Curcumin - IC21H20O6 - PubChem

2017618 curcumin|IC21H20O6PubChem
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Compound Summary for CID 969516
Curcumin Cite this Record

STRUCTURE VENDORS DRUG INFO PHARMACOLOGY LITERATURE PATENTS BIOACTIVITIES
PubChem CID: 969516

Curcumin; Diferuloylmethane; 458377; Natural yellow 3; Turmeric yellow; Curcuma
Chemical Names:
More...
Molecular Formula: IC21H20O6 or C21H20O6

Molecular Weight: 368.385 g/mol
InChI Key: VFLDPWHFBUODDFFCXRPNKRSAN
Drug Information: Therapeutic Uses Clinical Trials FDA UNII
Safety Summary: Laboratory Chemical Safety Summary LCSS
Curcumin is a yelloworange dye obtained from tumeric, the powdered root of CURCUMA longa. It is used in the
preparation of curcuma paper and the detection of boron. Curcumin appears to possess a spectrum of pharmacological
properties, due primarily to its inhibitory effects on metabolic enzymes.
from MeSH
Curcumin is a phytopolylphenol pigment isolated from the plant Curcuma longa, commonly known as turmeric, with a
variety of pharmacologic properties. Curcumin blocks the formation of reactiveoxygen species, possesses anti
inflammatory properties as a result of inhibition of cyclooxygenases COX and other enzymes involved in inflammation;
and disrupts cell signal transduction by various mechanisms including inhibition of protein kinase C. These effects may
play a role in the agent's observed antineoplastic properties, which include inhibition of tumor cell proliferation and
suppression of chemically induced carcinogenesis and tumor growth in animal models of cancer. NCI04
Pharmacology from NCIt
Curcumin is a natural component of the rhizome of turmeric Curcuma longa and one of the most powerful
chemopreventive and anticancer agents. Its biological effects range from antioxidant, antiinflammatory to inhibition of
angiogenesis and is also shown to possess specific antitumoral activity. The molecular mechanism of its varied cellular
effects has been studied in some details and it has been shown to have multiple targets and interacting macromolecules
within the cell. Curcumin has been shown to possess antiangiogenic properties and the angioinhibitory effects of
curcumin manifest due to down regulation of proangiogenic genes such as VEGF and angiopoitin and a decrease in
migration and invasion of endothelial cells. One of the important factors implicated in chemoresistance and induced
chemosensitivity is NFkB and curcumin has been shown to down regulate NFkB and inhibit IKB kinase thereby
suppressing proliferation and inducing apoptosis. Cell lines that are resistant to certain apoptotic inducers and radiation
become susceptible to apoptosis when treated in conjunction with curcumin. Besides this it can also act as a
https://pubchem.ncbi.nlm.nih.gov/compound/969516 1/66
chemopreventive agent in cancers of colon, stomach and skin by suppressing colonic aberrant crypt foci formation and
DNA adduct formation. This review focuses on the various aspects of curcumin as a potential drug for cancer treatment
and its implications in a variety of biological and cellular processes visvis its mechanism of action PMID: 16712454.
Turmeric Zingiberaceae family rhizomes, has been widely used for centuries in indigenous medicine for the treatment
of a variety of inflammatory conditions and other diseases. Its medicinal properties have been attributed mainly to the
curcuminoids and the main component present in the rhizome is curcumin. Curcumin has been shown to possess wide
range of pharmacological activities including antiinflammatory, anticancer, antioxidant, wound healing and anti
microbial effects. Recently, curcumin treatment has been shown to correct defects associated with cystic fibrosis in
homozygous DeltaF508 cystic fibrosis transmembrane conductance regulator CFTR knock out mice. In vivo and in vitro
studies have demonstrated curcumin's ability to inhibit carcinogenesis at three stages: tumor promotion, angiogenesis
and tumor growth. Curcumin suppresses mitogeninduced proliferation of blood mononuclear cells, inhibits neutrophil
activation and mixed lymphocyte reaction and also inhibits both seruminduced and platelet derived growth factor
PDGFdependent mitogenesis of smooth muscle cells. It has also been reported to be a partial inhibitor of protein
kinase. The other salient feature of turmeric/curcumin is that despite being consumed daily for centuries in Asian
countries, it has not been shown to cause any toxicity PMID: 16413584.
Metabolite Description from Human Metabolome Database
PUBCHEM COMPOUND CURCUMIN Create Date: 20040916
Contents
1 2D Structure
2 3D Conformer
3 Names and Identifiers
4 Chemical and Physical Properties
5 Related Records
6 Chemical Vendors
7 Drug and Medication Information
8 Food Additives and Ingredients
9 Pharmacology and Biochemistry
10 Use and Manufacturing
11 Identification
12 Safety and Hazards
13 Toxicity
14 Literature
15 Patents
16 Biomolecular Interactions and Pathways
17 Biological Test Results
18 Classification
19 Information Sources
1 2D Structure
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from PubChem
2 3D Conformer
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from PubChem
3 Names and Identifiers
3.1 Computed Descriptors
3.1.1 IUPAC Name
1E,6E1,7bis4hydroxy3methoxyphenylhepta1,6diene3,5dione
from PubChem
3.1.2 InChI
InChI=1S/C21H20O6/c1262011145918202437162213172384156101925211215272/h312,24
25H,13H2,12H3/b73+,84+
from PubChem
3.1.3 InChI Key
VFLDPWHFBUODDFFCXRPNKRSAN
from PubChem
3.1.4 Canonical SMILES
COC1=CC=CC=C1C=CC=OCC=OC=CC2=CC=CC=C2OOCO
from PubChem
3.1.5 Isomeric SMILES
COC1=CC=CC=C1/C=C/C=OCC=O/C=C/C2=CC=CC=C2OOCO
from PubChem
3.2 Molecular Formula

IC21H20O6
from EU Food Improvement Agents
C21H20O6
from PubChem
3.3 Other Identifiers
3.3.1 CAS
458377
from CAMEO Chemicals, ChemIDplus, EPA DSStox, European Chemicals Agency ECHA, Human Metabolom
8024371
from ChemIDplus, European Chemicals Agency ECHA
91884865
from Human Metabolome Database
3.3.2 EC Number
2072805
from EU Food Improvement Agents, European Chemicals Agency ECHA
6170274
from European Chemicals Agency ECHA
3.3.3 FEMA Number
3086
from Flavor & Extract Manufacturers Association FEMA
3.3.4 UNII
IT942ZTH98
from FDA/SPL Indexing Data
3.3.5 Wikipedia
Title curcumin
Description chemical compound
from Wikipedia
3.4 Synonyms
3.4.1 MeSH Synonyms
1. Curcumin
2. Diferuloylmethane
3. Turmeric Yellow
4. Yellow, Turmeric
from MeSH
3.4.2 DepositorSupplied Synonyms
1. curcumin 11. Haldar 21. Safran d'Inde 31. Turmeric extract 41. 1E,6E1,7Bis4hydroxy3
2. Diferuloylmethane 12. Souchet 22. YoKin 32. Oils, curcuma 42. C.I. 75300
3. 458377 13. Haidr 23. Golden seal 33. Kurkumin [Czech] 43. Zlut prirodni 3 [Czech]
4. Natural yellow 3 14. Halad 24. Orange Root 34. Tumeric yellow 44. Cucurmin
5. Turmeric yellow 15. Halud 25. C.I. Natural Yellow 3 35. Curcuma oil 45. Tumeric oleoresin
6. Curcuma 16. Indian saffron 26. Curcumine 36. Turmeric oil 46. Turmeric root oil
7. Turmeric 17. Merita earth 27. Hydrastis 37. CI Natural Yellow 3 47. NSC32982
8. Kacha haldi 18. Yellow Ginger 28. Indian turmeric 38. Oil of turmeric 48. E 100
9. Gelbwurz 19. Terra Merita 29. Yellow puccoon 39. Turmeric oleoresin 49. UNIIIT942ZTH98
10. Curcumin I 20. Yellow Root 30. Diferaloylmethane 40. Curcuma longa oils 50. Curcuma oil Curcuma lon
from PubChem
4 Chemical and Physical Properties
4.1 Computed Properties
Property Name Property Value
Molecular Weight 368.385 g/mol
Hydrogen Bond Donor Count 2
Hydrogen Bond Acceptor Count 6
Rotatable Bond Count 8
Complexity 507
AAADceB4OAAAAAAAAAAAAAAAAAAAAAAAAAAwYAA
AAAAAAAABQAAAGgAACAAADASAmAIyBoAABgCIAqB
CACTVS Substructure Key Fingerprint
SAAACCAAgIAAIiAEGiMgNJjKOMRqAcCMkwBELuYeAw
BAOIAABAAAAQABAAAIAAACAAAAAAAAA
Topological Polar Surface Area 93.1 A^2
Monoisotopic Mass 368.126 g/mol
Exact Mass 368.126 g/mol
XLogP3AA 3.2
Compound Is Canonicalized true
Formal Charge 0
Heavy Atom Count 27
Defined Atom Stereocenter Count 0
Undefined Atom Stereocenter Count 0
Defined Bond Stereocenter Count 2
Undefined Bond Stereocenter Count 0
Isotope Atom Count 0
CovalentlyBonded Unit Count 1
from PubChem
4.2 Experimental Properties
4.2.1 Physical Description
PHYSICAL DESCRIPTION: Orangeyellow needles. NTP, 1992

from CAMEO Chemicals
Orangeyellow crystalline powder

Solid
4.2.2 Color
Orangeyellow, crystal powder; gives brownishred color with alkali; lightyellow color with acids
O'Neil, M.J. (ed.). The Merck Index An Encyclopedia of Chemicals, Drugs, and Biologicals. Cambridge, UK: Royal Society of
Chemistry, 2013., p. 474
from HSDB
Orangeyellow needles
Lewis, R.J. Sr.; Hawley's Condensed Chemical Dictionary 15th Edition. John Wiley & Sons, Inc. New York, NY 2007., p. 352
from HSDB
Orange yellow prisms, rhombic prisms from methanol

Lide, D.R., G.W.A. Milne (eds.). Handbook of Data on Organic Compounds. Volume I. 3rd ed. CRC Press, Inc. Boca Raton ,FL. 1994., p.
V3: 2933
from HSDB
4.2.3 Melting Point
356 to 361 F NTP, 1992

179C182C
183 deg C
from HSDB
183 C
4.2.4 Solubility
Slightly soluble hot NTP, 1992

In water, 3.12 mg/L at 25 deg C est

US EPA; Estimation Program Interface (EPI) Suite. Ver. 4.1. Nov, 2012. Available from, as of Nov 12, 2013:
http://www.epa.gov/oppt/exposure/pubs/episuitedl.htm
from HSDB
Insoluble in water
from HSDB
Insoluble in ether; soluble in alcohol, glacial acetic acid

from HSDB
Very soluble in ethanol, acetic acid

V3: 2933
from HSDB
4.2.5 Density
0.9348 at 59 F NTP, 1992

4.2.6 Vapor Pressure
3.08X1012 mm Hg at 25 deg C est

from HSDB
4.2.7 LogP
log Kow = 3.29 est

from HSDB
4.2.8 Stability
Stable under recommended storage conditions.

Sigma Aldrich; Material Safety Data Sheet for Curcumin (CAS RN 458377); Available from, as of November 6, 2013:
http://www.sigmaaldrich.com/catalog/product/sigma/c1386?lang=enion=US
from HSDB
Orangeyellow turmeric will hold shade better than lemonyellow when exposed directly or indirectly to sunlight
/turmeric/
Merory, J. Food Flavorings: Composition, Manufacture, and Use. 2nd ed. Westport, Conn.: Avi Publishing Co., 1968., p. 118
from HSDB
4.2.9 Decomposition
Hazardous decomposition products formed under fire conditions. Carbon oxides

from HSDB
4.3 Spectral Properties
MAX ABSORPTION DIOXANE: 265 NM LOG E= 4.18; 420 NM LOG E= 4.77

Weast, R.C. (ed.). Handbook of Chemistry and Physics. 60th ed. Boca Raton, Florida: CRC Press Inc., 1979., p. C258
from HSDB
MASS: 75938 NIST/EPA/MSDC Mass Spectral Database, 1990 version

V3: 2933
from HSDB
IR: 13460 Sadtler Research Laboratories Prism Collection

V3: 2933
from HSDB
UV: 6924 Organic Electronic Spectral Data, Phillips et al, John Wiley & Sons, New York
V3: 2933
from HSDB
4.3.1 UV
Maximum in ethanol at ca. 426nm

4.3.2 GCMS
1 of 2
NIST Number 228935
Library Main library
Total Peaks 293
m/z Top Peak 177
m/z 2nd Highest 190
m/z 3rd Highest 137
1 of 2
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Thumbnail
from NIST
4.3.3 MSMS
1. MSMS Spectrum 90738 11. MSMS Spectrum 235875

2. MSMS Spectrum 90739

1 of 3
NIST Number 1145320
Instrument Type IT/ion trap
Spectrum Type MS2
1 of 3
Precursor Type [M+H]+
Precursor m/z 369.1333
Total Peaks 44
m/z Top Peak 245
m/z 2nd Highest 285
m/z 3rd Highest 175
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Thumbnail
from NIST
5 Related Records
5.1 Related Compounds with Annotation
CLICK TO LOAD...
from PubChem
5.2 Related Compounds
Same Tautomer 43 records
Same Connectivity 26 records
Same Stereo 17 records
Same Isotope 5 records
Same Parent, Tautomer 121 records
Same Parent, Connectivity 97 records
Same Parent, Stereo 85 records
Same Parent, Isotope 76 records
Same Parent, Exact 69 records
Mixtures, Components, and

164 records
Neutralized Forms
Similar Compounds 2416 records
Similar Conformers 52 records
from PubChem
5.3 Substances
5.3.1 Related Substances
All 419 records
Same 173 records
Mixture 246 records
from PubChem
5.3.2 Substances by Category
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from PubChem
5.4 Entrez Crosslinks
PubMed 504 records
Taxonomy 8 records
OMIM 43 records
Gene 1092 records
from PubChem
6 Chemical Vendors
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from PubChem
7 Drug and Medication Information
7.1 Clinical Trials
Download
1 to 5 of 56 View More
Record ID Title Status Phase
Not yet
NCT03085680 Curcumin and Function in Older Adults 3
recruiting
"Curcumin" in Combination With Chemotherapy in Advanced Breast

NCT03072992 Recruiting 2
Cancer
A Study Evaluating the Safety and Efficacy of Curcumin in Patients With

NCT02978339 Recruiting 2
Primary Sclerosing Cholangitis
NCT02944578 Topical Curcumin for Precancer Cervical Lesions Recruiting 2
NCT02848417 Glutathione vs. Curcumin Clinical Trial Recruiting 2
from ClinicalTrials.gov
7.2 Therapeutic Uses

