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Respiration
dr. Isra Thristy, M.Biomed
DEPARTMENT OF BIOCHEMISTRY
FACULTY OF MEDICINE
UNIVERSITAS MUHAMMADIYAH SUMATERA UTARA
2017
Learning Issues :
The process of the respiratory chain
The function of the respiratory chain
Mitochondrion
(g ATP/g tissue)
Heart 16
Brain 6
Kidneys 24
Liver 6
Skeletal Muscle (rest) 0.3
Skeletal Muscle (running) 23.6
Cells use GTP and CTP, as well as UTP and ATP, to form activated
intermediates.
Different anabolic pathways generally use different nucleotides as their
direct source of high phosphate bond energy:
UTP is used for combining sugars,
CTP in lipid synthesis, and
GTP in protein synthesis.
The high-energy phosphate bonds of UTP, GTP, and CTP are energetically
equivalent to ATP and are synthesized from ATP by nucleoside
diphosphokinases and nucleoside monophosphokinases.
Energy from fuel oxidation is converted to the high-energy phosphate bonds
of adenosine triphosphate (ATP) by the process of oxidative phosphorylation.
Most of the energy from oxidation of fuels in the TCA cycle and other
pathways is conserved in the form of the reduced electron-accepting
coenzymes, NADH and FAD(2H).
The electron transport chain oxidizes NADH and FAD(2H), and donates the
electrons to O2, which is reduced to H2O.
Energy from reduction of O2 is used for phosphorylation of adenosine
diphosphate (ADP) to ATP by ATP synthase (F0 ATPase).
The net yield of oxidative phosphorylation is approximately 2.5 moles of ATP
per mole of NADH oxidized, or 1.5 moles of ATP per mole of FAD(2H) oxidized.
Electron Transport Chain: Proteins
Electron transport
chain
Complex I
Alternate Entries
Complex II
(aka succinate
dehydrogenase)
Alternate Entries
Complex III
Complex IV
Fig 19-14
Chemiosmotic
Mechanism
Electron
transport chain
sets up an H+
gradient (proton
motive force).
Energy of the
pmf is harnessed
to make ATP.
Inhibitors of electron transport
Fig 19-6
Fatigue can result from iron-defeciency anemia, which
decreases Fe for Fe-S centers and cytochromes.
Cytochrome c2 oxidase, which contains the O2 binding site,
is inhibited by cyanide.
Mitochondrial DNA (mtDNA), which is maternally inherited,
encodes some of the subunits of the electron transport chain
complexes and ATP synthase.
Oxphos diseases are caused by mutations in nuclear DNA or
mt DNA that decrease mitochondrial capacity for oxidative
phosphorylation.
ATP synthesized from oxidative phosphorylation is actively transported
from the matrix to the intermembrane space by adenine nucleotide
translocase (ANT).
Porins form voltage-dependent anion channels (VDAC) through the outer
mitochondrial membrane for the diffusion of H2O, ATP metabolites, and
other ions.
Under certain types of stress, ANT, VDAC, and other proteins form a
nonspecific open channel known as the mitochondrial permeability
transition pore. This pore is associated with events that lead rapidly to
necrotic cell death.
Clinical aspects
Textbook of Biochemistry with Clinical Correlations, Devlin MT, Willey Liss, 2002/5th
ed.
Harper’s Biochemistry, Murray RK,Granner DK, Mayes PA, Lange MedicalBooks, Mc
Graw-Hill, 2003/26th ed.
Lippincott's illustrated reviews biochemistry, Denise r ferrier, 2014