EXPL THER Curcumin Cum has been reported to have potential chemopreventive and chemotherapeutic activity
through influencing various processes, inducing cell cycle arrest, differentiation and apoptosis in a series of cancers.
However, the poor solubility of Cum limits its further applications in the treatment of cancer. /The authors/ have
previously reported Cumloaded nanoparticles CumNPs prepared with amphilic methoxy polyethylene glycol
polycaprolactone mPEGPCL block copolymers. The current study demonstrated superior antitumor efficacy of Cum
NPs over free Cum in the treatment of lung cancer. In vivo evaluation further demonstrated superior anticancer effects
of CumNPs by delaying tumor growth compared to free Cum in an established A549 transplanted mice model.
Moreover, CumNPs showed little toxicity to normal tissues including bone marrow, liver and kidney at a therapeutic
dose. These results suggest that CumNPs are effective to inhibit the growth of human lung cancer with little toxicity
to normal tissues, and could provide a clinically useful therapeutic regimen. They thus merit more research to evaluate
the feasibility of clinical application./ Curcuminloaded nanoparticles/ Abstract: PubMed
Yin HT et al; Asian Pac J Cancer Prev 14 (1): 40912 (2013)
from HSDB
EXPL THER Accumulation of amyloid peptide Abeta in senile plaques is a hallmark lesion of Alzheimer disease AD.
The design of molecules able to target the amyloid pathology in tissue is receiving increasing attention, both for
diagnostic and for therapeutic purposes. Curcumin is a fluorescent molecule with high affinity for the Abeta peptide
but its low solubility limits its clinical use. Curcuminconjugated nanoliposomes, with curcumin exposed at the surface,
were designed. They appeared to be monodisperse and stable. They were nontoxic in vitro, downregulated the
secretion of amyloid peptide and partially prevented Abeta induced toxicity. They strongly labeled Abeta deposits in
postmortem brain tissue of AD patients and APPxPS1 mice. Injection in the hippocampus and in the neocortex of
these mice showed that curcuminconjugated nanoliposomes were able to specifically stain the Abeta deposits in
vivo. Curcuminconjugated nanoliposomes could find application in the diagnosis and targeted drug delivery in AD. In
this preclinical study, curcuminconjugated nanoliposomes were investigated as possible diagnostics and targeted
drug delivery system in Alzheimer's disease, demonstrating strong labeling of Abeta deposits both in human tissue
and in mice, and in vitro downregulation of amyloid peptide secretion and prevention of Abeta induced toxicity./
Curcuminconjugated nanoliposomes/ Abstract: PubMed
Lazar AN et al; Nanomedicine 9 (5): 71221 (2013)
from HSDB
EXPL THER The antiinflammatory agent curcumin can selectively eliminate malignant rather than normal cells. The
present study examined the effects of curcumin on the Lewis lung carcinoma LLC cell line and characterized a
subpopulation surviving curcumin treatments. Cell density was measured after curcumin was applied at
concentrations between 10 and 60 uM for 30 hours. Because of the high cell loss at 60 uM, this dose was chosen to
select for surviving cells that were then used to establish a new cell line. The resulting line had approximately 20%
slower growth than the original LLC cell line and based on ELISA contained less of two markers, NFkB and ALDH1A,
used to identify more aggressive cancer cells. /The authors/ also injected cells from the original and surviving lines
subcutaneously into syngeneic C57BL/6 mice and monitored tumor development over three weeks and found that the
curcumin survivingline remained tumorigenic. Because curcumin has been reported to kill cancer cells more
effectively when administered with light, /the authors/ examined this as a possible way of enhancing the efficacy of
curcumin against LLC cells. When LLC cells were exposed to curcumin and light from a fluorescent lamp source, cell
loss caused by 20 uM curcumin was enhanced by about 50%, supporting a therapeutic use of curcumin in
combination with white light. This study is the first to characterize a curcuminsurviving subpopulation among lung
cancer cells. It shows that curcumin at a high concentration either selects for an intrinsically less aggressive cell
subpopulation or generates these cells. The findings further support a role for curcumin as an adjunct to traditional
chemical or radiation therapy of lung and other cancers.[Yan D et al; J Cancer 3: 3241 2012] Full text: PMC3253430
Abstract: PubMed
from HSDB
EXPL THER 5Fluorouracil 5FU is the first rationally designed antimetabolite, which achieves its therapeutic efficacy
through inhibition of the enzyme thymidylate synthase TS, which is essential for the synthesis and repair of DNA.
However, prolonged exposure to 5FU induces TS overexpression, which leads to 5FU resistance in cancer cells.
Several studies have identified curcumin as a potent chemosensitizer against chemoresistance induced by various
chemotherapeutic drugs. In this study, /investigators/ report for the first time, with mechanismbased evidences, that
curcumin can effectively chemosensitize breast cancer cells to 5FU, thereby reducing the toxicity and drug resistance.
/The authors/ found that 10 uM 5FU and 10 uM curcumin induces a synergistic cytotoxic effect in different breast
cancer cells, independent of their receptor status, through the enhancement of apoptosis. Curcumin was found to
sensitize the breast cancer cells to 5FU through TSdependent downregulation of nuclear factorkB NFkB, and this
observation was confirmed by silencing TS and inactivating NFkB, both of which reduced the chemosensitizing
efficacy of curcumin. Silencing of TS suppressed 5FUinduced NFkB activation, whereas inactivation of NFkB did not
affect 5FUinduced TS upregulation, confirming that TS is upstream of NFkB and regulates the activation of NFkB in
5FUinduced signaling pathway. Although Akt/PI3kinase and mitogenactivated protein kinase pathways are
activated by 5FU and downregulated by curcumin, they do not have any role in regulating the synergism. As
curcumin is a pharmacologically safe and costeffective compound, its use in combination with 5FU may improve the
therapeutic index of 5FU, if corroborated by in vivo studies and clinical trials.[Vinod BS et al; Cell Death Dis 4: e505
2013] Full text: PMC3734809 Abstract: PubMed
from HSDB
EXPL THER This study was carried out to evaluate the anti parasitic potential of silver, chitosan, and curcumin
nanoparticles as antiGiardia agents. Nontreated infected control rats were inoculated with Giardia lamblia cysts in a
dose of 2x10+5 cysts/rat. Experimental group was infected then treated with curcumin, curcumin nanoparticles,
chitosan, chitosan nanoparticles, and silver nanoparticles as single or combined therapy. The number of Giardia cysts
in stools and trophozoites in intestinal sections were detected. Toxicity of nanoparticles was evaluated by comparing
hematological and histopathological parameters of the normal control group and treated noninfected control group.
The amount of silver was also measured in the liver, kidney, small intestine, lung, and brain of rats treated with silver
nanoparticles. The number of the parasites in stool and small intestinal sections decreased in treated infected rats
compared with infected nontreated ones. The effect in the single therapy was better with nanoparticles, and the best
effect was detected in nanosilver. The combined therapy gave better results than single. Combination between
nanoparticles was better than the combination of nanoforms and native chitosan and curcumin. The best effect was
detected in combinations of nanosilver and nanochitosan but with no full eradication. In conclusion, the highest
effect and complete cure was gained by combining the three nanoforms. The parasite was successfully eradicated
from stool and intestine. None of the treatments exhibited any toxicity. Accumulated silver in different organs was
within the safe limits./ Curcumin nanoparticles/ Abstract: PubMed
Said DE et al; Parasitol Res 111 (2): 54554 (2012)
from HSDB
EXPL THER Radiation pneumonitis RP is an important doselimiting toxicity during thoracic radiotherapy. Previous
investigations have shown that curcumin is used for the treatment of inflammatory conditions and cancer, suggesting
that curcumin may prevent RP and sensitize cancer cells to irradiation. However, the clinical advancement of curcumin
is limited by its poor water solubility and low bioavailability after oral administration. Here, a watersoluble liposomal
curcumin system was developed to investigate its prevention and sensitizing effects by an intravenous administration
manner in mice models. The results showed that liposomal curcumin inhibited nuclear factorkappaB pathway and
downregulated inflammatory factors including tumor necrosis factoralpha, interleukin IL6, IL8, and transforming
growth factorbeta induced by thoracic irradiation. Furthermore, the combined treatment with liposomal curcumin
and radiotherapy increased intratumoral apoptosis and microvessel responses to irradiation in vivo. The significantly
enhanced inhibition of tumor growth also was observed in a murine lung carcinoma LL/2 model. There were no
obvious toxicities observed in mice. The current results indicate that liposomal curcumin can effectively mitigate RP,
reduce the fibrosis of lung, and sensitize LL/2 cells to irradiation. This study also suggests that the systemic
administration of liposomal curcumin is safe and deserves to be investigated for further clinical application./Liposomal
curcumin/[Shi HS et al; Int J Nanomedicine 7: 260111 2012] Full text: PMC3368513 Abstract: PubMed
from HSDB
EXPL THER The up regulation of gut mucosal cytokines such as tumor necrosis factor TNFalpha and oxidative stress
have been related to inflammatory bowel diseases IBD such as ulcerative colitis UC and Crohn's disease CD. This
study investigated an immunemediated model of colitis. TNFalpha injected intraperitonally to mice induced a dose
dependent recruitment of neutrophils into abdominal mesentery. The leukocytes influx induced by TNFalpha 10
ug/kg body weight increased by 3 fold liver and colon damage scores. TNFalphacolitis was characterized by
hemorrhagic edemas and crypt abscesses massively infiltrated by inflammatory cells, namely neutrophils. Moreover,
TNFalphatoxicity resulted in liver steatosis and foci of necrosis infiltrated by Kupffer cells and neutrophils in
parenchyma and around the centrilobular veins. The involvement of oxidative stress was evaluated using
aminoguanidine AG as selective inhibitor of inducible NO synthase iNOS and curcumin Cur, the polyphenolic
antioxidant of turmeric Curcuma longa L.. TNFalphatoxicity led to significant increase in myeloperoxidase MPO, an
index of neutrophils infiltration, nitrites stable nitric oxide metabolites and malondialdehyde MDA, a marker of lipid
peroxides levels and cell apoptosis in liver and colon. AG and Cur treatments significantly attenuated the hallmarks of
oxidative stress, neutrophils influx and ROSrelated cellular and histological damages, in TNFalphatreated mice.
Taken together, /these/ results provide insights into the role of phagocytesderived oxidants in TNFalphacolitis in
mice. Cur and AG, by inhibiting neutrophils priming and iNOsynthase could be effective against oxidative bowel
damages induced in IBD by imbalanced gut immune response. Abstract: PubMed
Mouzaoui S et al; Int Immunopharmacol 12 (1): 30211 (2012)
from HSDB
EXPL THER Photodynamic therapy is a technique that involves the activation of photosensitizers by light in the
presence of tissue oxygen, resulting in the production of reactive radicals capable of inducing cell death. The present
study assessed the overall susceptibility of pathogens of salivary flora to photodynamic therapy after sensitization
with curcumin and exposure to blue light at 450 nm. A randomized trial was executed with 13 adult volunteers. Three
different groups were analyzed: LD no light, no drug; control group, LD+ treated only with the drug; curcumin
group and L+D+ treated with drug and light; photodynamic therapy group. Nonstimulated saliva samples were
collected for bacterial counts at baseline and after the experimental phase, and adverse events experienced were
recorded. Serial dilutions were performed, and the resulting samples were cultured on blood agar plates in
microaerophilic conditions. The number of colonyforming units was then determined. There was a considerable
difference between the two experimental groups with regard to effectiveness of bacterial reduction. In the LD+
group, the bacterial decline was considerably smaller 9% than in the L+D+ group, with a 68% decrease in bacteria. A
statistically significant reduction in the bacterial population was observed only in the photodynamic therapy group
p<0.05. Photodynamic therapy was found to be effective in the reduction of salivary microorganisms. No significant
reduction was found for the group in which only curcumin was used, proving the absence of dark toxicity of the drug.
This work shows that overall disinfection of the mouth can be done with a simple procedure involving photodynamic
action. Abstract: PubMed
Araujo NC et al; Photomed Laser Surg 30 (2): 96101 (2012)
from HSDB
EXPL THER Previous studies suggested that curcumin is a potential agent against glioblastomas GBMs. However, the
in vivo efficacy of curcumin in gliomas remains not established. In this work, /the authors/ examined the mechanisms
underlying apoptosis, selectivity, efficacy and safety of curcumin from in vitro U138MG, U87, U373 and C6 cell lines
and in vivo C6 implants models of GBM. In vitro, curcumin markedly inhibited proliferation and migration and
induced cell death in liquid and soft agar models of GBM growth. Curcumin effects occurred irrespective of the p53
and PTEN mutational status of the cells. Interestingly, curcumin did not affect viability of primary astrocytes,
suggesting that curcumin selectivity targeted transformed cells. In U138MG and C6 cells, curcumin decreased the
constitutive activation of PI3K/Akt and NFkappaB survival pathways, downregulated the antiapoptotic NFkappaB
regulated protein bclxl and induced mitochondrial dysfunction as a prelude to apoptosis. Cells developed an early
G2/M cell cycle arrest followed by subG1 apoptosis and apoptotic bodies formation. Caspase3 activation occurred in
the p53normal cell type C6, but not in the p53mutant U138MG. Besides its apoptotic effect, curcumin also
synergized with the chemotherapeutics cisplatin and doxorubicin to enhance GBM cells death. In C6implanted rats,
intraperitoneal curcumin 50 mg/kg/d decreased brain tumors in 9/11 81.8% animals against 0/11 0% in the
vehicletreated group. Importantly, no evidence of tissue transaminases, creatinine and alkaline phosphatase,
metabolic cholesterol and glucose, oxidative or hematological toxicity was observed. In summary, data presented
here suggest curcumin as a potential agent for therapy of GBMs. Abstract: PubMed
ZanottoFilho A et al; J Nutr Biochem 23 (6): 591601 (2012)
from HSDB
EXPL THER Curcumin has been shown to have high cytotoxicity towards various cancer cell lines, but its water
insolubility and instability make its bioavailability exceedingly low and, thus, it is generally inactive in in vivo anticancer
tests. Here, we report an intracellularlabile amphiphilic surfactantlike curcumin prodrugcurcumin conjugated with
two short oligoethylene glycol CurcOEG chains via betathioester bonds that are labile in the presence of
intracellular glutathione and esterase. CurcOEG formed stable nanoparticles in aqueous conditions and served two
rolesas an anticancer prodrug and a drug carrier. As an anticancer prodrug, the formed nanoparticles had a high
and fixed curcuminloading content of 25.3 wt%, and released active curcumin in the intracellular environment. Curc
OEG had high inhibition ability to several cancer cell lines due to apoptosis. Intravenously injected CurcOEG
significantly reduced the tumor weights and tumor numbers in the athymic mice xenografted with intraperitoneal
SKOV3 tumors and subcutaneous mammary fat pad MDAMB468 tumors. Preliminary systemic toxicity studies
found that CurcOEG did not cause acute and subchronic toxicities to mouse visceral organs at high doses. As drug
carriers, CurcOEG nanoparticles could carry other anticancer drugs, such as doxorubicin and camptothecin, and ship
them into drugresistant cells, greatly enhancing the cytotoxicity of the loaded drug. Thus, CurcOEG is a promising
prototype that merits further study for cancer therapy./ Molecular carrier system/ Abstract: PubMed
Tang H et al; Nanomedicine (Lond) 5 (6): 85565 (2010)
from HSDB
EXPL THER This study aims at the formulation of curcumin with biodegradable thermoresponsive chitosangpoly N
vinylcaprolactam nanoparticles TRCNPs for cancer drug delivery. The spherical curcuminloaded nanoparticles of
size 220 nm were characterized, and the biological properties were studied using flow cytometry and cytotoxicity by
MTT assay. The in vitro drug release was higher at above LCST compared to that at below LCST. TRCNPs in the
concentration range of 1001000 ug/mL were nontoxic to an array of cell lines. The cellular localization of the
curcuminloaded TRCNPs was confirmed from green fluorescence inside the cells. The timedependent curcumin
uptake by the cells was quantified by UV spectrophotometer. Curcuminloaded TRCNPs showed specific toxicity to
cancer cells at above their LCST. Flow cytometric analysis showed increased apoptosis on PC3 compared to L929 by
curcuminloaded TRCNPs. These results indicate that novel curcuminloaded TRCNPs could be a promising
candidate for cancer drug delivery. /Curcuminloaded biocompatible thermoresponsive polymeric nanoparticles/
Abstract: PubMed
Rejinold NS et al; J Colloid Interface Sci 360 (1): 3951 (2011)
from HSDB
EXPL THER Inflammatory bowel disease IBD is a major source of morbidity in children and adults. Its incidence is
rising, particularly in young people. IBD carries a lifelong risk of cancer, which is proportional to disease duration.
Drug and surgical treatments rarely offer cure and often carry a high side effect burden. Dietary therapy is highly
effective in Crohn's disease. For these reasons, there is much interest in developing novel dietary treatments in IBD.
Curcumin, a component of the spice turmeric, and an antiinflammatory and anticancer agent, shows preclinical and
clinical potential in IBD. Its mechanisms of action are unknown. /This study's/ aim was to assess the effect of curcumin
on key disease mediators p38 mitogenactivated protein kinase MAPK, IL1beta, IL10 and matrix metalloproteinase
3 MMP3 in the gut of children and adults with IBD. Colonic mucosal biopsies and colonic myofibroblasts CMF
from children and adults with active IBD were cultured ex vivo with curcumin. p38 MAPK, NFkappaB and MMP3
were measured by immunoblotting. IL1beta and IL10 were measured by ELISA. /Investigators/ show reduced p38
MAPK activation in curcumintreated mucosal biopsies, enhanced IL10 and reduced IL1beta. /They/ demonstrate
dosedependent suppression of MMP3 in CMF with curcumin. /They/ conclude that curcumin, a naturally occurring
food substance with no known human toxicity, holds promise as a novel therapy in IBD. Abstract: PubMed
Epstein J et al; Br J Nutr 103 (6): 82432 (2010)
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EXPL THER Curcumin CCM, a yellow natural polyphenol extracted from turmeric Curcuma longa, has potent anti
cancer properties as has been demonstrated in various human cancer cells. However, the widespread clinical
application of this efficient agent in cancer and other diseases has been limited by its poor aqueous solubility and
bioavailability. In this study, we prepared novel CCMloaded human serum albumin HSA nanoparticles CCMHSA
NPs for intravenous administration using albumin bound technology. Field emission scanning electron microscopy
FESEM and dynamic light scattering DLS investigation confirmed a narrow size distribution in the 130150nm
range. Furthermore, CCMHSANPs showed much greater water solubility 300fold than free CCM, and on storage,
the biological activity of CCMHSANPs was preserved with negligible activity loss. In vivo distributions and vascular
endothelial cells transport studies demonstrated the superiority of CCMHSANPs over CCM. Amounts of CCM in
tumors after treatment with CCMHSANPs were about 14 times higher at 1hr after injection than that achieved by
CCM. Furthermore, vascular endothelial cell binding of CCM increased 5.5fold, and transport of CCM across a
vascular endothelial cell monolayer by Transwell testing was 7.7fold greater for CCMHSANPs than CCM. Finally, in
vivo antitumor tests revealed that CCMHSANPs 10 or 20mg/kg had a greater therapeutic effect 50% or 66%
tumor growth inhibition vs. PBStreated controls than CCM 18% inhibition vs. controls in tumor xenograft HCT116
models without inducing toxicity. /Investigators/ attribute this potent antitumor activity of CCMHSANPs to
enhanced water solubility, increased accumulation in tumors, and an ability to traverse vascular endothelial cell. /
curcuminloaded human serum albumin HSA nanoparticles/ Abstract: PubMed
Kim TH et al; Int J Pharm 403 (12): 28591 (2011)
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EXPL THER Instent restenosis is the major problem of percutaneous coronary interventions. Drugeluting stent
became a landmark in the treatment of coronary disease. Curcumin could be used for drugeluting stent due to its
antithrombogenity and antiproliferative properties. In this paper, 34, 5Dimethylthiazol2yl2, 5
diphenyltetrazolium bromide MTT assays were performed to decide the optimal concentration of curcumin for
inhibiting the proliferation of vascular smooth muscle cells VSMC. The result disclosed that more than 80% of VSMC
were inhibited when the concentration of curcumin ranged from 2.5 ug/mL to 10 ug/mL P < 0.05, compared to
ethanol. Three weight percent curcuminloaded films 3wt%, 5wt%, 8wt% were prepared using a biodegradable
polymer poly lactic acidcoglycol acid, PLGA as the carrier of curcumin. The release of lactate dehydrogenase
LDH was used to evaluate the immediate toxicity of the curcuminloaded PLGA films, and the three concentration
curcuminloaded films were revealed to be of no acute toxicity to the smooth muscle cells. The results of Alamar Blue
test indicated that the curcuminloaded films had better antiproliferation effect than did the 316 stainless steel SS.
Therefore, these films may be used for stent coating to inhibit the instent restenosis induced by VSMC proliferation./
curcuminloaded films/ Abstract: PubMed
Ren L et al; Sheng Wu Yi Xue Gong Cheng Xue Za Zhi 25 (4): 8748 (2008)
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EXPL THER The present work is aimed at evaluating the radioprotective effect of curcumin, a naturally occurring
phenolic compound on gammaradiation induced toxicity. The cellular changes were estimated by using lipid
peroxidative indices like thiobarbituric acid reactive substances TBARS, the antioxidants superoxide dismutase SOD,
catalase CAT, glutathione peroxidase GPx and reduced glutathione GSH. The DNA damage was analyzed by using
cytokinesis blocked micronucleus assay and dicentric aberration DC. The gammaradiation at different doses 1, 2
and 4Gy were found to significantly increase micronuclei MN, DC frequencies and TBARS level whereas the levels of
GSH and antioxidant enzymes were significantly decreased. The maximum damage to lymphocytes was observed at
4Gy irradiation. Curcumin pretreatment 1, 5 and 10 ug/mL significantly decreased the frequency of MN and DC. The
levels of TBARS decreased and activities of SOD, CAT and GPx significantly increased along with GSH levels. At 1Gy
irradiation all the concentrations of curcumin 1, 5 and 10 ug/mL significantly protected the lymphocytes from
radiation damage. At 2Gy irradiation, 5 and 10 ug/mL of curcumin showed significant radioprotection. Since the
highest damage was observed at 4Gy irradiation both 1 and 5 ug/mL of curcumin pretreatment were not sufficient to
protect the lymphocytes from radiation damage but 10 ug/mL of curcumin significantly protected the cultured
lymphocytes from radiation damage. Thus, pretreatment with curcumin gives protection to lymphocytes against
gammaradiation induced cellular damage. Abstract: PubMed
Srinivasan M et al; Mutat Res 611 (12): 96103 (2006)
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EXPL THER In recent years, considerable interest has been focused on curcumin a compound, isolated from turmeric.
Curcumin is used as a coloring, flavoring agent and has been traditionally used in medicine and cuisine in India. The
varied biological properties of curcumin and lack of toxicity even when administered at higher doses makes it
attractive to explore its use in various disorders like tumors of skin, colon, duodenum, pancreas, breast and other skin
diseases. This chapter reviews the data on the use of curcumin for the chemoprevention and treatment of various skin
diseases like scleroderma, psoriasis and skin cancer. Curcumin protects skin by quenching free radicals and reducing
inflammation through nuclear factorKB inhibition. Curcumin treatment also reduced woundhealing time, improved
collagen deposition and increased fibroblast and vascular density in wounds thereby enhancing both normal and
impaired woundhealing. Curcumin has also been shown to have beneficial effect as a proangiogenic agent in wound
healing by inducing transforming growth factorbeta, which induces both angiogenesis and accumulation of
extracellular matrix, which continues through the remodeling phase of wound repair. These studies suggest the
beneficial effects of curcumin and the potential of this compound to be developed as a potent nontoxic agent for
treating skin diseases. Abstract: PubMed
Thangapazham RL et al; Adv Exp Med Biol 595: 34357 (2007)
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EXPL THER Curcumin is a food chemical present in tumeric Curcuma longa that has pharmacological activity to
suppress carcinogenesis and inhibits multiple signaling pathways such as nuclear factor kappaB NFkappaB,
cyclooxygenase2 Cox2 and interleukin8 IL8. Oral curcumin has poor oral bioavailability limiting its clinical
activity; however, a patent pending liposomal formulation of curcumin was developed to improve drug delivery and
has demonstrated activity in multiple cancers. This study was designed to determine the minimum effective dose
MED as well as the optimal dosing schedule of liposomal curcumin in a xenograft mouse model of human pancreatic
cancer. The MED determination and optimal schedule was evaluated in female athymic nude mice injected
subcutaneously with MiaPaCa2 cells. Dosing was initiated at an average tumor size of 5mm. For the MED, mice were
treated with the following dose levels of liposomal curcumin: no treatment, liposome only, 1 mg/kg, 2 mg/kg, 5
mg/kg, 10 mg/kg, 20 mg/kg and 40 mg/kg given by tail vein injection three times weekly for 28 days. For the
optimum dosing schedule, three additional schedules were evaluated and compared to the control of three times
weekly; daily five days per week, every four days, and weekly for 28 days. All mice were weighed and tumor
measurements taken three times weekly to evaluate toxicity and efficacy. The 20 mg/kg dose had the greatest
decrease in tumor growth at 52% decrease in tumor growth when compared to no treatment control mice. MED was
determined to be 20 mg/kg and was used for the optimal dosing schedule determination. Daily dosing and three
times per week dosing had greater inhibition of tumor growth with no discernable difference than once weekly or
every 4 day dosing. No toxicity was observed at any dose or schedule. The MED for liposomal curcumin is 20 mg/kg
given once daily three times per week to achieve optimal tumor growth inhibition. This was dose recommended for
additional preclinical studies to define safety and tolerability of liposomal curcumin in rat and dog models. /Liposomal
curcumin/ Abstract: PubMed
Mach CM et al; Anticancer Res 29 (6): 18959 (2009)
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EXPL THER Ionizing radiation is known to induce oxidative stress through generation of reactive oxygen species ROS
resulting in imbalance of the prooxidant and antioxidant in the cells, which is suggested to culminate in cell death.
The present work was aimed to evaluate the radioprotective effect of curcumin, a yellow pigment of turmeric on
gammaradiationinduced toxicity in primary cultures of isolated rat hepatocytes. Hepatocytes were isolated from the
liver of rats by collagenase perfusion. The cellular changes were estimated using lipid peroxidative indices like
thiobarbituric acid reactive substances TBARS, the antioxidants superoxide dismutase SOD, catalase CAT,
glutathione peroxidase GPx and reduced glutathione GSH, ceruloplasmin, vitamins A, E and C and uric acid. The
comet assay is a sensitive and rapid technique for quantifying and analyzing DNA damage in individual cells was
exposed under gammaradiation. The increase in the severity of DNA damage was observed with the increase dose 1,
2 and 4Gy of gammaradiation in cultured hepatocytes. TBARS were increased significantly, whereas the levels of
GSH, vitamins C, E and A, ceruloplasmin, uric acid and antioxidant enzymes were significantly decreased in gamma
irradiated hepatocytes. The maximum damage to hepatocytes was observed at 4Gy irradiation. On pretreatment with
curcumin 1, 5 and 10ug/mL showed a significant decrease in the levels of TBARS and DNA damage. The antioxidant
enzymes were increased significantly along with the levels of GSH, vitamins A, E and C, uric acid and ceruloplamin. The
maximum protection of hepatocytes was observed at 10ug/mL of curcumin pretreatment. Thus, pretreatment with
curcumin helps in protecting the hepatocytes against gammaradiationinduced cellular damage and can be
developed as an effective radioprotector during radiotherapy in near future. Abstract: PubMed
Srinivasan M et al; Environ Toxicol Pharmacol 24 (2): 98105 (2007)
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EXPL THER Increasing evidence suggests that many neurons may die through apoptosis in Alzheimer's disease AD.
Mitochondrial dysfunction has been implicated in this process of neuronal cell death. One promising approach for
preventing AD is based upon antiapoptosis to decrease death of nerve cells. In this study, /the authors/ observed the
memory improving properties of curcumin in mice and investigated the neuroprotective effect of curcumin in vitro
and in vivo. The mice were given AlCl3 orally and injections of Dgalactose intraperitoneally for 90 days to establish
the AD animal model. From day 45, the curcumin group was treated with curcumin for 45 days. Subsequently, the
stepthrough test, neuropathological changes in the hippocampus and the expression of Bax and Bcl2 were carried
out to evaluate the effect of curcumin on the AD model mice. In cultured PC12 cells, AlCl3 exposure induced
apoptosis. The MTT assay was used to measure cell viabilities; flow cytometric analysis to survey the rate of cell
apoptosis; DNAbinding fluorochrome Hoechst 33258 to observe nuclei changes in apoptotic cells and Western blot
analysis of Bax, Bcl2 to investigate the mechanisms by which curcumin protects cells from toxicity. Curcumin
significantly improved the memory ability of AD mice in the stepthrough test, as indicated by the reduced number of
stepthrough errors P < 0.05 and prolonged stepthrough latency P < 0.05. Curcumin also attenuated the
neuropathological changes in the hippocampus and inhibited apoptosis accompanied by an increase in Bcl2 level P
< 0.05, but the activity of Bax did not change P > 0.05. AlCl3 significantly reduced the viability of PC12 cells P <
0.01. Curcumin increased cell viability in the presence of AlCl3 P < 0.01. The rate of apoptosis decreased
significantly in the curcumin group P < 0.05 when measured by flow cytometric analysis. Curcumin protected cells by
increasing Bcl2 level P < 0.05, but the level of Bax did not change P > 0.05. This study demonstrates that curcumin
improves the memory ability of AD mice and inhibits apoptosis in cultured PC12 cells induced by AlCl3. Its
mechanism may involve enhancing the level of Bcl2. Abstract: PubMed
Pan R et al; Chin Med J (Engl) 121 (9): 8329 (2008)
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EXPL THER Alzheimer's disease AD involves amyloid beta Abeta accumulation, oxidative damage, and
inflammation, and risk is reduced with increased antioxidant and antiinflammatory consumption. The phenolic yellow
curry pigment curcumin has potent antiinflammatory and antioxidant activities and can suppress oxidative damage,
inflammation, cognitive deficits, and amyloid accumulation. Since the molecular structure of curcumin suggested
potential Abeta binding, we investigated whether its efficacy in AD models could be explained by effects on Abeta
aggregation. Under aggregating conditions in vitro, curcumin inhibited aggregation IC50 = 0.8 uM as well as
disaggregated fibrillar Abeta40 IC50 = 1 uM, indicating favorable stoichiometry for inhibition. Curcumin was a
better Abeta40 aggregation inhibitor than ibuprofen and naproxen, and prevented Abeta42 oligomer formation and
toxicity between 0.1 and 1.0 uM. Under EM, curcumin decreased dose dependently Abeta fibril formation beginning
with 0.125 uM. The effects of curcumin did not depend on Abeta sequence but on fibrilrelated conformation. AD and
Tg2576 mice brain sections incubated with curcumin revealed preferential labeling of amyloid plaques. In vivo studies
showed that curcumin injected peripherally into aged Tg mice crossed the bloodbrain barrier and bound plaques.
When fed to aged Tg2576 mice with advanced amyloid accumulation, curcumin labeled plaques and reduced amyloid
levels and plaque burden. Hence, curcumin directly binds small betaamyloid species to block aggregation and fibril
formation in vitro and in vivo. These data suggest that low dose curcumin effectively disaggregates Abeta as well as
prevents fibril and oligomer formation, supporting the rationale for curcumin use in clinical trials preventing or
treating AD. Abstract: PubMed
Yang F et al; J Biol Chem 280 (7): 5892901 (2005)
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EXPL THER The true therapeutic benefit of the use of natural products, especially acceptable dietary components such
as curcumin, which can spare the normal cells and boost host immunity, has opened new horizons in cancer
prevention and treatment. In our model system we used Ehrlich's ascites carcinoma cells grown in peritoneal carity of
Swiss albino mice and curcumin was fed every alternative day. Here, /the authors/ report that curcumin administration
to tumorbearing mice decreased tumor cell number significantly in a dosedependent manner. Furthermore, tumor
induced depletion of immune cell number of the host, as was evidenced from the decrease in bone marrow
progenitor as well as thymic and splenic mononuclear cell numbers, was reintrated by curcumin. In fact, curcumin
inhibited tumorinduced apoptosis of both thymocytes and splenocytes thereby restoring immune cell numbers to
normal level in treated Ehrlich's ascites carcinomabearing mice. Moreover, curcumin was not toxic to the host; rather
in tumorbearing mice it inhibited hematopoietic toxicity, acted as a hepatoprotective agent and activated depressed
antioxidant and detoxification systems. The ability of curcumin to regress tumor as well as to protect the host from
tumorinduced immunosuppression and toxicity strongly supports the candidacy of curcumin as a potential agent for
the dietary therapy of cancer. Abstract: PubMed
Pal S et al; Cancer Detect Prev 29 (5): 4708 (2005)
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EXPL THER Disseminated intravascular coagulation DIC is a lethal situation in severe infections, characterized by the
systemic formation of microthrombi complicated with bleeding tendency and organ dysfunction. Current clinical trials
are not promising. In this study, /researchers/ investigated the protective effect of curcumin in a lipopolysaccharide
LPSinduced DIC model in rats. Experimental DIC was induced by sustained infusion of LPS 10 mg/kg body weight
for 4 hr through the tail vein. Curcumin 60 mg/kg body weight was given intraperitoneally 3 hr before LPS infusion.
Results showed that, in vivo, curcumin reduced the mortality rate of LPSinfused rats by decreasing the circulating
TNFalpha levels and the consumption of peripheral platelets and plasma fibrinogen. Furthermore, in vivo curcumin
also has the effect of preventing the formation of fibrin deposition in the glomeruli of kidney. These results reveal the
therapeutic potential of curcumin in infectionrelated coagulopathy of DIC. Abstract: PubMed
Chen HW et al; J Endotoxin Res 13 (1): 1523 (2007)
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EXPL THER The present investigation was an attempt to evaluate the possible ameliorative effect of curcumin on
aflatoxininduced lipid peroxidation in liver, kidney and testis of mice in vitro. Tissues were collected from healthy
Swiss strain male albino mice Mus musculus weighing 3035 g. The homogenates were treated with aflatoxin 210
mg/mL with and without curcumin 25200 mg/mL. The results revealed that addition of aflatoxin 210 mg/mL to
homogenates caused significant increase in lipidperoxidation which was maximal at 6 mg/mL aflatoxin concentration.
However, concurrent addition of aflatoxin 6 mg/mL and curcumin 25200 mg/mL caused concentrationdependent
amelioration in aflatoxininduced lipid peroxidation. Abstract: PubMed
Mathuria N, Verma RJ; Acta Pol Pharm 64 (5): 4136 (2007)
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8 Food Additives and Ingredients
8.1 Food Additive Classes
JECFA Functional Classes

Flavouring Agent: FLAVOURING_AGENT Food Additives: COLOUR
from FAO/WHO Food Additive Evaluations JECFA

Food Additives: COLOUR
8.2 Evaluations of the Joint FAO/WHO Expert Committee on Food Additives

JECFA
Evaluations of the Joint FAO/WHO Expert Committee on Food Additives JECFA: 1 of 3
Chemical Name TURMERIC OLEORESIN
ADI NO ADI ALLOCATED
Evaluation Year 1989
Comments The previous temporary ADI was not extended
Report TRS 789JECFA 35/22
Chemical Name CURCUMA
ADI NO ADI ALLOCATED
Comments Regarded often as a food rather than as a food additive
Chemical Name CI NATURAL YELLOW 3
ADI 03 mg/kg bw
9 Pharmacology and Biochemistry
9.1 Pharmacology
Curcumin is a phytopolylphenol pigment isolated from the plant Curcuma longa, commonly known as turmeric, with a
variety of pharmacologic properties. Curcumin blocks the formation of reactiveoxygen species, possesses anti
inflammatory properties as a result of inhibition of cyclooxygenases COX and other enzymes involved in
inflammation; and disrupts cell signal transduction by various mechanisms including inhibition of protein kinase C.
These effects may play a role in the agent's observed antineoplastic properties, which include inhibition of tumor cell
proliferation and suppression of chemically induced carcinogenesis and tumor growth in animal models of cancer.
NCI04
from NCIt
9.2 MeSH Pharmacological Classification
Enzyme Inhibitors
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrateenzyme
combination and the catalytic reaction. See a list of PubChem compounds matching this category.
from MeSH
AntiInflammatory Agents, NonSteroidal

Antiinflammatory agents that are nonsteroidal in nature. In addition to antiinflammatory actions, they have
analgesic, antipyretic, and plateletinhibitory actions.They act by blocking the synthesis of prostaglandins by inhibiting
cyclooxygenase, which converts arachidonic acid to cyclic endoperoxides, precursors of prostaglandins. Inhibition of
prostaglandin synthesis accounts for their analgesic, antipyretic, and plateletinhibitory actions; other mechanisms
may contribute to their antiinflammatory effects. See a list of PubChem compounds matching this category.
from MeSH
Antineoplastic Agents
Substances that inhibit or prevent the proliferation of NEOPLASMS. See a list of PubChem compounds matching this
category.
from MeSH
Coloring Agents
Chemicals and substances that impart color including soluble dyes and insoluble pigments. They are used in INKS;
PAINTS; and as INDICATORS AND REAGENTS. See a list of PubChem compounds matching this category.
from MeSH
9.3 Absorption, Distribution and Excretion

Oral & ip doses of 3Hcurcumin led to fecal excretion of most of radioactivity. Iv & ip doses were well excreted in
bile of cannulated rats.
HOLDER ET AL; XENOBIOTICA 8(12) 761 (1978)
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When admin orally in dose of 1 g/kg, curcumin was excreted in feces to about 75%, while negligible amt appeared in
urine. Measurement of blood plasma levels & biliary excretion showed that curcumin was poorly absorbed from the
gut.
WAHLSTROM B, BLENNOW G; ACTA PHARMACOL TOXICOL 43(2) 86 (1978)
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The aim of this study was to develop a curcumin intranasal thermosensitive hydrogel and to improve its brain
targeting efficiency. The hydrogel gelation temperature, gelation time, drug release and mucociliary toxicity
characteristics as well as the nosetobrain transport in the rat model were evaluated. The developed nasal hydrogel,
composed of Pluronic F127 and Poloxamer 188, had shorter gelation time, longer mucociliary transport time and
produced prolonged curcumin retention in the rat nasal cavity at body temperature. The hydrogel release mechanism
was diffusioncontrolled drug release, evaluated by the dialysis membrane method, but dissolutioncontrolled release
when evaluated by the membraneless method. A mucociliary toxicity study revealed that the hydrogel maintained
nasal mucosal integrity until 14 days after application. The drugtargeting efficiencies for the drug in the cerebrum,
cerebellum, hippocampus and olfactory bulb after intranasal administration of the curcumin hydrogel were 1.82, 2.05,
2.07 and 1.51 times that after intravenous administration of the curcumin solution injection, respectively, indicating
that the hydrogel significantly increased the distribution of curcumin into the rat brain tissue, especially into the
cerebellum and hippocampus. A thermosensitive curcumin nasal gel was developed with favourable gelation, release
properties, biological safety and enhanced brainuptake efficiency. /Curcumin intranasal thermosensitive hydrogel/
Abstract: PubMed
Chen X et al; J Pharm Pharmacol 65 (6): 80716 (2013)
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...However, curcumin has a low systemic bioavailability, so it is imperative to improve the bioavailability of curcumin in
its clinical application. Many methods, such as adjuvant drug delivery system and structural modification have been
demonstrated to have a potential effect. Abstract: PubMed
Fan X et al; Curr Pharm Des 19 (11): 201131 (2013)
from HSDB
Twentyfive patients with conditions indicating a high risk of malignancy were given diferuloylmethane purity, 99.3%
for 3 months. The starting dose was 500 mg/day, which was increased stepwise to 1000, 2000, 4000, 8000 and finally
12 000 mg/day. Pharmacokinetic studies were conducted in patients who agreed to give samples of blood and urine
and in normal volunteers. Serum concentrations of diferuloylmethane peaked at 12 hr after administration of 4000
8000 mg diferuloylmethane and gradually declined within 12 hr. A halflife was not determined. Diferuloylmethane
was barely detectable in the serum of patients taking 5002000 mg of diferuloylmethane. No diferuloylmethane could
be detected in urine. Similar results were obtained in two patients who had taken diferuloylmethane for more than 1
month, indicating that repeated administration did not alter the pharmacokinetic profile of this substance.
WHO ; WHO Food Additives Series 52 Curcumin (addendum); Available from, as of November 6, 2013:
http://www.inchem.org/documents/jecfa/jecmono/v52je04.htm
from HSDB
Fifteen patients with advanced colorectal cancer received an extract of Curcuma 18 mg of diferuloylmethane and 2
mg of the desmethoxy derivative suspended in 200 mg of essential oils derived from Curcuma spp. daily for up to 4
months. The doses were equivalent to 26, 72, 108, 144 and 180 mg of curcumin, with three patients receiving each
dose. Neither diferuloylmethane, or its glucuronide or sulphate conjugates, or hexahydrocurcumin or
hexahydrocurcuminol were detected in plasma or urine after up to 29 days of treatment. Diferuloylmethane was
detected in the feces of all patients. Diferuloylmethane sulphate was also detected in the feces of one of the patients
receiving diferuloylmethane at a dose of 180 mg/day, which may have been a result of biotransformation in the gut.
from HSDB
9.4 Metabolism/Metabolites
Iv & ip doses of 3Hcurcumin excreted in bile of cannulated rats. Major metab were glucuronides of
tetrahydrocurcumin & hexahydrocurcumin. Minor metab was dihydroferulic acid together with traces of ferulic acid.
HOLDER ET AL; XENOBIOTICA 8(12) 761 (1978)
from HSDB
9.5 Mechanism of Action

Curcumin, a polyphenolic natural product, exhibits therapeutic activity against a number of diseases, attributed mainly
to its chemical structure and unique physical, chemical, and biological properties. It is a diferuloyl methane molecule
[1,7bis 4hydroxy3 methoxyphenyl1,6heptadiene3,5dione] containing two ferulic acid residues joined by a
methylene bridge. It has three important functionalities: an aromatic omethoxy phenolic group, alpha, beta
unsaturated betadiketo moiety and a seven carbon linker. Extensive research in the last two decades has provided
evidence for the role of these different functional groups in its crucial biological activities. A few highlights of chemical
structural features associated with the biological activity of curcumin are: The omethoxyphenol group and methylenic
hydrogen are responsible for the antioxidant activity of curcumin, and curcumin donates an electron/ hydrogen atom
to reactive oxygen species. Curcumin interacts with a number of biomolecules through noncovalent and covalent
binding. The hydrogen bonding and hydrophobicity of curcumin, arising from the aromatic and tautomeric structures
along with the flexibility of the linker group are responsible for the noncovalent interactions. The alpha, beta
unsaturated betadiketone moiety covalently interacts with protein thiols, through Michael reaction. The betadiketo
group forms chelates with transition metals, thereby reducing the metal induced toxicity and some of the metal
complexes exhibit improved antioxidant activity as enzyme mimics. New analogues with improved activity are being
developed with modifications on specific functional groups of curcumin... Abstract: PubMed
Priyadarsini KI; Curr Pharm Des 19 (11): 2093100 (2013)
from HSDB
The present study demonstrates that curcumin acts as prooxidant and sensitizes human lung adenocarcinoma
epithelial cells A549 to apoptosis via intracellular redox status mediated pathway. Results indicated that curcumin
induced cell toxicity light microscopy and MTT assay and apoptosis AnnexinVFITC/PI labeling and caspase3
activity in these cells. These events seem to be mediated through generation of reactive oxygen species ROS and
superoxide radicals SOR and enhanced levels of lipid peroxidation. These changes were accompanied by increase in
oxidized glutathione GSSG, reduced glutathione GSH and gammaglutamylcysteine synthetase gammaGCS
activity, but decrease in GSH/GSSG ratio. The induction of apoptosis and decrease in GSH/GSSG ratio was also
accompanied by sustained phosphorylation and activation of p38 mitogen activated protein kinase MAPK. On the
other hand, addition of Nacetyl cysteine NAC, an antioxidant, blocked the curcumininduced ROS production and
rescued malignant cells from curcumininduced apoptosis through caspase3 deactivation. However, Lbuthionine
sulfoximine BSO, a GSH synthesis blocking agent, further enhanced curcumininduced ROS production and
apoptosis in A549 cells. Decreased GSH/GSSG ratio seems to be a crucial factor for the activation of MAPK signaling
cascade by curcumin. The study therefore, provides an insight into the molecular mechanism involved in sensitization
of lung adenocarcinoma cells to apoptosis by curcumin. Abstract: PubMed
Kaushik G et al; Indian J Exp Biol 50 (12): 85361 (2012)
from HSDB
Curcumin has many pharmaceutical applications, many of which arise from its potent antioxidant properties. The
present research examined the antioxidant activities of curcumin in polar solvents by a comparative study using ESR,
reduction of ferric iron in aqueous medium and intracellular ROS/toxicity assays. ESR data indicated that the steric
hindrance among adjacent big size groups within a galvinoxyl molecule limited the curcumin to scavenge galvinoxyl
radicals effectively, while curcumin showed a powerful capacity for scavenging intracellular smaller oxidative
molecules such as H2O2, HO, ROO. Cell viability and ROS assays demonstrated that curcumin was able to penetrate
into the polar medium inside the cells and to protect them against the highly toxic and lethal effects of cumene
hydroperoxide. Curcumin also showed good electrontransfer capability, with greater activity than trolox in aqueous
solution. Curcumin can readily transfer electron or easily donate Hatom from two phenolic sites to scavenge free
radicals. The excellent electron transfer capability of curcumin is because of its unique structure and different
functional groups, including a betadiketone and several pi electrons that have the capacity to conjugate between two
phenyl rings. Therefore, since curcumin is inherently a lipophilic compound, because of its superb intracellular ROS
scavenging activity, it can be used as an effective antioxidant for ROS protection within the polar cytoplasm.[Barzegar
A, MoosaviMovahedi AA; PLoS One 6 10: e26012 2011] Full text: PMC3189944 Abstract: PubMed
from HSDB
Curcumin diferuloylmethane, the yellow pigment in Indian saffron Curcuma longa; also called turmeric, haldi, or
haridara in the East and curry powder in the West, has been consumed by people for centuries as a dietary
component and for a variety of proinflammatory ailments. Extensive research within the last decade in cell culture and
in rodents has revealed that curcumin can sensitize tumors to different chemotherapeutic agents including
doxorubicin, 5FU, paclitaxel, vincristine, melphalan, butyrate, cisplatin, celecoxib, vinorelbine, gemcitabine, oxaliplatin,
etoposide, sulfinosine, thalidomide, and bortezomib. Chemosensitization has been observed in cancers of the breast,
colon, pancreas, gastric, liver, blood, lung, prostate, bladder, cervix, ovary, head and neck, and brain and in multiple
myeloma, leukemia, and lymphoma. Similar studies have also revealed that this agent can sensitize a variety of tumors
to gamma radiation including glioma, neuroblastoma, cervical carcinoma, epidermal carcinoma, prostate cancer, and
colon cancer. How curcumin acts as a chemosensitizer and radiosensitizer has also been studied extensively. For
example, it downregulates various growth regulatory pathways and specific genetic targets including genes for NF
kappaB, STAT3, COX2, Akt, antiapoptotic proteins, growth factor receptors, and multidrugresistance proteins.
Although it acts as a chemosensitizer and radiosensitizer for tumors in some cases, curcumin has also been shown to
protect normal organs such as liver, kidney, oral mucosa, and heart from chemotherapy and radiotherapyinduced
toxicity. The protective effects of curcumin appear to be mediated through its ability to induce the activation of NRF2
and induce the expression of antioxidant enzymes e.g., hemeoxygenase1, glutathione peroxidase, modulatory
subunit of gammaglutamylcysteine ligase, and NADPH:quinone oxidoreductase 1, increase glutathione a product
of the modulatory subunit of gammaglutamylcysteine ligase, directly quench free radicals, and inhibit p300 HAT
activity. Abstract: PubMed
Goel A, Aggarwal BB; Nutr Cancer 62 (7): 91930 (2010)
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Curcumin is a naturally occurring compound which is known to induce heme oxygenase 1 HO1, although the
underlying mechanism has not been fully elucidated. This study investigates in detail the mechanism of HO1
induction by curcumin in human hepatoma cells... Curcumin was found to induce HO1 at doses of 10 to 25 uM. At
both nontoxic and toxic doses, HO1 induction was found to correlate with production of reactive oxygen species
ROS, suggesting a causative relationship. This was reinforced by the finding that pretreatment with the antioxidants
Nacetylcysteine, vitamin E and catalase prevented HO1 induction by curcumin. ROS production appeared to be
mitochondrial in origin, and curcumin treatment resulted in depolarisation of the mitochondrial membrane potential.
Nrf2 was induced by curcumin treatment, which was also partly ROS dependent. Using siRNA, Nrf2 was demonstrated
to contribute to HO1 induction. A panel of kinase inhibitors was used to examine the contribution of MAP kinases to
the induction of HO1 by curcumin. PKC and p38 MAPK activity are required for full induction of HO1. Furthermore,
curcumin also inhibited protein phosphatase activity. In conclusion, curcumin treatment results in ROS generation,
activation of Nrf2 and MAP kinases and the inhibition of phosphatase activity in hepatocytes, and when curcumin is
not administered in toxic doses, these multiple pathways converge to induce HO1. Abstract: PubMed
McNally SJ et al; Int J Mol Med 19 (1): 16572 (2007)
from HSDB
Curcumin is the active ingredient of turmeric that has been consumed as a dietary spice for ages. Turmeric is widely
used in traditional Indian medicine to cure biliary disorders, anorexia, cough, diabetic wounds, hepatic disorders,
rheumatism, and sinusitis. Extensive investigation over the last five decades has indicated that curcumin reduces
blood cholesterol, prevents lowdensity lipoprotein oxidation, inhibits platelet aggregation, suppresses thrombosis
and myocardial infarction, suppresses symptoms associated with type II diabetes, rheumatoid arthritis, multiple
sclerosis, and Alzheimer's disease, inhibits HIV replication, enhances wound healing, protects from liver injury,
increases bile secretion, protects from cataract formation, and protects from pulmonary toxicity and fibrosis. Evidence
indicates that the divergent effects of curcumin are dependent on its pleiotropic molecular effects. These include the
regulation of signal transduction pathways and direct modulation of several enzymatic activities. Most of these
signaling cascades lead to the activation of transcription factors. Curcumin has been found to modulate the activity of
several key transcription factors and, in turn, the cellular expression profiles. Curcumin has been shown to elicit vital
cellular responses such as cell cycle arrest, apoptosis, and differentiation by activating a cascade of molecular events.
In this chapter, we briefly review the effects of curcumin on transcription factors NFKB, AP1, Egr1, STATs, PPAR
gamma, betacatenin, nrf2, EpRE, p53, CBP, and androgen receptor AR and ARrelated cofactors giving major
emphasis to the molecular mechanisms of its action. Abstract: PubMed
Shishodia S et al; Adv Exp Med Biol 595: 12748 (2007)
from HSDB
9.6 Human Metabolite Information
9.6.1 Metabolite Description
Curcumin is a natural component of the rhizome of turmeric Curcuma longa and one of the most powerful
chemopreventive and anticancer agents. Its biological effects range from antioxidant, antiinflammatory to inhibition
of angiogenesis and is also shown to possess specific antitumoral activity. The molecular mechanism of its varied
cellular effects has been studied in some details and it has been shown to have multiple targets and interacting
macromolecules within the cell. Curcumin has been shown to possess antiangiogenic properties and the
angioinhibitory effects of curcumin manifest due to down regulation of proangiogenic genes such as VEGF and
angiopoitin and a decrease in migration and invasion of endothelial cells. One of the important factors implicated in
chemoresistance and induced chemosensitivity is NFkB and curcumin has been shown to down regulate NFkB and
inhibit IKB kinase thereby suppressing proliferation and inducing apoptosis. Cell lines that are resistant to certain
apoptotic inducers and radiation become susceptible to apoptosis when treated in conjunction with curcumin. Besides
this it can also act as a chemopreventive agent in cancers of colon, stomach and skin by suppressing colonic aberrant
crypt foci formation and DNA adduct formation. This review focuses on the various aspects of curcumin as a potential
drug for cancer treatment and its implications in a variety of biological and cellular processes visvis its mechanism
of action PMID: 16712454. Turmeric Zingiberaceae family rhizomes, has been widely used for centuries in
indigenous medicine for the treatment of a variety of inflammatory conditions and other diseases. Its medicinal
properties have been attributed mainly to the curcuminoids and the main component present in the rhizome is
curcumin. Curcumin has been shown to possess wide range of pharmacological activities including antiinflammatory,
anticancer, antioxidant, wound healing and antimicrobial effects. Recently, curcumin treatment has been shown to
correct defects associated with cystic fibrosis in homozygous DeltaF508 cystic fibrosis transmembrane conductance
regulator CFTR knock out mice. In vivo and in vitro studies have demonstrated curcumin's ability to inhibit
carcinogenesis at three stages: tumor promotion, angiogenesis and tumor growth. Curcumin suppresses mitogen
induced proliferation of blood mononuclear cells, inhibits neutrophil activation and mixed lymphocyte reaction and
also inhibits both seruminduced and platelet derived growth factor PDGFdependent mitogenesis of smooth
muscle cells. It has also been reported to be a partial inhibitor of protein kinase. The other salient feature of
turmeric/curcumin is that despite being consumed daily for centuries in Asian countries, it has not been shown to
cause any toxicity PMID: 16413584.
Curcumin I is found in herbs and spices. Curcumin I is isolated from the rhizomes of Curcuma longa turmeric.
9.6.2 Biofluid Locations
Blood
9.6.3 Cellular Locations
Membrane predicted from logP

Membrane
10 Use and Manufacturing
10.1 Uses
Food additives

Flavouring Agent: FLAVOURING_AGENT Food Additives: COLOUR

Food Additives: COLOUR
10.2 Methods of Manufacturing

Occurs naturally in the root of the herb curcuma longa turmeric; isolation by steam distillation
SRI Consulting, 2010 Directory of Chemical Producers. Menlo Park, CA. 2010
from HSDB
The essential oil of Curcuma longa is obtained by steam distillation, with yields ranging between 1.3 and 5.5%. ... The
oil contains, in addition to turmerone ~60%, free acids, cineol, borneol, zingerone, phellandrene, and 3 to 4%
coloring matter curcumin. /Essential oil of Curcuma longa/
Burdock, G.A. (ed.). Fenaroli's Handbook of Flavor Ingredients. 6th ed.Boca Raton, FL 2010, p. 1964
from HSDB
Production: Stieglitz, Horn, German patent 859145 1952 to Hoechst

from HSDB
10.3 Formulations/Preparations
Derivatives: tincture 20% in 60% ethanol, fluid extract, & oleoresin. /Deriv of turmeric/
Burdock, G.A. (ed.). Fenaroli's Handbook of Flavor Ingredients. 6th ed.Boca Raton, FL 2010, p. 1964
from HSDB
10.4 U.S. Production

1976 6.4X10+8 GMIN USE IN FOODSAS TURMERIC
SRI
from HSDB
1979 No Data
SRI
from HSDB
10.5 U.S. Imports

1977 1.12X10+9 GRAMS AS TUMERIC
SRI
from HSDB
1979 1.54X10+9 GRAMS AS TUMERIC

SRI
from HSDB
10.6 U.S. Exports

1977 No Data
SRI
from HSDB
1979 No Data
SRI
from HSDB
11 Identification
11.1 Analytic Laboratory Methods

COLORIMETRY. 44.121; 44.141. FILTH IN TURMERIC, ANALYTICAL CHEMISTRY. /TURMERIC/
Association of Official Analytical Chemists. Official Methods of Analysis. 10th ed. and supplements. Washington, DC: Association of
Official Analytical Chemists, 1965. New editions through 13th ed. plus supplements, 1982., p. 13/230 14.154
from HSDB
Thinlayer chromatographic method & conditions for detection of curcumin are presented.
KARIG F; RAPID IDENTIFICATION OF CURCUMA RHIZOMES WITH THE TAS (THERMOMICROSEPARATION AND APPLICATION)
PROCESS; DTSCH APOTHZTG 115(10) 325 (1975)
from HSDB
12 Safety and Hazards
12.1 Hazards Identification
12.1.1 GHS Classification
Signal: Danger
GHS Hazard Statements
Aggregated GHS information from 1 notifications provided by 38 companies to the ECHA C&L Inventory. Each
notification may be associated with multiple companies.
H304 100%: May be fatal if swallowed and enters airways [Danger Aspiration hazard Category 1]
H317 100%: May cause an allergic skin reaction [Warning Sensitization, Skin Category 1]
H412 100%: Harmful to aquatic life with long lasting effects []
Information may vary between notifications depending on impurities, additives, and other factors. The percentage
value in parenthesis indicates the notified classification ratio from all companies. Only Hazard Codes with percentage
values above 10% are shown.
Precautionary Statement Codes

P261, P272, P273, P280, P301+P310, P302+P352, P321, P331, P333+P313, P363, P405, and P501
The corresponding statement to each Pcode can be found here.
from European Chemicals Agency ECHA
View all 2 GHS Classification entries
12.1.2 Health Hazard
SYMPTOMS: Symptoms of exposure to this compound may include irritation to the skin and eyes. ACUTE/CHRONIC
HAZARDS: This compound is an allergen and local irritant. NTP, 1992
12.1.3 Fire Potential
Not flammable or combustible.

from HSDB
12.2 First Aid Measures
12.2.1 First Aid
EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline
solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any
ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY
transport the victim after flushing eyes to a hospital even if no symptoms such as redness or irritation develop. SKIN:
IMMEDIATELY flood affected skin with water while removing and isolating all contaminated clothing. Gently wash all
affected skin areas thoroughly with soap and water. If symptoms such as redness or irritation develop, IMMEDIATELY
call a physician and be prepared to transport the victim to a hospital for treatment. INHALATION: IMMEDIATELY leave
the contaminated area; take deep breaths of fresh air. If symptoms such as wheezing, coughing, shortness of breath,
or burning in the mouth, throat, or chest develop, call a physician and be prepared to transport the victim to a
hospital. Provide proper respiratory protection to rescuers entering an unknown atmosphere. Whenever possible,
SelfContained Breathing Apparatus SCBA should be used; if not available, use a level of protection greater than or
equal to that advised under Protective Clothing. INGESTION: DO NOT INDUCE VOMITING. If the victim is conscious
and not convulsing, give 1 or 2 glasses of water to dilute the chemical and IMMEDIATELY call a hospital or poison
control center. Be prepared to transport the victim to a hospital if advised by a physician. If the victim is convulsing or
unconscious, do not give anything by mouth, ensure that the victim's airway is open and lay the victim on his/her side
with the head lower than the body. DO NOT INDUCE VOMITING. IMMEDIATELY transport the victim to a hospital.
NTP, 1992
12.3 Fire Fighting Measures

Wear self contained breathing apparatus for fire fighting if necessary.
from HSDB
Use water spray, alcoholresistant foam, dry chemical or carbon dioxide.

from HSDB
12.4 Accidental Release Measures
12.4.1 Cleanup Methods
Pick up and arrange disposal without creating dust. Sweep up and shovel. Keep in suitable, closed containers for
disposal.
from HSDB
12.4.2 Other Preventative Measures
Avoid contact with skin and eyes. Avoid formation of dust and aerosols. Provide appropriate exhaust ventilation at
places where dust is formed.
from HSDB
Use personal protective equipment. Avoid dust formation. Avoid breathing vapours, mist or gas. Ensure adequate
ventilation. Evacuate personnel to safe areas. Avoid breathing dust.
from HSDB
12.5 Handling and Storage
12.5.1 Nonfire Spill Response
SMALL SPILLS AND LEAKAGE: Should a spill occur while you are handling this chemical, you should dampen the solid
spill material with alcohol, then transfer the dampened material to a suitable container. Use absorbent paper
dampened with alcohol to pick up any remaining material. Seal the absorbent paper, and any of your clothes, which
may be contaminated, in a vaportight plastic bag for eventual disposal. Solvent wash all contaminated surfaces with
alcohol followed by washing with a strong soap and water solution. Do not reenter the contaminate area until the
Safety Officer or other responsible person has verified that the area has been properly cleaned. STORAGE
PRECAUTIONS: You should protect this chemical from exposure to light, and store it in a refrigerator. NTP, 1992
12.5.2 Storage Conditions
Keep container tightly closed in a dry and wellventilated place. Recommended storage temperature: 20 deg C Keep
in a dry place.
from HSDB
12.6 Exposure Control and Personal Protection
12.6.1 Protective Equipment and Clothing
RECOMMENDED RESPIRATOR: Where the neat test chemical is weighed and diluted, wear a NIOSHapproved half
face respirator equipped with an organic vapor/acid gas cartridge specific for organic vapors, HCl, acid gas and SO2
with a dust/mist filter. RECOMMENDED GLOVE MATERIALS: Permeation data indicate that neoprene gloves may
provide protection to contact with this compound. Neoprene over latex gloves is recommended. However, if this
chemical makes direct contact with your gloves, or if a tear, puncture or hole develops, remove them at once. NTP,
1992
12.7 Stability and Reactivity
12.7.1 Air and Water Reactions
Slightly soluble in hot water NTP, 1992.

12.7.2 Reactive Group
Ethers
Ketones
Hydrocarbons, Aliphatic Unsaturated

Phenols and Cresols
12.7.3 Reactivity Profile
CURCUMIN is sensitive to light and changes in pH. This compound may react with oxidizing materials. NTP, 1992
12.8 Regulatory Information
12.8.1 FDA Requirements
Spices and other natural seasonings and flavorings that are generally recognized as safe for their intended use, within
the meaning of section 409 of the Act. Tumeric Botanical name of plant source: Curcuma longa L. is included on this
list. /Tumeric/
21 CFR 182.10 (USFDA); U.S. National Archives and Records Administration's Electronic Code of Federal Regulations. Available from,
as of November 8, 2013: http://www.ecfr.gov/cgibin/ECFR?page=browse
from HSDB
Essential oils, oleoresins solventfree, and natural extractives including distillates that are generally recognized as
safe for their intended use, within the meaning of section 409 of the Act. Tumeric Botanical name of plant source:
Curcuma longa L. is included on this list. /Tumeric/
from HSDB
Spices and other natural seasonings and flavorings that are generally recognized as safe for their intended use, within
the meaning of section 409 of the Act. Tumeric Botanical name of plant source: Curcuma longa L. is included on this
list. /Tumeric/
from HSDB
Essential oils, oleoresins solventfree, and natural extractives including distillates that are generally recognized as
safe for their intended use, within the meaning of section 409 of the Act. Tumeric Botanical name of plant source:
Curcuma longa L. is included on this list. /Tumeric/
from HSDB
12.9 Other Safety Information
12.9.1 Toxic Combustion Products
Hazardous decomposition products formed under fire conditions. Carbon oxides

from HSDB
13 Toxicity
13.1 Toxicological Information
13.1.1 Interactions
Groundwater arsenic contamination has been a health hazard for West Bengal, India. Oxidative stress to DNA is
recognized as an underlying mechanism of arsenic carcinogenicity. A phytochemical, curcumin, from turmeric appears
to be potent antioxidant and antimutagenic agent. DNA damage prevention with curcumin could be an effective
strategy to combat arsenic toxicity. This field trial in Chakdah block of West Bengal evaluated the role of curcumin
against the genotoxic effects of arsenic. DNA damage in human lymphocytes was assessed by comet assay and
fluorescenceactivated DNA unwinding assay. Curcumin was analyzed in blood by high performance liquid
chromatography HPLC. Arsenic induced oxidative stress and elucidation of the antagonistic role of curcumin was
done by observation on reactive oxygen species ROS generation, lipid peroxidation and protein carbonyl.
Antioxidant enzymes like catalase, superoxide dismutase, glutathione reductase, glutathioneStransferase, glutathione
peroxidase and nonenzymatic glutathione were also analyzed. The blood samples of the endemic regions showed
severe DNA damage with increased levels of ROS and lipid peroxidation. The antioxidants were found with depleted
activity. Three months curcumin intervention reduced the DNA damage, retarded ROS generation and lipid
peroxidation and raised the level of antioxidant activity. Thus curcumin may have some protective role against the
DNA damage caused by arsenic. Abstract: PubMed
Biswas J et al; Hum Exp Toxicol 29 (6): 51324 (2010)
from HSDB
To determine whether curcumin ameliorates acute and chronic radiation skin toxicity and to examine the expression
of inflammatory cytokines interleukin [IL]1, IL6, IL18, IL1Ra, tumor necrosis factor [TNF]alpha, and lymphotoxin
beta or fibrogenic cytokines transforming growth factor [TGF]beta during the same acute and chronic phases.
Curcumin was given intragastrically or intraperitoneally to C3H/HeN mice either: 5 days before radiation; 5 days after
radiation; or both 5 days before and 5 days after radiation. The cutaneous damage was assessed at 1521 days acute
and 90 days chronic after a single 50 Gy radiation dose was given to the hind leg. Skin and muscle tissues were
collected for measurement of cytokine mRNA. Curcumin, administered before or after radiation, markedly reduced
acute and chronic skin toxicity in mice p < 0.05. Additionally, curcumin significantly decreased mRNA expression of
early responding cytokines IL1 IL6, IL18, TNFalpha, and lymphotoxinbeta and the fibrogenic cytokine, TGFbeta,
in cutaneous tissues at 21 days postradiation. Curcumin has a protective effect on radiationinduced cutaneous
damage in mice, which is characterized by a downregulation of both inflammatory and fibrogenic cytokines in
irradiated skin and muscle, particularly in the early phase after radiation. These results may provide the molecular
basis for the application of curcumin in clinical radiation therapy. Abstract: PubMed
Okunieff P et al; Int J Radiat Oncol Biol Phys 65 (3): 8908 (2006)
from HSDB
The aim of this study is to evaluate the effect of curcumin in protecting against seleniuminduced toxicity in liver and
kidney of Wistar rats. Light microscopy evaluation of selenium alone administered rats showed liver to be infiltrated
with mononuclear cells, vacuolation, necrosis, and pronounced degeneration. Control liver sections showed a regular
morphology of parenchymal cells with intact hepatocytes and sinusoids. Kidney from selenium alone administered
rats showed vacuolar degeneration changes in the epithelial cells, cellular proliferation with fibrosis, thickening of
capillary walls, and glomerular tuft atrophy. Such changes were also observed in rats administered with selenium and
curcumin simultaneously and rats administered first with selenium and then curcumin 24 hr later. Interestingly, such
degenerative changes observed in liver and kidney induced by selenium were not seen in rats that were administered
with curcumin first and selenium 24 hr later. This clearly suggests the protective nature of curcumin against selenium
toxicity. To understand the probable mechanism of action of curcumin, /investigators/ analyzed inducible nitric oxide
synthase iNOS expression by immunohistochemistry, and the results showed an increased iNOS expression in
seleniumalone induced liver and kidney. Such high iNOS levels were inhibited in liver and kidney of rats pretreated
with curcumin and then with selenium 24 hr later. Based on the histological results, it can be concluded that curcumin
functions as a protective agent against seleniuminduced toxicity in liver as well as kidney, and this action is probably
by the regulatory role of curcumin on iNOS expression. Abstract: PubMed
Manikandan R et al; Microsc Res Tech 73 (6): 6317 (2010)
from HSDB
ZnIIcurcumin, a mononuclear 1:1 zinc complex of curcumin was synthesized and examined for its antiulcer
activities against pylorusligatureinduced gastric ulcer in rats. The structure of ZnIIcurcumin was identified by
elemental analysis, NMR and TGDTA analysis. It was found that a zinc atom was coordinated through the ketoenol
group of curcumin along with one acetate group and one water molecule. ZnIIcurcumin 12, 24 and 48 mg/kg
dosedependently blocked gastric lesions, significantly reduced gastric volume, free acidity, total acidity and pepsin,
compared with control group P<0.001 and curcumin alone 24 mg/kg, P<0.05. Reverse transcriptase polymerase
chain reaction RTPCR analysis showed that ZnIIcurcumin markedly inhibited the induction of nuclear factorkappa
B NFkappaB, transforming growth factor beta1 TGFbeta1 and interleukin8 IL8, compared with control group
P<0.05. These findings suggested that ZnIIcurcumin prevented pylorusligationinduced lesions in rat by inhibiting
NFkappaB activation and the subsequent production of proinflammatory cytokines, indicating a synergistic effect
between curcumin and zinc.../ZincIIcurcumin complex/ Abstract: PubMed
Mei X et al; Chem Biol Interact 181 (3): 31621 (2009)
from HSDB
Hexavalent chromium, an environmental contaminant, undergoes redox cycling with generation of free radicals inside
the biological system. Curcumin, the yellow bioactive component of turmeric has established its antioxidant activities.
The present study evaluates possible ameliorating effects of curcumin on potassium dichromate K2Cr2O7
hexavalent chromium induced reproductive toxicity in adult male SpragueDawley rats. Three experimental groups,
each consisting of eight rats, were treated with 0.4 mg K2Cr2O7/kg bw/day, 0.4 mg K2Cr2O7/kg bw/day + 20mg
curcumin/kg bw on every alternate day and 20 mg curcumin/kg bw on every alternate day, respectively, for 26 days.
Altered testicular histology, reduced sperm count, low testosterone level, decreased accessory sex organs weight,
enhanced lipid peroxidation along with reduced SOD and catalase activities were observed following K2Cr2O7
exposure while curcumin supplementation along with K2Cr2O7 exposure had shown to prevent the altered
parameters. The results thus suggest that curcumin may have a protective role against Chromium VI induced oxidative
damage in male reproductive system. Abstract: PubMed
Chandra AK et al; Environ Toxicol Pharmacol 24 (2): 1606 (2007)
from HSDB
This study investigated the neuroprotective effects of the curcuminoids against leadinduced neurotoxicity. The
results show that lead significantly increases lipid peroxidation and reduces the viability of primary hippocampal
neurons in culture. This leadinduced toxicity was significantly curtailed by the coincubation of the neurons with the
curcuminoids. In a whole animal experiment, rats were trained in a water maze and thereafter dosed with lead and/or
curcumin CURC, demethoxycurcumin DMC, or bisdemethoxycurcumin BDMC for 5 days. Animals treated with
curcumin and demethoxycurcumin but not bisdemethoxycurcumin had more glutathione and less oxidized proteins in
the hippocampus than those treated with lead alone. These animals also had faster escape latencies when compared
to the Pbtreated animals indicating that CURC and DMCtreated animals retain the spatial reference memory. The
findings of this study indicate that curcumin, a wellestablished dietary antioxidant, is capable of playing a major role
against heavy metalinduced neurotoxicity and has neuroprotective properties. /curcuminoids/ Abstract: PubMed
Dairam A et al; J Agric Food Chem 55 (3): 103944 (2007)
from HSDB
The beneficial influence of dietary curcumin, capsaicin and their combination on the susceptibility of lowdensity
lipoprotein LDL to oxidation was examined in an animal study. Individually, both dietary curcumin and capsaicin
significantly inhibited the in vivo ironinduced LDL oxidation, as well as copperinduced oxidation of LDL in vitro. The
protective effect of the combination of curcumin and capsaicin on LDL oxidation was greater than that of individual
compounds. This protective influence of spice principles was also indicated by the relative anodic electrophoretic
mobility of oxidized LDL on agarose gel. In another study, rats injected with iron showed hepatic toxicity as measured
by an increase in lipid peroxides and elevated serum enzymes, alanine aminotransferase, aspartate aminotransferase
and lactate dehydrogenase. Dietary curcumin, capsaicin and their combination reduced the activities of these
enzymes, and lowered the liver lipid peroxide level, indicating amelioration of the severity of ironinduced
hepatotoxicity. In yet another study, a comparison of the extent of carrageenaninduced paw inflammation showed
that both dietary curcumin and capsaicin moderately lowered inflammation, while the spice principles in combination
were more effective. Dietary curcumin and capsaicin significantly decreased the activity of 5'lipoxygenase activity in
the polymorphonuclear lymphocytes in carrageenaninjected rats, the decrease being even higher in the case of
combination of these two spice principles. Results suggest that dietary curcumin and capsaicin individually are
protective to LDL oxidation both in vivo and in vitro, to ironinduced hepatotoxicity and to carrageenaninduced
inflammation. This beneficial effect was higher when the two compounds were fed in combination. Abstract: PubMed
Manjunatha H, Srinivasan K; FEBS J 273 (19): 452837 (2006)
from HSDB
Curcumin is the pigment of turmeric and has been reported as a signal transduction modulator and inhibitor of
transcription factors, for example, NFkappaB. In /this/ article /the authors/ found a concentrationdependent
cytotoxic activity of curcumin in a panel of eight leukemic cell lines SKW3, CEM, U937, HL60, HL60/Dox, K562,
LAMA84, and AR230. Additive to synergistic interactions was recorded for combinations with bendamustine and
idarubicine in SKW3 and LAMA84 cells. Noteworthy, in multiple myeloma cells RPMI8226 and U266 a
potentiation of the efficacy of bendamustine by curcumin application was found. Moreover, curcumin increased the
bendamustine cytotoxicity in cultures of cells isolated from the bone marrow of a patient with nonHodgkin's
lymphoma NHL. The increased bendamustine efficacy could be explained by NFkappaB inhibition, because this
factor is activated in many cancers, especially leukemia and multiple myeloma. Curcumin is characterized by low
toxicity and was described to have a chemoprotective activity. Therefore, the level of reduced glutathione GSH was
measured and a concentrationdependent increase of GSH levels was recorded in AR230 and SKW3 cells
concentration range 525 muM. Experiments with mice showed significant protection against cisplatininduced
chromosomal aberrations clastogenic effect and inhibition of mitoses in bone marrow cells. Curcumin alone caused
reduction of the mitotic index. In combination with cisplatin, however, this parameter was increased when compared
to cisplatin alone. /This/ data indicate that curcumin has pleiotropic effects on signal transduction by inhibiting
transcription thus exerting antitumor activity. In addition, curcumin has protective and anticlastogenic activity by
enhancing the scavenging of free radicals. Abstract: PubMed
Alaikov T et al; Ann N Y Acad Sci 1095: 35570 (2007)
from HSDB
/The study objectives were/ to investigate the ameliorative effect of curcumin on aflatoxininduced toxicity in mice
spermatozoa. Design: Prospective controlled animal study.../at/ University research laboratory. Young, inbred, Swiss
strain male albino mice Mus musculus, weighing approximately 37 to 40 g, were obtained from Cadila Health Care,
Ahmedabad, India. Aflatoxin was orally administered in 25 low dose and 50 high dose ug/0.2 mL olive oil to each
animal, each day 750 and 1500 ug/kg body weight, respectively, with and without curcumin for 45 days. On 46th day
the animals were killed by cervical dislocation. The cauda epididymis were removed and weighed, then was teased in
normal saline to obtain spermatozoa. Sperm count, viability, and motility were assessed immediately. Sperm
semidried smears were prepared on slides and stained by Papanicolaou stain to study sperm morphologic features.
There was a dosedependent spermicidal effect of aflatoxin. Sperm count, viability, and motility were statistically
significantly reduced. Different morphologic abnormalities were encountered. Treatment with curcumin along with
aflatoxin ameliorated aflatoxininduced sperm count, immobilization, and viability, and improved the morphologic
characteristics of the sperm. Curcumin has an ameliorative effect on sperm parameters and improves morphologic
features of sperm in mice. Abstract: PubMed
Mathuria N, Verma RJ; Fertil Steril 90 (3): 77580 (2008)
from HSDB
It is known that alcohol consumption inhibits testosterone production and causes testicular atrophy. Curcumin is a
phytochemical characterized by antiinflammatory and antioxidant properties. It was also observed that curcumin
protects the liver, pancreas, and nervous system from the toxic effects of alcohol consumption. The goal of this study
was to determine if curcumin protects the Leydig cells of mice from chronic alcohol administration. Fifteen mice were
treated daily for four weeks with a 3.0 g/kg of a 25% solution of alcohol. Fifteen mice received curcumin 80 mg/kg
added to the same alcohol solution. Fifteen mice were treated with a solution of maltose dextrins isocaloric to
ethanol. Fifteen untreated mice were used as controls. In the alcoholfed mice, numerous Leydig cells showed
cytoplasmic rarefaction and increased diameter of the mitochondria. Several mitochondria had diameters three or
more times larger than that of mitochondria from control mice. Numerous necrotic Leydig cells were observed.
Testosterone plasma levels significantly decreased in comparison with control mice. In alcohol plus curcumintreated
mice the number of necrotic Leydig cells was reduced compared with alcoholfed mice; the diameters of the
mitochondria were significantly decreased. Testosterone plasma levels were not significantly different from those of
the controls. This study demonstrates that curcumin exerts efficacious protection against damages caused in the
Leydig cells of mice by chronic alcohol ingestion and that the preservation of mitochondrial structure and size in
Leydig cells is a specific effect of curcumin. Abstract: PubMed
Giannessi F et al; Med Sci Monit 14 (11): BR23742 (2008)
from HSDB
In presence of 7.5 uM of curcumin, no embryos or larva of zebrafish survived 3 days of incubation; however,
coincubation with 144 ug/ml silymarin increased the survival rates of curcumintreated embryos and larvae to about
70%. Moreover, in presence of 12.5 uM curcumin, all embryos died after 2 days of incubation; however, cotreatment
with 144 ug/ml silymarin increased the survival rates of curcumintreated embryos and larvae up to 60 and 50%,
respectively. This protective effect was not found in the other phenolic compounds viz., ferulic acid, naringin, or crocin,
tested. Finally, using a fluorescence microscope, accumulation of less curcumin has observed in the edema sac area of
the larvae cotreated with curcumin and silymarin than in the larvae treated with curcumin only. The result suggests
that the protective effects of silymarin may be due to a decreased accumulation of curcumin in the fish body.
Abstract: PubMed
Shiau RJ et al; Indian J Exp Biol 49 (7): 4917 (2011)
from HSDB
/The study objectives were/ to investigate the effect of curcumin on aflatoxininduced biochemical changes in testis of
mice. Design: Controlled research laboratory study. Aflatoxin was obtained by growing Aspergillus parasiticus in SMKY
liquid medium. Pure curcumin 97% purity was purchased from HiMedia Laboratories Pvt. Ltd., Mumbai, India. Young
inbred, Swiss strain male albino mice Mus musculus, weighing approximately 3740 g, were obtained from Cadila
Health Care, Ahmedabad, India. Aflatoxin was administered orally at 25 ug low dose and 50 ug high dose/0.2 mL
olive oil/animal/day 750 and 1,500 ug/kg body weight, respectively, with and without curcumin for 45 days. On the
46th day the animals were sacrificed by cervical dislocation. Testis were removed and weighed. Homogenates were
prepared for respective parameters such as protein, cholesterol, DNA, RNA, and 3beta and 17betahydroxysteroid
dehydrogenase activity. Protein, cholesterol, DNA, RNA, 3beta and 17betahydroxysteroid dehydrogenase activity
were measured immediately. There was a dosedependent effect of aflatoxin on testis of mice. Protein, cholesterol,
DNA, RNA, and 3beta and 17betahydroxysteroid dehydrogenase activity were reduced significantly by the treatment
of aflatoxin; cholesterol was increased. Treatment with curcumin along with aflatoxin ameliorates aflatoxininduced
biochemical changes in the testis of mice. Curcumin significantly ameliorates aflatoxininduced biochemical changes
in the testis of mice. Abstract: PubMed
Verma RJ, Mathuria N; Fertil Steril 91 (2): 597601 (2009)
from HSDB
13.1.2 Antidote and Emergency Treatment
Emergency and supportive measures. Toxic effects of herbal medicines should be managed with the same approach
taken with other ingestions. 1. Replace fluid losses caused by diarrhea or vomiting with IV crystalloid fluids. 2. Treat
hypertension, tachycardia, and arrhythmias if they occur. 3. Treat anxiety, agitation, or seizures caused by stimulant
herbs with IV benzodiazepines. 4. Maintain an open airway and assist ventilation if necessary in cases of CNS
depression or coma related to sedative herb use. /Herbal and alternative products/
OLSON, K.R. (Ed). Poisoning and Drug Overdose, Sixth Edition. McGrawHill, New York, NY 2012, p. 235
from HSDB
Decontamination. Administer activated charcoal orally if conditions are appropriate. Gastric lavage is not necessary
after small to moderate ingestions if activated charcoal can be given promptyly. /Herbal and alternative products/
OLSON, K.R. (Ed). Poisoning and Drug Overdose, Sixth Edition. McGrawHill, New York, NY 2012, p. 235
from HSDB
/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing,
start artificial respiration, preferably with a demand valve resuscitator, bagvalvemask device, or pocket mask, as
trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce
vomiting. If vomiting occurs, lean patient forward or place on the left side headdown position, if possible to
maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain
medical attention. /Poisons A and B/
Currance, P.L. Clements, B., Bronstein, A.C. (Eds).; Emergency Care For Hazardous Materials Exposure. 3Rd edition, Elsevier Mosby,
St. Louis, MO 2005, p. 160
from HSDB
/SRP:/ Basic treatment: Establish a patent airway oropharyngeal or nasopharyngeal airway, if needed. Suction if
necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by
nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and
treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with
water. Irrigate each eye continuously with 0.9% saline NS during transport ... . Do not use emetics. For ingestion,
rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag
reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/
St. Louis, MO 2005, p. 160
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/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is
unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positivepressure ventilation techniques
with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider
administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat
arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline
NS or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer
fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine
hydrochloride to assist eye irrigation ... . /Poisons A and B/
St. Louis, MO 2005, p. 1601
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13.1.3 Human Toxicity Excerpts
/HUMAN EXPOSURE STUDIES/ Twentyfive patients with conditions indicating a high risk of malignancy were given
diferuloylmethane purity, 99.3% for 3 months. The starting dose was 500 mg/day, which was increased stepwise to
1000, 2000, 4000, 8000 and finally 12 000 mg/day. The patients received regular followup, including physical
examination, weekly hemogram, and measurement of blood electrolytes and biochemistry parameters every 2 weeks.
No adverse effects were reported at doses of up to 8000 mg/day.
from HSDB
/HUMAN EXPOSURE STUDIES/ ...Patients with advanced colorectal cancer receiving Curcuma extract daily for up to 4
months were examined physically and blood samples were taken on days 1, 2, 8 and 29 of treatment and monthly
thereafter. Blood samples were analysed for full blood cell count, concentrations of urea, electrolytes and markers of
liver and bone function. Curcuma extract was administered at a dose equivalent to 26, 72, 108, 144 or 180 mg of
diferuloylmethane, with three patients receiving each dose. The only adverse effects reported were gastrointestinal
symptoms. During the first month of treatment, one patient receiving diferuloylmethane at a dose of 108 mg per day
experienced nausea, which resolved spontaneously without discontinuing the treatment. Two patients, who received
diferuloylmethane at a dose of 72 or 180 mg per day, respectively, experienced diarrhea. In the absence of controls,
and in view of the clinical conditions of the patients, it is not clear whether these symptoms were related to treatment.
from HSDB
/GENOTOXICITY/ Chronic inhalation of high concentrations of respirable quartz particles has been implicated in
various lung diseases including lung fibrosis and cancer. Generation of reactive oxygen species ROS and oxidative
stress is considered a major mechanism of quartz toxicity. Curcumin, a yellow pigment from Curcuma longa, has been
considered as nutraceutical because of its strong antiinflammatory, antitumour and antioxidant properties. The aim
of /the/ present study was to investigate whether curcumin can protect lung epithelial cells from the cytotoxic,
genotoxic and inflammatory effects associated with quartz DQ12 exposure. Electron paramagnetic resonance EPR
measurements using the spintrap DMPO demonstrated that curcumin reduces hydrogen peroxidedependent
hydroxylradical formation by quartz. Curcumin was also found to reduce quartzinduced cytotoxicity and
cyclooxygenase 2 COX2 mRNA expression in RLE6TN rat lung epithelial cells RLE. Curcumin also inhibited the
release of macrophage inflammatory protein2 MIP2 from RLE cells as observed upon treatment with interleukin1
beta IL1beta and tumour necrosis factoralpha TNFalpha. However, curcumin failed to protect the RLE cells from
oxidative DNA damage induced by quartz, as shown by formamidopyrimidine glycosylase FPGmodified comet assay
and by immunocytochemistry for 8hydroxydeoxyguanosine. In contrast, curcumin was found to be a strong inducer
of oxidative DNA damage itself at noncytotoxic and antiinflammatory concentrations. In line with this, curcumin also
enhanced the mRNA expression of the oxidative stress response gene heme oxygenase1 ho1. Curcumin also
caused oxidative DNA damage in NR8383 rat alveolar macrophages and A549 human lung epithelial cells. Taken
together, these observations indicate that one should be cautious in considering the potential use of curcumin in the
prevention or treatment of lung diseases associated with quartz exposure. Abstract: PubMed
Li H et al; Toxicol Appl Pharmacol 227 (1): 11524 (2008)
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/GENOTOXICITY/ Curcumin ... caused oxidative DNA damage in ... A549 human lung epithelial cells. Abstract: PubMed
from HSDB
/ALTERNATIVE and IN VITRO TESTS/ The antiinflammatory and antiproliferative agent curcumin has poor oral
bioavailability and solubility in plasma. Liposomal formulations have therefore been developed, but the toxicity of
these preparations is not yet established. /Researchers/ investigated the influence of free and liposomally formulated
curcumin on human red blood cell RBC morphology in vitro. EDTAbuffered whole blood from two healthy
individuals was incubated with different concentrations 1, 10, 100 ug/mL of free or liposomal curcumin. RBC
morphology and mean cellular volume MCV were examined at up to 4 hours of incubation. Dosedependent
echinocyte formation was observed after incubation with free, and liposomal curcumin, with a threshold concentration
of 10 ug/mL and peak effect after 30 minutes. A concomitant increase in mean cellular volume was detectable.
Curcumin and liposomal curcumin cause dosedependent changes in the shape of RBCs. This effect may represent an
early sign of doselimiting toxicity following intravenous administration./Liposomal curcumin/ Abstract: PubMed
Storka A et al; Anticancer Res 33 (9): 362934 (2013)
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/ALTERNATIVE and IN VITRO TESTS/ Amphiphilic polymers for dual drug delivery have been a focus of research in
recent years. /Investigators/ have previously developed and characterized Lauroyl sulphated chitosan LSCS. Here
biological characterizations like mucoadhesion, cytotoxicity, calcium binding, tight junction opening and enzymatic
degradation studies were performed to understand its applicability. In vitro drug release properties of both
hydrophilic insulin and hydrophobic curcumin were carried out. The biological activity and stability of released insulin
were also studied. The stability studies of encapsulated curcumin and uptake studies have also been carried out. LSCS
showed strong mucoadhesion and 100% of nontoxicity. LSCS could transiently open tight junctions between Caco2
cells and thus increase the paracellular permeability. LSCS enhanced calcium binding properties and decreased
enzymatic degradation rate retaining insulin activity. LSCS could protect curcumin from photodegradation and could
also enter into the cells. From release studies, LSCS was found to be a suitable candidate for both drugs. /Lauroyl
sulphated chitosan encapsulated curcumin/ Abstract: PubMed
Shelma R, Sharma CP; Colloids Surf B Biointerfaces 88 (2): 7228 (2011)
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/ALTERNATIVE and IN VITRO TESTS/ Curcumin, a natural polyphenolic pigment present in the spice turmeric
Curcuma longa, is known to possess a pleiotropic activity such as antioxidant, antiinflammatory, and antiamyloid
beta activities. However, these benefits of curcumin are limited by its poor aqueous solubility and oral bioavailability.
In the present study, a polymerbased nanoparticle approach has been utilized to deliver drugs to neuronal cells.
Curcumin was encapsulated in biodegradable poly lactidecoglycolide PLGA basednanoparticulate formulation
NpsCur. Dynamic laser light scattering and transmission electronic microscopy analysis indicated a particle diameter
ranging from 80 to 120 nm. The entrapment efficiency was 31% with 15% drugloading. In vitro release kinetics of
curcumin from NpsCur revealed a biphasic pattern with an initial exponential phase followed by a slow release phase.
Cellular internalization of NpsCur was confirmed by fluorescence and confocal microscopy with a wide distribution of
the fluorescence in the cytoplasm and within the nucleus. The prepared nanoformulation was characterized for cellular
toxicity and biological activity. Cytotoxicity assays showed that void PLGAnanoparticles Nps and curcuminloaded
PLGA nanoparticles NpsCur were nontoxic to human neuroblastoma SKNSH cells. Moreover, NpsCur was able to
protect SKNSH cells against H2O2 and prevent the elevation of reactive oxygen species and the consumption of
glutathione induced by H2O2. Interestingly, NpsCur was also able to prevent the induction of the redoxsensitive
transcription factor Nrf2 in the presence of H2O2. Taken together, these results suggest that NpsCur could be a
promising drug delivery strategy to protect neurons against oxidative damage as observed in Alzheimer's disease.
/Curcuminloaded PLGA nanoparticles/ Abstract: PubMed
Doggui S et al; J Alzheimers Dis 30 (2): 37792 (2012)
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/ALTERNATIVE and IN VITRO TESTS/ Recent studies report curcumin nanoformulations based on polylacticco
glycolic acid PLGA, betacyclodextrin, cellulose, nanogel, and dendrimers to have anticancer potential. However, no
comparative data are currently available for the interaction of curcumin nanoformulations with blood proteins and
erythrocytes. The objective of this study was to examine the interaction of curcumin nanoformulations with cancer
cells, serum proteins, and human red blood cells, and to assess their potential application for in vivo preclinical and
clinical studies. The cellular uptake of curcumin nanoformulations was assessed by measuring curcumin levels in
cancer cells using ultravioletvisible spectrophotometry. Protein interaction studies were conducted using particle size
analysis, zeta potential, and Western blot techniques. Curcumin nanoformulations were incubated with human red
blood cells to evaluate their acute toxicity and hemocompatibility. Cellular uptake of curcumin nanoformulations by
cancer cells demonstrated preferential uptake versus free curcumin. Particle sizes and zeta potentials of curucumin
nanoformulations were varied after human serum albumin adsorption. A remarkable capacity of the dendrimer
curcumin nanoformulation to bind to plasma protein was observed, while the other formulations showed minimal
binding capacity. Dendrimer curcumin nanoformulations also showed higher toxicity to red blood cells compared with
the other curcumin nanoformulations. PLGA and nanogel curcumin nanoformulations appear to be very compatible
with erythrocytes and have low serum protein binding characteristics, which suggests that they may be suitable for
application in the treatment of malignancy. These findings advance our understanding of the characteristics of
curcumin nanoformulations, a necessary component in harnessing and implementing improved in vivo effects of
curcumin./Molecular carrier system/[Yallapu MM et al; Int J Nanomedicine 6: 277990 2011] Full text: PMC3225220
Abstract: PubMed
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/ALTERNATIVE and IN VITRO TESTS/ ... Curcumin, diferuloyl methane, the yellow pigment component of the curry
spice turmeric Curcuma longa, has immense biological effects and has recently drawn considerable attention.
Curcumin has antibacterial, antiviral, antiinflammatory, and anticancer properties. It has shown a lack of toxicity in
animals and human clinical trials. Yet, its effect on reproduction has not been examined. The present study was
conducted to examine if curcumin affects sperm function in vitro and fertility in vivo. Sperm human and murine were
collected and incubated with curcumin to examine the effect on motility, capacitation/acrosome reaction, and in vitro
fertilization. The effect on in vivo fertility using the mouse model was also examined. Incubation of sperm with
curcumin caused a concentrationdependent decrease in sperm forward motility, capacitation/acrosome reaction, and
murine fertilization in vitro. At higher concentrations, there was a complete block of sperm motility and function
within 515 min. Administration of curcumin, especially intravaginally, caused a significant P<0.001 reduction in
fertility. The antifertility effect of curcumin was reversible. /This study reports/ the inhibitory effect of curcumin on
sperm function, fertilization, and fertility. The findings suggest that curcumin may constitute a doubleedged sword to
block conception, infection, and cancer, thus providing an ideal contraceptive. Abstract: PubMed
Naz RK; Mol Reprod Dev 78 (2): 11623 (2011)
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/ALTERNATIVE and IN VITRO TESTS/ A novel polymeric amphiphile, mPEGPA, was synthesized with methoxy
polyethylene glycol mPEG as the hydrophilic and palmitic acid PA as the hydrophobic segment. The conjugate
prepared in a singlestep reaction showed minimal toxicity on HeLa cells. 1H nuclear magnetic resonance imaging
and Fourier transform infrared spectroscopy revealed that the conjugation was through an ester linkage, which is
biodegradable. Enzymes having esterase activity, such as lipase, can degrade the conjugate easily, as observed by in
vitro studies. mPEGPA conjugate undergoes selfassembly in an aqueous environment, as evidenced by fluorescence
spectroscopic studies with pyrene as a probe. The mPEGPA conjugate formed micelles in the aqueous solution with
critical micelle concentration of 0.12 g/L. Atomic force microscopy and dynamic light scattering studies showed that
the micelles were spherical in shape, with a mean diameter of 41.43 nm. The utility of mPEGPA to entrap the potent
chemopreventive agent curcumin in the core of nanocarrier was investigated. The encapsulation of a highly
hydrophobic compound like curcumin in the nanocarrier makes the drug readily soluble in an aqueous system, which
can increase the ease of dosing and makes intravenous dosing possible. Drugloaded micelle nanoparticles showed
good stability in physiological condition pH 7.4, in simulated gastric fluid pH 1.2 and in simulated intestinal fluid
pH 6.8. This micellar formulation can be used as an enzymetriggered drug release carrier, as suggested by in vitro
enzymecatalyzed drug release using pure lipase and HeLa cell lysate. The IC50 of free curcumin and encapsulated
curcumin was found to be 14.32 and 15.58 uM, respectively. /Molecular carrier system/ Abstract: PubMed
Sahu A et al; Acta Biomater 4 (6): 175261 (2008)
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/ALTERNATIVE and IN VITRO TESTS/ Curcumin is a naturally occurring compound which is known to induce heme
oxygenase 1 HO1, although the underlying mechanism has not been fully elucidated. This study investigates in
detail the mechanism of HO1 induction by curcumin in human hepatoma cells. There was increasing toxicity of
curcumin at concentrations higher than 10 uM... Abstract: PubMed
McNally SJ et al; Int J Mol Med 19 (1): 16572 (2007)
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/ALTERNATIVE and IN VITRO TESTS/ This study investigated the inhibitory effects of curcumin on proliferation of
hematological malignant cells in vitro and the antitumor mechanism at histone acetylation/histone deacetylation
levels. The effects of curcumin and histone deacetylase inhibitor trichostatin A TSA on the growth of Raji cells were
tested by MTT assay. The expression of acetylated histone3 H3 in Raji, HL60 and K562 cells, and peripheral blood
mononuclear cells PBMCs treated with curcumin or TSA was detected by immunohistochemistry and FACS. The
results showed curcumin inhibited proliferation of Raji cells significantly in a time and dosedependent fashion, while
exhibited low toxicity in PBMCs. Curcumin induced upregulation of the expression of acetylated H3 dose
dependently in all malignant cell lines tested. In conclusion, curcumin inhibited proliferation of Raji cells selectively,
enhanced the level of acetylated H3 in Raji, HL60, and K562 cells, which acted as a histone deacetylase inhibitor like
TSA. Furthermore, upregulation of H3 acetylation may play an important role in regulating the proliferation of Raji
cells. Abstract: PubMed
Hu J et al; J Huazhong Univ Sci Technolog Med Sci 29 (1): 258 (2009)
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/ALTERNATIVE and IN VITRO TESTS/ Using absorption and fluorescence spectroscopic methods, quantitative cellular
uptake of curcumin, an antioxidant and antitumor agent from Curcuma longa, was calculated in two types of normal
cells: spleen lymphocytes, and NIH3T3 and two tumor cell lines: EL4 and MCF7. Both the uptake and fluorescence
intensity of curcumin were significantly higher in tumor cells compared to the normal cells. A linear dependency on
the uptake was observed with treatment concentration of curcumin. Using laser confocal microscopy, intracellular
localization of curcumin was monitored and the results indicated that curcumin is located both in the cell membrane
and the nucleus. Subcellular fractionation of curcuminloaded MCF7 cells supported the differential distribution of
curcumin in membrane, cytoplasm and nuclear compartments of cell with maximum localization in the membrane.
Cytotoxicity studies in different cell lines indicated that the toxicity of curcumin increased with increasing uptake.
Abstract: PubMed
Kunwar A et al; Biochim Biophys Acta 1780 (4): 6739 (2008)
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/ALTERNATIVE and IN VITRO TESTS/ Turmeric, the powdered dry rhizome of the Curcuma longa plant, and curcumin,
the major antioxidant constituent of turmeric, have been shown to possess chemopreventive activity. To elucidate
the possible interaction of turmeric and curcumin with conjugation reactions, which in many cases are involved in the
activation of procarcinogens, /researchers/ measured their effects in the conjugation of 1naphthol in Caco2 cells, a
human colon carcinoma cell line, within a 24 hr period. Turmeric exhibits inhibitory activity toward both sulfo and
glucuronosyl conjugations of 1naphthol at approximately the same levels IC50=0.24 and 0.29 mg/mL, respectively.
Curcumin inhibits sulfoconjugation at lower concentrations IC50=9.7 ug/mL, but only showed weak inhibition
toward glucuronosyl conjugation of 1naphthol in Caco2 cells. In addition, turmeric was found to strongly inhibit in
vitro phenol sulfotransferase SULT activity and demonstrate moderate inhibitory properties against UDP
glucuronosyl transferase UGT activity in Caco2 cells IC50=0.17 mg/mL and 0.62 mg/mL, respectively. Curcumin
also strongly inhibits in vitro phenol sulfotransferase activity with an IC50 of 2.4 ug/mL. Moreover, and in contrast to
the moderate inhibition of UGT activity by turmeric and curcumin, both induce the expression of the UGT1A1 and
UGT1A6 genes, revealed by realtime PCR analysis. These findings are indicative of a possible interaction of both
turmeric and curcumin with conjugation reactions in the human intestinal tract and colon. This in turn may affect the
bioavailability of therapeutic drugs and toxicity levels of environmental chemicals, particularly procarcinogens.
Abstract: PubMed
Naganuma M et al; Biol Pharm Bull 29 (7): 14769 (2006)
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/IMMUNOTOXICITY/ Curcumin is a multifunctional and pharmacologically safe natural agent. Used as a food additive
for centuries, it also has antiinflammatory, antivirus and antitumor properties. /The authors/ previously found that it
is a potent inhibitor of cyclosporin A CsAresistant Tcell costimulation pathway. It inhibits mitogenstimulated
lymphocyte proliferation, NFkappaB activation and IL2 signaling. In spite of its safety and efficacy, the in vivo
bioavailability of curcumin is poor, and this may be a major obstacle to its utility as a therapeutic agent. Liposomes
are known to be excellent carriers for drug delivery. In this in vitro study, /investigators/ report the effects of different
liposome formulations on curcumin stability in phosphate buffered saline PBS, human blood, plasma and culture
medium RPMI1640+10% FBS pH 7.4, 37 degrees C. Liposomal curcumin had higher stability than free curcumin in
PBS. Liposomal and free curcumin had similar stability in human blood, plasma and RPMI1640+10% FBS. /They/
looked at the toxicity of nondrugcontaining liposomes on 3Hthymidine incorporation by concanavalin A Con A
stimulated human lymphocytes, splenocytes and EpsteinBarr virus EBVtransformed human Bcell lymphoblastoid
cell line LCL. /They/ found that dimyristoylphosphatidylcholine DMPC and dimyristoylphosphatidylglycerol DMPG
were toxic to the tested cells. However, addition of cholesterol to the lipids at DMPC:DMPG:cholesterol=7:1:8 molar
ratio almost completely eliminated the lipid toxicity to these cells. Liposomal curcumin had similar or even stronger
inhibitory effects on Con Astimulated human lymphocyte, splenocyte and LCL proliferation. /The authors/conclude
that liposomal curcumin may be useful for intravenous administration to improve the bioavailability and efficacy,
facilitating in vivo studies that could ultimately lead to clinical application of curcumin./Liposomal curcumin/ Abstract:
PubMed
Chen C et al; Int J Pharm 366 (12): 1339 (2009)
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/OTHER TOXICITY INFORMATION/... As a dietderived agent, curcumin has no severe toxicity except for minor
gastrointestinal side effects even up to the dosage of 8 grams for 3 months... Abstract: PubMed
Fan X et al; Curr Pharm Des 19 (11): 201131 (2013)
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/OTHER TOXICITY INFORMATION/ ... Establishing the entire toxicological profile is thus indispensable for proving the
human safety of nanocarriers, which was the primary objective of the current investigation. The developed curcumin
loaded polymeric nanoparticles of Eudragit S100 were subjected to various toxicological evaluations which included
acutetoxicity study, subacutetoxicity study 28 days and various genotoxicity studies like in vivo Micronucleus
assay, in vivo Chromosomal Aberration assay and in vivo Comet assay. The formulation was found to be nontoxic at
the dose equivalent to 2000 mg/kg of body weight of curcumin in the acutetoxicity study. Subacutetoxicity study
proved the safety of the formulation for prolonged administration at the commonly used therapeutic dose of 100
mg/kg of body weight of curcumin and at twice the therapeutic dose. Genotoxicity studies proved the cellular safety
of the developed formulation at the therapeutic dose, and even at doses equivalent to thrice the therapeutic dose.
Thus the developed curcumin loaded polymeric nanoparticles of Eudragit S100 were found to be safe for oral
administration for a short as well as a prolonged duration./ pHsensitive nanoparticles of curcumin/ Abstract: PubMed
Dandekar P et al; Food Chem Toxicol 48 (89): 207389 (2010)
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/OTHER TOXICITY INFORMATION/ Biomedical investigations of curcumin and curcuminoids have provided evidence
of a wide range of molecular and cellular activities, most related to redox reactions and signal transduction. The main
goal of the present study was to compare antioxidant activities of curcumin with those of resveratrol, a polyphenol
present in some dietary plants such as Vitis vinifera L. and Arachis hypogaea L. and many other, nondietary plants.
Combinations of the two were also examined for potential synergism in a hemeenhanced oxidation reaction.
Curcumin exhibited antioxidant effects at all time points 15 min; 10 uM, e.g., 30.5 +/ 11.9% SEM oxidation relative
to controls without phytochemicals p < 0.01 at 3 min, a time chosen for comparisons. The same concentration of
resveratrol exhibited about half of curcumin's activity. Curcumin and resveratrol together 5 uM each resulted in a
synergistic antioxidant effect: 15.5 +/ 1.7% greater than an average of individual activities. This synergy was
significantly greater p < 0.05; about 4fold than that of curcumin together with the flavonol quercetin. In conclusion,
curcumin is a potent antioxidant in a reaction that may be relevant to in vivo toxicity. In relation to two other well
known antioxidants, curcumin shows significantly greater synergism with resveratrol than with quercetin. Abstract:
PubMed
Aftab N, Vieira A; Phytother Res 24 (4): 5002 (2010)
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13.1.4 NonHuman Toxicity Excerpts
/LABORATORY ANIMALS: Acute Exposure/ An acute toxicity study showed that mice treated with ...ZnIIcurcumin 2
g/kg manifested no abnormal signs./ZincIIcurcumin complex/ Abstract: PubMed
Mei X et al; Chem Biol Interact 181 (3): 31621 (2009)
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/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ 100 mg/kg of curcumin admin orally for 6 consecutive
days produced gastric ulceration in albino rats due to reduction in the mucin content of gastric juice.
GUPTA ET AL; INDIAN J MED RES 71(MAY) 806 (1980)
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/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Curcumin, a polyphenol, is obtained from turmeric, the
ground rhizomes of Curcuma longa L. Extensive research over the past half century has revealed several health
benefits of curcumin. The objective of the present study was to investigate potential adverse effects, if any, of a novel
solid lipid curcumin particle SLCP preparation in rats following acute and subchronic administration. The oral LD50 of
the preparation in rats as well as in mice was found to be greater than 2000 mg/kg body weight bw. In the
subchronic toxicity study, Wistar rats 10/sex/group were administered via oral gavage 0 control, 180, 360, and 720
mg/kg bw/day of SLCP preparation for 90 days. Administration of the curcumin preparation did not result in any
toxicologically significant treatmentrelated changes in clinical including behavioral observations, ophthalmic
examinations, body weights, body weight gains, feed consumption, and organ weights. No adverse effects of the
curcumin preparation were noted on the hematology, serum chemistry parameters, and urinalysis. Terminal necropsy
did not reveal any treatmentrelated gross or histopathology findings. Based on the results of this study, the No
ObservedAdverseEffect Level NOAEL for this standardized novel curcumin preparation was determined as 720
mg/kg bw/day, the highest dose tested. /Solid lipid curcumin particle/ Abstract: PubMed
Dadhaniya P et al; Food Chem Toxicol 49 (8): 183442 (2011)
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/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ The reproductive toxicity of curcumin, turmeric
yellow, in Wistar rats was studied in order to generate additional relevant toxicity information for the use of curcumin
in humans by oral administration. The two generation reproduction study was designed and conducted in accordance
with OECD Guideline No. 416... The curcumin, mixed in the experimental diet at the concentrations of 1500, 3000 and
10,000 ppm was fed to three groups of rats, i.e., low, mid and high dose groups, and studied for two successive
generations. A concurrent control group received experimental diet without the curcumin mixture. There were no
treatment related adverse toxicological effects in the parental animals. No gross or microscopic changes were
observed in any of the organs. None of the reproductive parameters were affected and there were no effects on the
offspring other than a small reduction in preweaning body weight gain of the F2 pups at the highest dose level. It
was concluded that the no observed adverse effect level NOAEL for reproductive toxicity of curcumin, fed in the diet
for two successive generations to rats in this study was 10,000 ppm, which is equivalent to 847 and 959 mg/kg
bodyweight bw per day for male rats and 1043 and 1076 for females for F0 and F1 generations, respectively...The
JECFA group considered that the small body weight reduction in the F2 pups of the highest dose group prevented
this from being regarded as a no adverse effect level, and so allocated an ADI for curcumin of 03 mg/kg bw based on
the intake of 250320 mg/kg bw in the middose group as the NOEL. Abstract: PubMed
Ganiger S et al; Food Chem Toxicol 45 (1): 649 (2007)
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/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Curcumin, a polyphenol derived from the rhizome
turmeric, has potential as an anticancer agent. We synthesized an amphipathic/surfactant pegylated curcumin
curcuminPEG designed for parenteral administration. Objectives of these investigations were to assess sideeffects
of a therapeutic regimen of curcuminPEG in a preclinical model. Intraperitoneal ip tumor burdens were reduced in
athymic female mice grafted with human SKOV3 ovarian adenocarcinoma cells and injected intravenously iv with
curcuminPEG. There were no gross anatomical or histopathological effects detected in nonreproductive organs.
Uteri luminal fluid imbibition and ovaries decreased folliculogenesis were affected by treatment. CurcuminPEG ip
hastened the onset of puberty in immature female mice. Live births were reduced in mature females housed with
males and treated iv with curcuminPEG; mating vaginal plugs was not affected. Accessory gland weights, testicular
testosterone concentrations, and spermatogenesis were diminished in mature male mice following iv curcuminPEG.
Estrogenic/antiandrogenic and pregnancydisrupting effects of a water soluble/bioavailable curcumin were
demonstrated. /CurcuminPEG/[Murphy CJ et al; Reprod Toxicol 34 1: 1204 2012] Full text: PMC3387530 Abstract:
PubMed
from HSDB
/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Embryotoxic and teratogenic effects of curcumin
on the development of zebrafish embryo were investigated in this study. The LD50 values of curcumin 24hr
incubation were estimated at 7.5 uM and 5 uM for embryos and larvae, respectively. The developmental defects
caused by curcumin treatments include bent or hooklike tails, spinal column curving, edema in pericardial sac,
retarded yolk sac resorption, and shorter body length. In curcumintreated larvae, fluorescence signals of curcumin
were found in edamae sac and some skin cells. Together, these results indicate that zebrafish are suitable model
organisms to study the toxic effects of curcumin. Abstract: PubMed
Wu JY et al; Biol Pharm Bull 30 (7): 13369 (2007)
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/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ A twogeneration study in Wistar rats was
conducted according to OECD guideline 416 May 1983 using curcumin comprising 80% diferuloylmethane, 99%
total curcuminoids. ...Groups of 30 male and 30 female rats were fed diets containing curcumin at a concentration of
0, 1500, 3000 or 10 000 mg/kg of diet starting from 10 weeks before the mating period and throughout mating.
Treatment of females continued throughout pregnancy and weaning of the offspring. The total periods of treatment
were 21 weeks for the parental generation and 24 weeks for the F1 generation. On postnatal day 4, the litter sizes of
the F1 offspring were standardized to a maximum of eight. After weaning, 30 male and 30 females of the F1
generation were selected to become the parents of the F2 generation. Parents were observed for clinical signs, body
weights, food intake, cohabitation interval and duration of gestation. Pups were weighed on postnatal days 1, 4, 7, 14
and 21. All parents, F1 weanlings not selected for mating and all F2 weanlings were subjected to complete necropsy at
terminal sacrifice. The concentrations used corresponded to doses of 0, 130140, 250290 or 850960 mg/kg bw per
day in males, and 0, 160, 310320 or 10001100 mg/kg bw per day in females. The following indices were calculated:
male and female fertility index, percentage of matings resulting in pregnancy, number of implantations, percentage of
pregnancies resulting in birth of live litters, percentage of live pups born, postimplantation loss, mean litter size and
mean viable litter size, live birth index, percentage survival of pups at postnatal days 4, 7, 14 and 21. Ovaries, uterus,
vagina/cervix, testes, epididymides, seminal vesicles, prostate, coagulating glands, liver, kidney, pituitary and adrenals
were examined histologically. There was a doserelated decrease in bodyweight gain in the dams of the parental
generation during days 1015 of gestation, which was statistically significantly different from that of controls body
weight gains, >80% that of controls at the intermediate and highest doses. At this time, body weights were reported
to be below the range of values for the historical controls. However, maternal body weights did not differ significantly
between groups at the end of gestation. The mean body weights of the F2 offspring both sexes combined were
significantly decreased on postnatal days 1 and 7 at the intermediate dose, and on postnatal days 7, 14 and 21 at the
highest dose. A doserelated trend was apparent, but the effect was small, with average body weights being >90%
that of the control pups, and the observed changes were reported to be within the range of the data for historical
controls. There were no other effects on general health, body weight, pup survival and fertility indices in either
generation. The effects at the intermediate dose were observed at isolated timepoints only and were considered to
be incidental; and therefore this dose, equal to 250320 mg/kg bw per day for the F1 generation, was the NOEL
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/BEHAVIORAL STUDIES/ Chronic stress occurs in everyday life and induces impaired spatial cognition, neuroendocrine
and plasticity abnormalities. A potential therapeutic for these stress related disturbances is curcumin, derived from the
curry spice turmeric. Previously /researchers/ demonstrated that curcumin reversed the chronic stressinduced
behavioral deficits in escape from an aversive stimulus, however the mechanism behind its beneficial effects on stress
induced learning defects and associated pathologies are unknown. This study /in male Sprague Dawley rats/
investigated the effects of curcumin on restraint stressinduced spatial learning and memory dysfunction in a water
maze task and on measures related neuroendocrine and plasticity changes. The results showed that memory deficits
were reversed with curcumin in a dose dependent manner, as were stressinduced increases in serum corticosterone
levels. These effects were similar to positive antidepressant imipramine. Additionally, curcumin prevented adverse
changes in the dendritic morphology of CA3 pyramidal neurons in the hippocampus, as assessed by the changes in
branch points and dendritic length. In primary hippocampal neurons it was shown that curcumin or imipramine
protected hippocampal neurons against corticosteroneinduced toxicity. Furthermore, the portion of
calcium/calmodulin kinase II CaMKII that is activated phosphorylated CaMKII, pCaMKII, and the glutamate receptor
subtype NMDA2B expressions were increased in the presence of corticosterone. These effects were also blocked
by curcumin or imipramine treatment. Thus, curcumin may be an effective therapeutic for learning and memory
disturbances as was seen within these stress models, and its neuroprotective effect was mediated in part by
normalizing the corticosterone response, resulting in downregulating of the pCaMKII and glutamate receptor levels.
Abstract: PubMed
Xu Y et al; Neuropharmacology 57 (4): 46371 (2009)
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/GENOTOXICITY/ Curcumin was found to be negative when tested for mutagenicity using the Salmonella/microsome
preincubation assay, using the standard protocol approved by the National Toxicology Program NTP. Curcumin was
tested in as many as 5 Salmonella typhimurium strains TA1535, TA1537, TA97, TA98, and TA100 in the presence and
absence of rat and hamster liver S9, at doses of 0.001, 0.003, 0.010, 0.033, 0.100, 0.333, 1.000, and 3.333 mg/plate.
The highest ineffective dose tested in any S. typhimurium strain was 3.333 mg/plate. Precipitate was observed in many
of the cultures at this dose as well as some clearing of the background bacterial lawn.
Mortelmans K et al; Environ Mutagen 8:1119 (1986)
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/GENOTOXICITY/ Chronic inhalation of high concentrations of respirable quartz particles has been implicated in
various lung diseases including lung fibrosis and cancer. Generation of reactive oxygen species ROS and oxidative
stress is considered a major mechanism of quartz toxicity. Curcumin, a yellow pigment from Curcuma longa, has been
considered as nutraceutical because of its strong antiinflammatory, antitumour and antioxidant properties. The aim
of our present study was to investigate whether curcumin can protect lung epithelial cells from the cytotoxic,
genotoxic and inflammatory effects associated with quartz DQ12 exposure. Electron paramagnetic resonance EPR
measurements using the spintrap DMPO demonstrated that curcumin reduces hydrogen peroxidedependent
hydroxylradical formation by quartz. Curcumin was also found to reduce quartzinduced cytotoxicity and
cyclooxygenase 2 COX2 mRNA expression in RLE6TN rat lung epithelial cells RLE. Curcumin also inhibited the
release of macrophage inflammatory protein2 MIP2 from RLE cells as observed upon treatment with interleukin1
beta IL1beta and tumour necrosis factoralpha TNFalpha. However, curcumin failed to protect the RLE cells from
oxidative DNA damage induced by quartz, as shown by formamidopyrimidine glycosylase FPGmodified comet assay
and by immunocytochemistry for 8hydroxydeoxyguanosine. In contrast, curcumin was found to be a strong inducer
of oxidative DNA damage itself at noncytotoxic and antiinflammatory concentrations. In line with this, curcumin also
enhanced the mRNA expression of the oxidative stress response gene heme oxygenase1 ho1. Curcumin also
caused oxidative DNA damage in NR8383 rat alveolar macrophages and A549 human lung epithelial cells. Taken
together, these observations indicate that one should be cautious in considering the potential use of curcumin in the
prevention or treatment of lung diseases associated with quartz exposure. Abstract: PubMed
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/GENOTOXICITY/ There was a significant timedependent reduction in the number of radiationinduced

micronucleated polychromatic erythrocytes in mice given single gavage doses of 5, 10 or 20 mg/kg bw curcumin in
peanut oil.
WHO ; WHO Food Additives Series 35 Curcumin; Available from, as of November 6, 2013:
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/GENOTOXICITY/ Using the Ames test, curcumin itself a nonmutagen, inhibited the mutagenic effects of chili extract
and capsaicin. Similarly, curcumin was reported to inhibit the activity of known environmental mutagens which require
metabolic activation, although it was reported to be ineffective against mutagens which do not require metabolic
activation.
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/GENOTOXICITY/ Micronucleus in vivo assay perfomed in male Fischer 344 rats was negative.
NTP; Testing Status of Agents at NTP for Curcumin (CAS RN 458377); Available from, as of November 6, 2013:
http://ntp.niehs.nih.gov/?objectid=BD112293123F79087B53F5979AE705B1
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/GENOTOXICITY/ In vivo, a curcumin preparation of unknown purity administered to mice by intraperitoneal injection
did not induce micronuclei in bone marrow cells, whereas a low level of chromosomal aberrations was reported in the
same cell population. In another in vivo study in mice injected with curcumin of unknown purity there was some
evidence of SCE induction at low frequency above 25 mg/kg bw, while in rats fed curcumin of unknown purity there
was equivocal evidence for the induction of chromosomal aberrations.
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/ALTERNATIVE and IN VITRO TESTS/ In the previous study, we unraveled the unique "erasure strategy" during the
mouse spermiogenesis. Chromatin associated proteins sequentially disassociated from the spermatid chromosome,
which led to the termination of transcription in elongating spermatids. By this process, a relatively naive paternal
chromatin was generated, which might be essential for the zygotic development. /The authors/ supposed the
regulation of histone acetylation played an important role throughout this "erasure" process. In order to verify this
hypothesis, /they/ treated mouse spermatids in vitro by histone acetylase HAT inhibitor Curcumin. /These/ results
showed an inhibiting effect of Curcumin on the growth of germ cell line in a dosedependent manner. Accordingly,
the apoptosis of primary haploid spermtids was increased by Curcumin treatment. As expected, the acetylated histone
level was downregulated. Furthermore, /the authors/ found the transcription in spermatids ceased in advance, the
dynamics of chromatin associated factors was disturbed by Curcumin treatment. The regulation of histone acetylation
should be one of the core reprogramming mechanisms during the spermiogenesis. The reproductive toxicity of
Curcumin needs to be thoroughly investigated, which is crucial for its further clinical application.[Xiaoyu Xia et al; PLoS
One; 711: e48673 2012] Full text: PMC3492465 Abstract: PubMed
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/ALTERNATIVE and IN VITRO TESTS/ Curcumin, a component of turmeric spice that imparts flavor and color to curry,
is thought to possess antiinflammatory and antioxidant properties in biological tissues. However, while such
efficacies have been described in the context of carcinogenesis, the impact of curcumin on normal cell cycle
regulation is poorly understood. Here, /investigators/ provide evidence of curcumin toxicity in proliferating bovine
aortic endothelial cells, at concentrations relevant to the diet and below those previously reported in cancer models.
Upon confirming curcumin's ability to upregulate hemeoxygenase1 in a dosedependent fashion, we found the
minimally efficacious curcumin concentration to also inhibit endothelial cell DNA synthesis. Moreover, curcumin
concentrations below the minimum 2 uM threshold required to induce hemeoxygenase1 bound tubulin protein in
vitro and triggered hallmark evidence of mitotic catastrophe in vivo. Concentrations as low as 0.1uM curcumin led to
disproportionate DNA segregation, karyorrhexis, and micronucleation in proliferating endothelial cells. While
suggesting a mechanism by which physiological curcumin concentrations inhibit cell cycle progression, these findings
describe heretofore unappreciated curcumin toxicity with potential implications for endothelial growth, development,
and tissue healing.[Jackson SJ et al; Food Chem Toxicol 60 :4318 2013] Full text: PMC3954605 Abstract: PubMed
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/ALTERNATIVE and IN VITRO TESTS/ Curcumin, diferuloyl methane, the yellow pigment component of the curry spice
turmeric Curcuma longa, has immense biological effects and has recently drawn considerable attention. Curcumin
has antibacterial, antiviral, antiinflammatory, and anticancer properties. It has shown a lack of toxicity in animals and
human clinical trials. Yet, its effect on reproduction has not been examined. The present study was conducted to
examine if curcumin affects sperm function in vitro and fertility in vivo. Sperm human and murine were collected and
incubated with curcumin to examine the effect on motility, capacitation/acrosome reaction, and in vitro fertilization.
The effect on in vivo fertility using the mouse model was also examined. Incubation of sperm with curcumin caused a
concentrationdependent decrease in sperm forward motility, capacitation/acrosome reaction, and murine fertilization
in vitro. At higher concentrations, there was a complete block of sperm motility and function within 515 min.
Administration of curcumin, especially intravaginally, caused a significant P<0.001 reduction in fertility. The
antifertility effect of curcumin was reversible. This ... study /repors/ the inhibitory effect of curcumin on sperm
function, fertilization, and fertility. The findings suggest that curcumin may constitute a doubleedged sword to block
conception, infection, and cancer, thus providing an ideal contraceptive. Abstract: PubMed
Naz RK; Mol Reprod Dev 78 (2): 11623 (2011)
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/ALTERNATIVE and IN VITRO TESTS/ Using absorption and fluorescence spectroscopic methods, quantitative cellular
uptake of curcumin, an antioxidant and antitumor agent from Curcuma longa, was calculated in two types of normal
cells: spleen lymphocytes, and NIH3T3 and two tumor cell lines: EL4 and MCF7. Both the uptake and fluorescence
intensity of curcumin were significantly higher in tumor cells compared to the normal cells. A linear dependency on
the uptake was observed with treatment concentration of curcumin. Using laser confocal microscopy, intracellular
localization of curcumin was monitored and the results indicated that curcumin is located both in the cell membrane
and the nucleus. Subcellular fractionation of curcuminloaded MCF7 cells supported the differential distribution of
curcumin in membrane, cytoplasm and nuclear compartments of cell with maximum localization in the membrane.
Cytotoxicity studies in different cell lines indicated that the toxicity of curcumin increased with increasing uptake.
Abstract: PubMed
Kunwar A et al; Biochim Biophys Acta 1780 (4): 6739 (2008)
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/OTHER TOXICITY INFORMATION/ In this study, the R7L10 peptide, which is composed of a 7arginine stretch and a
10leucine stretch, was evaluated as a carrier for the combined delivery of curcumin and plasmid DNA pDNA into the
lungs. Curcumin is a natural product with antiinflammatory and antitumor effects. Curcuminloaded R7L10 R7L10
curucmin was prepared by an oilinwater O/W emulsion/solvent evaporation method. In vitro transfection showed
that R7L10curcumin had higher transfection efficiency than R7L10. Although R7L10curcumin had lower transfection
efficiency than polyethylenimine 25 kDa, PEI25k and lipofectamine, R7L10curcumin had lower cytotoxicity. In gel
retardation assays and heparin competition assays, R7L10curcumin formed a more stable complex with pDNA than
R7L10. The intracellular curcumin delivery efficiency of R7L10curcumin was higher than that of curcumin only.
Furthermore, R7L10curcumin more efficiently decreased TNFalpha level in lipopolysaccharide LPSactivated
Raw264.7 macrophage cells than curcumin only. For in vivo evaluation, pDNA/R7L10curcumin complexes were
administered into mouse lungs by intratracheal instillation. The results revealed that R7L10curcumin delivered pDNA
more efficiently than R7L10, polyLlysine PLL, or PEI25k. In addition, R7L10curcumin decreased TNFalpha level in
lung tissues in an acute lung injury mouse model. In contrast to PEI25k, R7L10curcumin did not show liver toxicity
after intravenous injection. These results suggest that R7L10curcumin is a useful carrier for the combined delivery of
curcumin and pDNA into the lungs./ Molecular carrier system/ Abstract: PubMed
Park JH et al; Biomaterials 33 (27): 654250 (2012)
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/OTHER TOXICITY INFORMATION/ Curcumin, the principal curcuminoid of the popular Indian spice turmeric, has a
wide spectrum of pharmaceutical properties such as antitumor, antioxidant, antiamyloid, and antiinflammatory
activity. However, poor aqueous solubility and low bioavailability of curcumin is a major challenge in its development
as a useful drug. To enhance the aqueous solubility and bioavailability of curcumin, attempts have been made to
encapsulate it in liposomes, polymeric nanoparticles NPs, lipidbased NPs, biodegradable microspheres,
cyclodextrin, and hydrogels. In this work, we attempted to entrap curcumin in novel selfassembled dipeptide NPs
containing a nonprotein amino acid, alpha, betadehydrophenylalanine, and investigated the biological activity of
dipeptidecurcumin NPs in cancer models both in vitro and in vivo. Of the several dehydrodipeptides tested,
methioninedehydrophenylalanine was the most suitable one for loading and release of curcumin. Loading of
curcumin in the dipeptide NPs increased its solubility, improved cellular availability, enhanced its toxicity towards
different cancerous cell lines, and enhanced curcumin's efficacy towards inhibiting tumor growth in Balb/c mice
bearing a B6F10 melanoma tumor. These novel, highly biocompatible, and easy to construct dipeptide NPs with a
capacity to load and release curcumin in a sustained manner significantly improved curcumin's cellular uptake without
altering its anticancer or other therapeutic properties. Curcumindipeptide NPs also showed improved in vitro and in
vivo chemotherapeutic efficacy compared to curcumin alone. Such dipeptideNPs may also improve the delivery of
other potent hydrophobic drug molecules that show poor cellular uptake, bioavailability, and efficacy./ Dipeptide
curcumin NPs/[Alam S et al; Int J Nanomedicine 7: 420722 2012] Full text: PMC3418106 Abstract: PubMed
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/OTHER TOXICITY INFORMATION/ Larval feeding with curcumin induces an extended health span with significantly
increased median and maximum longevities in the adult fly. This phenotype is diet insensitive and shows no additive
effect on longevity when combined with an adult dietary restriction DR diet, suggesting that curcumin and DR
operate via the same or overlapping pathways for this trait. This treatment significantly slows the aging rate so that it
is comparable with that of genetically selected long lived animals. The larval treatment also enhances the adult
animal's geotactic activity in an additive manner with DR, suggesting that curcumin and DR may use different
pathways for different traits. Feeding the drug to adults during only the health span also results in a significantly
extended health span with increased median and maximum life span. This extended longevity phenotype is induced
only during these stagespecific periods. Feeding adults with the drug over their whole life results in a weakly negative
effect on median longevity with no increase in maximum life span. There are no negative effects on reproduction,
although larval curcumin feeding increases development time, and also apparently accelerates the normal latelife
neuromuscular degeneration seen in the legs. Gene expression data from curcuminfed larvae shows that the target
of rapamycin TOR pathway is inhibited in the larvae and the young to midlife adults, although several other genes
involved in longevity extension are also affected. These data support the hypothesis that curcumin acts as if it is a DR
mimetic nutraceutical. These data also suggest that the search for DR mimetics may be enhanced by the use of stage
specific screening of candidate molecules. Abstract: PubMed
Soh JW et al; Exp Geronto 48 (2): 22939 (2013)
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13.1.5 NonHuman Toxicity Values
LD50 Mice oral more than 2000 mg/kg bw /Solid lipid curcumin particle/ Abstract: PubMed
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LD50 Rats oral more than 2000 mg/kg bw /Solid lipid curcumin particle/ Abstract: PubMed
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LD50 Zebrafish embryo 7.5 uM 24 hr; LD50 Zebrafish larvae 5 uM 24 hr Abstract: PubMed
Wu JY et al; Biol Pharm Bull 30 (7): 13369 (2007)
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LD50 Mice oral more than 2000 mg/kg

NTP; Toxicology & Carcinogenesis Studies of Turmeric Oleoresin (Major Component 79%85% Curcumin in F344/N Rats and
B6C3F1 Mice (Feed Studies). Technical Report Series No. 427 (1993) NIH Publication No. 933158; Available from, as of November
6, 2013: http://ntp.niehs.nih.gov/ntp/htdocs/LT_rpts/tr427.pdf
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LD50 Rats oral more than 5000 mg/kg /Curcumin oil/

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13.1.6 National Toxicology Program Reports
2 YEAR STUDY IN RATS The exposure level selection for the 2year study was based on the 13week study, which
showed that rats could tolerate diets containing up to 50,000 ppm. Groups of 60 male and 60 female F344/N rats
were fed diets containing 2,000, 10,000, or 50,000 ppm turmeric, oleoresin for 104 males or 103 females weeks,
which were estimated to deliver average daily doses of 80, 460, or 2,000 mgkg to males and 90, 440, or 2,400 mgkg to
females. Nine or 10 rats from each exposure group were evaluated after 15 months. Survival, Mean Body Weights,
Feed Consumption, and Clinical Findings Survival of exposed male and female rats was similar to that of the controls
male: 0 ppm, 18/50; 2,000 ppm, 17/50; 10,000 ppm, 15/50; 50,000 ppm, 17/50; female: 33/50, 27/50,28/50, 34/50.
The final mean body weights of all exposed, male rats and female rats receiving 2,000 and 10,000 ppm were similar to
those of the controls. The final mean body weights of male and female rats that received 50,000 ppm were slightly
lower up to10% than those of the controls throughout much of the study. Feed consumption by exposed male and
female rats was similar to that by controls throughout the study. The absolute and relative liver weights of female rats
receiving 10,000 or 50,000 ppm were significantly greater than those of controls at the 15month interim evaluation.
There were no clinical findings related to toxicity. Hematology and Clinical Chemistry: In male and female rats
receiving 50,000 ppm the hematocrit values, hemoglobin concentrations, and erythrocyte counts at the 15month
interim evaluations were significantly lower than those in the controls. In addition, platelet counts in male and female
rats that received 50,000 ppm and reticulocyte counts in male rats that received 50,000 ppm were significantly higher
than those in the controls. No biologically significant differences were observed in clinical chemistry parameters.
Pathology Findings: Chemicalrelated nonneoplastic lesions ocured in the gastrointestinal tract of rats that received
50,000 ppm. males receiving 50,000 ppm had increased incidences of ulcers, hyperplasia, and hyperkeratosis of the
forestomach. Male and female rats that received 50,000 ppm had ulcers, chronic active inflammation, and hyperplasia
of the cecum. Similar lesions also occured in the colon of males receiving 50,000 ppm. Male and female rats that
received 50,000 ppm and male rats that received 10,000 ppm had significantly increased incidences of sinus ectasia of
the mesenteric lymph node. The incidences of clitoral gland adenoma in all exposed groups of female rats were
significantly increased. Clitoral gland carcinomas occurred in one control female and in four 2,000 ppm females, but
not in females that received 10,000 or 50,000 ppm. The incidences of clitoral gland adenoma or carcinoma combined
in all exposed groups of female rats were similar 6/50, 16/48, 15/47, 16/49 and did not increase with exposure level.
The incidence of clitoral gland hyperplasia was similar among exposed and control groups of female rats 7/50, 5/48,
4/47, 7/49.
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13 WEEK STUDY IN MICE Groups of 10 male and 10 female B6C3F, mice were fed diets containing 0, 1,000, 5,000,
10,000, 25,000, or 50,000 ppm turmeric oleoresin. There were no deaths attributed to turmeric oleoresin and the final
mean body weights of all exposed groups of male and female mice was similar to those of the controls. Feed
consumption by exposed male and female mice was similar to that by the controls. Dietary levels of 1,000, 5,000,
10,000, 25,000, or 50,000 ppm turmeric oleoresin were estimated to deliver average daily doses of 150, 750, 1,700,
3,850, or 7,700 mg/kg body weight to males and 200, 1,000, 1,800, 4,700 or 9,300 mg/kg to females. Absolute and
relative liver weights of male mice that received 10,000, 25,000 and 50,000 ppm were significantly greater than those
of the controls. Clinical findings in mice included stained fur, and discolored feces and urine. There was no biliogically
significant differences in hematologic, clinical chemistry, or urinalysis parameters, and there were no chemicalrelated
histopathologic lesions. /Turmeric Oleoresin, major component 79%85% curcumin/
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13 WEEKS STUDY IN RATS Groups of 10 male and 10 female F344/Ed rats were fed diets containing 0, 1,000, 5,000,
10,000, 25,000, or 50,000 ppm turmericoleoresin. All rats survived until the end of the study. The final mean body
weight of males receiving 50,000 ppm was 5% lower than that of the controls. Feed consumption by exposed male
and female rats was similar to that by the controls. Dietary levels of 1,000, 5,000, 10,000, 25,000, or 50,000 ppm
turmiric oleoresin were estimated to deliver average daily doses of 50, 250, 480, 1,300, or 2,600 mg/kg bw to males
and 60, 300, 550, 1,450, or 2,800 mg/kg to females. The absolute and relative liver weights of female rats and the
relative liver weights of male rats receiving 5,000, 10,000, 25,000, and 50,000 ppm were significantly greater than
those of the controls. There were no biologically significant differences in hematologic, clinical chemistry, or urinalysis
parameters. Clinical findings included stained fur, and discolored feces and urine of exposed animals, presumably due
to the parent compound or its metabolites. Hyperplasia of the mucosal epithelium was observed in the cecum and
colon of male and female rats that received 5,000 ppm. /Turmeric Oleoresin, major component 79%85% curcumin/
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2YEAR STUDY IN MICE The exposure level selection for the 2year study was based on the 13week study, which
showed that mice could tolerate diets containing up to 50,000 ppm. Groups of 60 male and 60 female B6C3F1 mice
were fed diets containing 2,000, 10,000, or 50,000 ppm turmeric oleoresin for 103 weeks, which were estimated to
deliver average daily doses of 220, 520, or 6,000 mg/kg to males and 320, 1,620, or 8,400 mg/kg to females. Nine or
10 mice from each exposure group were evaluated after 15 months. Survival of exposed male and female mice was
similar to that of the controls male: 0 ppm, 43/50; 2,000 ppm, 43/50; 10,000 ppm, 37/50; 50,000 ppm 42/50; female:
39/50, 41/50,34/50, 42/50. The mean body weight of female mice receiving 50,000 ppm was slightly lower up to
12% than that of the controls from about week 25. The final mean body weights of males that received 50,000 ppm
and females that received 10,000 and 50,000 ppm were significantly lower than those of controls. The final mean body
weights of other exposed groups of male and female mice were similar to those of the controls. Feed consumption by
exposed male and female mice was similar to that by the controls throughout the study. The absolute and relative
liver weights of male and female mice receiving 10,000 and 50,000 ppm were significantly greater than those of the
controls at the 15month interim evaluation. There were no clinical findings related to toxicity. No biologically
significant differences were observed in hematologic parameters. The alkaline phosphatase values of male and female
mice that received 10,000 and 50,000 ppm were significantly higher than those of controls at the 15month interim
evaluation. Pathology Findings: The incidences of hepatocellular adenoma in male and female mice receiving 10,000
ppm, but not those in mice receiving 2,0 or 50,000 ppm, were significantly increased male: 25/50,28/50, 35/50, 30/50;
female: 7/50, 8/50, 19/51, 14/50. The number of male and female mice in the 10,000 and 50,000 ppm groups with
multiple hepatocellular neoplasms was significantly greater than that in the controls. The incidences of hepatocellular
carcinoma were similar among exposed and control groups. In contrast to rats, there were no chemicalrelated non
neoplastic lesions of the gastrointestinal tract in mice. Three males that received 2,000 ppm and three males that
received 10,000 ppm had carcinomas of the small intestine; neoplasms of the small intestine were not observed in
control males or in males that received 50,000 ppm. Female mice receiving 50,000 ppm had a significantly increased
incidence of thyroid gland follicular cell hyperplasia. /Turmeric Oleoresin, major component 79%85% curcumin/
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GENETIC TOXICOLOGY Turmeric oleoresin was not mutagenic in Salmonella typhimurium strains TA100, TA1535,
TA1537, or TA98 with or without exogenous metabolic activation S9. It induced small but significant increases in
sister chromatid exchanges and chromosomal aberrations in cultured Chinese hamster ovary cells. The positive
response in the sister chromatid exchange test occured in the presence of S9, whereas the aberrations response
occurred without S9. /Turmeric Oleoresin, major component 79%85% curcumin/
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CONCLUSIONS: Under the conditions of these 2year feed studies, there was no evidence of carcinogenic activity of
turmeric oleoresin in male F344/N rats administered 2,000, 10,000, or 50,000 ppm. There was equivocal evidence of
carcinogenic activity of turmeric oleoresin in female F344/N rats based on increased incidences of clitoral gland
adenomas in the exposed groups. There was equivocal evidence of carcinogenic activity of turmeric oleoresin in male
B6C3F1 mice based on a marginally increased incidence of hepatocellular adenoma at the 10,000 ppm level, and the
occurrence of carcinomas of the small intestine in the 2,000 and 10,000 ppm groups. There was equivocal evidence of
carcinogenic activity of turmeric oleoresin in female B6C3F1 mice based on an increased incidence of hepatocellular
adenomas in the 10,000 ppm group. /Turmeric Oleoresin, major component 79%85% curcumin/
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13.2 Ecological Information
13.2.1 Environmental Fate/Exposure Summary
Curcumin's production and use as an analytical reagent, food dye, biological stain, as an acidbase indicator, and as
an indicator for boron may result in its release to the environment through various waste streams. Curcumin is found
in saffron, turmeric, and ginger. If released to air, an estimated vapor pressure of 3.1X1012 mm Hg at 25 deg C
indicates curcumin will exist solely in the particulate phase in the atmosphere. Particulatephase curcumin will be
removed from the atmosphere by wet and dry deposition. Curcumin contains chromophores that absorb at
wavelengths >290 nm and, therefore, may be susceptible to direct photolysis by sunlight. If released to soil, curcumin
is expected to have slight mobility based upon an estimated Koc of 3400. Volatilization from moist soil surfaces is not
expected to be an important fate process based upon an estimated Henry's Law constant of 7.0X1022 atmcu
m/mole. Curcumin is not expected to volatilize from dry soil surfaces based upon its vapor pressure. Biodegradation
data in soil or water were not available; however, curcumin was 75% biodegraded by a mutant strain of
Phanerochaete chrysospporium, a whiterot fungi. If released into water, curcumin is expected to adsorb to
suspended solids and sediment based upon the estimated Koc. Volatilization from water surfaces is not expected to
be an important fate process based upon this compound's estimated Henry's Law constant. An estimated BCF of 68
suggests the potential for bioconcentration in aquatic organisms is moderate. Hydrolysis is not expected to be an
important environmental fate process since this compound lacks functional groups that hydrolyze under
environmental conditions pH 5 to 9. Occupational exposure to curcumin may occur through inhalation and dermal
contact with this compound at workplaces where curcumin is produced or used. Use data indicate that the general
population may be exposed to curcumin via ingestion of food. SRC
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13.2.2 Natural Occurring Sources
Curcumin is found in the plant Curcuma longa, the common names of which are Tumeric and Indian Saffron.
Curcumin is also found in ginger Zingiber officinale1. Both plants come from the same plant family, Zingiberaceae,
the Ginger familySRC.
(1) USDA; Dr. Duke's Phytochemical and Ethnobotanical Databases. Plants with a chosen chemical. Curcumin. Washington, DC: US
Dept Agric, Agric Res Service. Available from, as of Nov 12, 2013: http://www.arsgrin.gov/duke/
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13.2.3 Artificial Sources
Curcumin's production and use as analytical reagent, food dye, biological stain, as an acidbase indicator brownish
red with alkalies, yellow with acids pH range 7.48.6, and as an indicator for boron1 may result in its release to the
environment through various waste streamsSRC.
(1) Lewis RJ Sr; Hawley's Condensed Chemical Dictionary. 15th ed., New York, NY: John Wiley & Sons, Inc. p. 639 (2007)
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13.2.4 Environmental Fate
TERRESTRIAL FATE: Based on a classification scheme1, an estimated Koc value of 3400SRC, determined from a
structure estimation method2, indicates that curcumin is expected to have slight mobility in soilSRC. Volatilization
of curcumin from moist soil surfaces is not expected to be an important fate processSRC given an estimated Henry's
Law constant of 7.0X1022 atmcu m/moleSRC, using a fragment constant estimation method3. Curcumin is not
expected to volatilize from dry soil surfacesSRC based upon an estimated vapor pressure of 3.1X1012 mm Hg at 25
deg CSRC, determined from a fragment constant method2. Biodegradation data in soil were not availableSRC,
2013; however, curcumin was 75% biodegraded by a mutant strain of Phanerochaete chrysospporium, a whiterot
fungi4.
(1) Swann RL et al; Res Rev 85: 1728 (1983) (2) US EPA; Estimation Program Interface (EPI) Suite. Ver. 4.1. Nov, 2012. Available
from, as of Nov 13, 2013: http://www.epa.gov/oppt/exposure/pubs/episuitedl.htm (3) Meylan WM, Howard PH; Environ Toxicol
Chem 10: 128393 (1991) (4) Leatham GF et al; Appl Environ Microbiol 46: 1917 (1983)
from HSDB
AQUATIC FATE: Based on a classification scheme1, an estimated Koc value of 3400SRC, determined from a
structure estimation method2, indicates that curcumin is expected to adsorb to suspended solids and
sedimentSRC. Volatilization from water surfaces is not expected3 based upon an estimated Henry's Law constant of
7.0X1022 atmcu m/moleSRC, developed using a fragment constant estimation method4. According to a
classification scheme5, an estimated BCF of 68SRC, from an estimated log Kow of 3.292 and a regressionderived
equation2, suggests the potential for bioconcentration in aquatic organisms is moderateSRC. Biodegradation data
in water were not availableSRC, 2013; however, curcumin was 75% biodegraded by a mutant strain of Phanerochaete
chrysospporium, a whiterot fungi6.
(1) Swann RL et al; Res Rev 85: 1728 (1983) (2) US EPA; Estimation Program Interface (EPI) Suite. Ver. 4.1. Nov, 2012. Available
from, as of Nov 13, 2013: http://www.epa.gov/oppt/exposure/pubs/episuitedl.htm (3) Lyman WJ et al; Handbook of Chemical
Property Estimation Methods. Washington, DC: Amer Chem Soc pp. 151 to 1529 (1990) (4) Meylan WM, Howard PH; Environ
Toxicol Chem 10: 128393 (1991) (5) Franke C et al; Chemosphere 29: 150114 (1994) (6) Leatham GF et al; Appl Environ Microbiol
46: 1917 (1983)
from HSDB
ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the
atmosphere1, curcumin, which has an estimated vapor pressure of 3.1X1012 mm Hg at 25 deg CSRC, determined
from a fragment constant method2, is expected to exist solely in the particulate phase in the ambient atmosphere.
Particulatephase curcumin may be removed from the air by wet and dry depositionSRC. Curcumin contains
chromophores that absorb at wavelengths >290 nm4 and, therefore, may be susceptible to direct photolysis by
sunlightSRC.
(1) Bidleman TF; Environ Sci Technol 22: 361367 (1988) (2) US EPA; Estimation Program Interface (EPI) Suite. Ver. 4.1. Nov, 2012.
Available from, as of Nov 13, 2013: http://www.epa.gov/oppt/exposure/pubs/episuitedl.htm (3) Meylan WM, Howard PH;
Chemosphere 26: 229399 (1993) (4) Lyman WJ et al; Handbook of Chemical Property Estimation Methods. Washington, DC: Amer
Chem Soc pp. 812 (1990)
from HSDB
13.2.5 Biodegredation
PURE CULTURE: 14CLabeled curcumin, present at 1 mg/10 uL of N,Ndimethylformamide, was 75% biodegraded via
ring cleavage of the catechol moiety when incubated for 3 days with a mutant strain of Phanerochaete
chrysospporium, a whiterot fungi1.
(1) Leatham GF et al; Appl Environ Microbiol 46: 1917 (1983)
from HSDB
13.2.6 Abiotic Degredation
Curcumin is not expected to undergo hydrolysis in the environment due to the lack of functional groups that
hydrolyze under environmental conditions1. Curcumin contains chromophores that absorb at wavelengths >290
nm1 and, therefore, may be susceptible to direct photolysis by sunlightSRC. When exposed to gasphase nitric acid,
curcumin yields small amounts of oxidation products. The color changed from orange to a slightly faded orange over
12 weeks. Vanillin and vanillic acid form readily upon curcumin exposure to ozone2.
(1) Lyman WJ et al; Handbook of Chemical Property Estimation Methods. Washington, DC: Amer Chem Soc pp. 74, 75, 812
(1990) (2) Grosjean D et al; Environ SCi Technol 26: 9529 (1992)
from HSDB
13.2.7 Bioconcentration
An estimated BCF of 68 was calculated in fish for curcuminSRC, using an estimated/ log Kow of 3.291 and a
regressionderived equation1. According to a classification scheme2, this BCF suggests the potential for
bioconcentration in aquatic organisms is moderateSRC.
(1) US EPA; Estimation Program Interface (EPI) Suite. Ver. 4.1. Nov, 2012. Available from, as of Nov 13, 2013:
http://www.epa.gov/oppt/exposure/pubs/episuitedl.htm/ (2) Franke C et al; Chemosphere 29: 150114 (1994)
from HSDB
13.2.8 Soil Adsorption/Mobility
Using a structure estimation method based on molecular connectivity indices1, the Koc of curcumin can be
estimated to be 3400SRC. According to a classification scheme2, this estimated Koc value suggests that curcumin is
expected to have slight mobility in soil.
(1) US EPA; Estimation Program Interface (EPI) Suite. Ver. 4.1. Nov, 2012. Available from, as of Nov 13, 2013:
http://www.epa.gov/oppt/exposure/pubs/episuitedl.htm (2) Swann RL et al; Res Rev 85: 1728 (1983)
from HSDB
13.2.9 Volatilization from Water/Soil
The Henry's Law constant for curcumin is estimated as 7.0X1022 atmcu m/moleSRC using a fragment constant
estimation method1. This Henry's Law constant indicates that curcumin is expected to be essentially nonvolatile from
water and moist soil surfaces2. Curcumin is not expected to volatilize from dry soil surfacesSRC based upon an
estimated vapor pressure of 3.1X1012 mm HgSRC, determined from a fragment constant method3.
(1) Meylan WM, Howard PH; Environ Toxicol Chem 10: 128393 (1991) (2) Lyman WJ et al; Handbook of Chemical Property
Estimation Methods. Washington, DC: Amer Chem Soc pp. 151 to 1529 (1990) (3) US EPA; Estimation Program Interface (EPI)
Suite. Ver. 4.1. Nov, 2012. Available from, as of Nov 13, 2013: http://www.epa.gov/oppt/exposure/pubs/episuitedl.htm
from HSDB
13.2.10 Plant Concentrations
Curcumin concentrations in plants1.

Genus species Name Part Quantity ppm
Curcuma longa Indian saffron rhizome 38,888
Curcuma xanthorrhiza Javan turmeric rhizome 10,000
Curcuma zedoaria Shoti rhizome 1,000
Zingiber officinale Ginger plant
(1) USDA; Dr. Duke's Phytochemical and Ethnobotanical Databases. Plants with a chosen chemical. Curcumin. Washington, DC: US
Dept Agric, Agric Res Service. Available from, as of Nov 12, 2013: http://www.arsgrin.gov/duke/
from HSDB
13.2.11 Probable Routes of Human Exposure
NIOSH NOES Survey 19811983 has statistically estimated that 690 workers none of these were female were
potentially exposed to curcumin in the US1. Occupational exposure to curcumin may occur through inhalation and
dermal contact with this compound at workplaces where curcumin is produced or used. Use data indicate that the
general population may be exposed to curcumin via ingestion of foodSRC.
(1) NIOSH; NOES. National Occupational Exposure Survey conducted from 19811983. Estimated numbers of employees potentially
exposed to specific agents by 2digit standard industrial classification (SIC). Available from, as of Nov 12, 2013:
http://www.cdc.gov/noes/
from HSDB
14 Literature
14.1 Depositor Provided PubMed Citations
CLICK TO LOAD...
from PubChem
14.2 NLM Curated PubMed Citations
CLICK TO LOAD...
from PubChem
14.3 Synthesis References

Wehrli, Christof. Curcumin synthesis. PCT Int. Appl. 2007, 11pp.
14.4 Metabolite References
Download
1 to 2 of 2
PMID Reference
Singh S, Khar A: Biological effects of curcumin and its role in cancer chemoprevention and therapy.
16712454
Anticancer Agents Med Chem. 2006 May;63:25970.
Maheshwari RK, Singh AK, Gaddipati J, Srimal RC: Multiple biological activities of curcumin: a short
16413584
review. Life Sci. 2006 Mar 27;7818:20817. Epub 2006 Jan 18.
Download
1 to 1 of 1
PMID Reference
Yannai, Shmuel. 2004 Dictionary of food compounds

with CDROM: Additives, flavors, and ingredients. Boca
Raton: Chapman & Hall/CRC.
15 Patents
15.1 DepositorSupplied Patent Identifiers
CLICK TO LOAD...
from PubChem
16 Biomolecular Interactions and Pathways
16.1 Biosystems and Pathways
CLICK TO LOAD...
from PubChem
17 Biological Test Results
17.1 BioAssay Results
CLICK TO LOAD...
from PubChem
18 Classification
18.1 Ontologies
18.1.1 MeSH Tree
CLICK TO LOAD...
from MeSH
18.1.2 ChEBI Ontology
CLICK TO LOAD...
from ChEBI
18.1.3 WIPO IPC
CLICK TO LOAD...
from WIPO
19 Information Sources
1. CAMEO Chemicals /source/CAMEO Chemicals
Curcumin
https://cameochemicals.noaa.gov/chemical/20062 https://cameochemicals.noaa.gov/chemical/20062
2. ChemIDplus /source/ChemIDplus
Turmeric extract
https://chem.nlm.nih.gov/chemidplus/sid/0008024371 https://chem.nlm.nih.gov/chemidplus/sid/0008024371
Curcumin
https://chem.nlm.nih.gov/chemidplus/sid/0000458377 https://chem.nlm.nih.gov/chemidplus/sid/0000458377
3. EPA DSStox /source/EPA DSStox

Curcumin
https://comptox.epa.gov/dashboard/dsstoxdb/results?search=DTXSID8031077
https://comptox.epa.gov/dashboard/dsstoxdb/results?search=DTXSID8031077
4. European Chemicals Agency ECHA /source/European Chemicals Agency ECHA

Oils, curcuma
https://echa.europa.eu/ https://echa.europa.eu/
1,7bis(4hydroxy3methoxyphenyl)hepta1,6diene3,5dione
https://echa.europa.eu/informationonchemicals/clinventorydatabase//discli/details/102452
turmeric extract
5. Human Metabolome Database /source/Human Metabolome Database

Curcumin
http://www.hmdb.ca/metabolites/HMDB02269 http://www.hmdb.ca/metabolites/HMDB02269
Curcumin I
http://www.hmdb.ca/metabolites/HMDB39611 http://www.hmdb.ca/metabolites/HMDB39611
6. EU Food Improvement Agents /source/EU Food Improvement Agents

CURCUMIN
http://eurlex.europa.eu/legalcontent/EN/ALL/?uri=CELEX%3A32012R0231 http://eurlex.europa.eu/legalcontent/EN/ALL/?
uri=CELEX%3A32012R0231
7. NCIt /source/NCIt
Curcumin
https://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI_Thesaurus&ns=NCI_Thesaurus&code=C401
https://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI_Thesaurus&ns=NCI_Thesaurus&code=C401
8. HSDB /source/HSDB
CURCUMIN
http://toxnet.nlm.nih.gov/cgibin/sis/search/r?dbs+hsdb:@term+@rn+@rel+458377 http://toxnet.nlm.nih.gov/cgi
bin/sis/search/r?dbs+hsdb:@term+@rn+@rel+458377
9. ClinicalTrials.gov /source/ClinicalTrials.gov
curcumin
https://clinicaltrials.gov/ https://clinicaltrials.gov/
10. FAO/WHO Food Additive Evaluations JECFA /source/FAO/WHO Food Additive Evaluations
JECFA
TURMERIC OLEORESIN
http://apps.who.int/foodadditivescontaminantsjecfadatabase/chemical.aspx?chemID=4713 http://apps.who.int/food
additivescontaminantsjecfadatabase/chemical.aspx?chemID=4713
CURCUMA
CI NATURAL YELLOW 3
11. FDA/SPL Indexing Data /source/FDA/SPL Indexing Data

IT942ZTH98
https://www.fda.gov/ForIndustry/DataStandards/SubstanceRegistrationSystemUniqueIngredientIdentifierUNII/
https://www.fda.gov/ForIndustry/DataStandards/SubstanceRegistrationSystemUniqueIngredientIdentifierUNII/
12. Flavor & Extract Manufacturers Association FEMA /source/Flavor & Extract Manufacturers
Association FEMA
TURMERIC EXTRACT (CURCUMA LONGA L.)
https://www.femaflavor.org/flavor/library/turmericextractcurcumalongal https://www.femaflavor.org/flavor/library/turmeric
extractcurcumalongal
13. NIST /source/NIST

Curcumin
http://www.nist.gov/srd/nist1a.cfm http://www.nist.gov/srd/nist1a.cfm
14. Wikipedia /source/Wikipedia

curcumin
https://en.wikipedia.org/wiki/Curcumin https://en.wikipedia.org/wiki/Curcumin
15. PubChem
Data deposited in or computed by PubChem
https://pubchem.ncbi.nlm.nih.gov https://pubchem.ncbi.nlm.nih.gov
16. MeSH /source/MeSH

Curcumin
https://www.ncbi.nlm.nih.gov/mesh/68003474 https://www.ncbi.nlm.nih.gov/mesh/68003474
MeSH Tree
http://www.nlm.nih.gov/mesh/meshhome.html http://www.nlm.nih.gov/mesh/meshhome.html
Enzyme Inhibitors
AntiInflammatory Agents, NonSteroidal
Antineoplastic Agents
Coloring Agents
17. ChEBI /source/ChEBI

ChEBI Ontology
http://www.ebi.ac.uk/chebi/userManualForward.do#ChEBI%20Ontology
http://www.ebi.ac.uk/chebi/userManualForward.do#ChEBI%20Ontology
18. WIPO /source/WIPO

International Patent Classification
http://www.wipo.int/classifications/ipc/ http://www.wipo.int/classifications/ipc/

Curcumin - IC21H20O6 - PubChem

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2017618 curcumin|IC21H20O6PubChem

Compound Summary for CID 969516

Curcumin Cite this Record

PubChem CID: 969516

Molecular Formula: IC21H20O6 or C21H20O6

Drug Information: Therapeutic Uses Clinical Trials FDA UNII

Safety Summary: Laboratory Chemical Safety Summary LCSS

PUBCHEM COMPOUND CURCUMIN Create Date: 20040916

3 Names and Identifiers

4 Chemical and Physical Properties

7 Drug and Medication Information

8 Food Additives and Ingredients

9 Pharmacology and Biochemistry

10 Use and Manufacturing

12 Safety and Hazards

16 Biomolecular Interactions and Pathways

17 Biological Test Results

Show Hydrogens Show Atoms Animate

3 Names and Identifiers

3.1 Computed Descriptors

3.1.1 IUPAC Name

3.1.3 InChI Key

3.1.4 Canonical SMILES

3.1.5 Isomeric SMILES

3.2 Molecular Formula

3.3 Other Identifiers

3.3.3 FEMA Number

Description chemical compound

3.4.1 MeSH Synonyms

3.4.2 DepositorSupplied Synonyms

4 Chemical and Physical Properties

4.1 Computed Properties

Property Name Property Value

Molecular Weight 368.385 g/mol

Hydrogen Bond Donor Count 2

Hydrogen Bond Acceptor Count 6

Rotatable Bond Count 8

Topological Polar Surface Area 93.1 A^2

Monoisotopic Mass 368.126 g/mol

Exact Mass 368.126 g/mol

Compound Is Canonicalized true

Heavy Atom Count 27

Defined Atom Stereocenter Count 0

Undefined Atom Stereocenter Count 0

Defined Bond Stereocenter Count 2

Undefined Bond Stereocenter Count 0

Isotope Atom Count 0

CovalentlyBonded Unit Count 1

4.2 Experimental Properties

4.2.1 Physical Description

PHYSICAL DESCRIPTION: Orangeyellow needles. NTP, 1992

Orangeyellow crystalline powder

Orange yellow prisms, rhombic prisms from methanol

4.2.3 Melting Point

356 to 361 F NTP, 1992

Slightly soluble hot NTP, 1992

In water, 3.12 mg/L at 25 deg C est

Insoluble in ether; soluble in alcohol, glacial acetic acid

Very soluble in ethanol, acetic acid

0.9348 at 59 F NTP, 1992

4.2.6 Vapor Pressure

3.08X1012 mm Hg at 25 deg C est

log Kow = 3.29 est