Influence of Selenife and Fourteen Trace Elements

on Cataractogenesis in the Rot

Thomas R. Shearer, Ruth 5. Anderson, and Jim L. Brirron
The purposes of these experiments were to measure the influence of 14 trace elements on cataractogenesis and to test if these trace elements could prevent cataracts induced by selenium. On days
5-9 postpartum, suckling white rats received daily subcutaneous injections of either selenium (0.15
pinoles Se, as Na 2 SeO 3 , per pup) or selenium plus one of 14 other trace elements (separate subcutaneous injection) at one to five times the molar concentration of selenium. The frequency and severity
of cataracts at three locations in the lens were assessed by slit-lamp examination on day 26-28
postpartum. Seven ions were found to be effective in preventing selenium-induced cataracts (% protection): mercuric (100%), silver (80%), cyanide (75%), arsenite (75%), cadmium (60%), and cupric
(44%). Tellurite ion offered only 20% protection, while ferrous, zinc, lead, chromic, molybdate, tungstate, and vanadate ions provided no protection against selenium-induced cataract. No significant
differences were found between the concentrations of selenium in the lenses of control and cataractous
lenses when measured approximately three weeks after selenium injection. Except for selenium, none
of the trace minerals alone caused cataracts under our experimental conditions. In addition to subcutaneous injection of selenium, oral administration of this element was also found to cause cataract.
It was concluded that among the ions studied, selinite was a powerful and rapid promoter of nuclear
cataract formation, and that the protective ions may serve as useful probes for elucidating the mechanism of selenium-induced cataracts. Invest Ophthalmol Vis Sci 24:417-423, 1983

ticular proteins from rats receiving selenium. Selenium is also noted for its interaction with other trace
minerals,7 and we recently reported that cadmium
ameliorated the frequency of selenium-induced cataract.8 However, the lens contains a variety of other
trace minerals,9 yet it is not known if other trace elements modify selenium-induced cataracts. Most of
the selenium taken in by man is from the diet, yet
there is no evidence on whether or not oral administration of selenium is cataractogenic. Thus, the purposes of the experiments described below were: (1)
to compare 14 trace elements to selenium in their
abilities to promote cataract in the animal model,(2)
to determine if other trace elements ameliorate selenium-induced cataract, and (3) to determine if oral
administration of selenium promotes cataract formation.

Several laboratories have recently shown that injections of elevated quantities of the trace mineral
selenium to rats during the suckling period caused
the formation of bilateral nuclear cataracts.1"4 These
cataracts are interesting because of their speed of formation (3 days)4 and because they may be useful
models for cataracts caused by oxidant stressors. Selenium-induced cataracts have been characterized
histologically,' and several important biochemical
changes have been noted. For example, glutathione
and proteinaceous sulfhydryl levels were decreased,4
while the ratio of insoluble to soluble proteins and
H2O2 were increased in lenses of rats with seleniuminduced cataract5. Hess et al6 recently reported changes
in specific peptides in the soluble and insoluble lenFrom the Departments of Biochemistry and Ophthalmology,
The Oregon Health Sciences University, Portland, Oregon.
Presented in part at the Annual Meeting of the Association for
Research in Vision and Ophthalmology, Sarasota, Florida, May
1982.
Supported by NIH grant EY-3600 from the National Eye Institute and by the R. Blaine Bramble Medical Research Foundation.
Submitted for publication June 17, 1982.
Reprint requests: Thomas R. Shearer, PhD, Departments of
Biochemistry and Ophthalmology, The Oregon Health Sciences
University, Portland, OR 97201.

Materials and Methods

Injection Experiments
Nineteen Sprague-Dawley derived, albino female
rats (Simonsen Laboratories, Inc., Gilroy, CA) with
their litters of pups were individually housed in polypropylene breeding cages with cellulose bedding material. The animals received laboratory chow (Wayne
Lab Blox, F-6, Continental Grain Co., Chicago, IL)

0146-0404/83/0400/417/$ 1.15 Association for Research in Vision and Ophthalmology

417

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418

INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE / April 1983

Table 1. Cataractogenesis by selenite

and other trace minerals

Element
Selenium
Tellurium
Arsenic
Molybdenum
Tungsten
Vanadium
Cyanide
Zinc
Iron
Lead
Cadmium
Copper
Silver
Chromium
Mercury

Ionic
form

Compound
injected

SeO 3 =
TeO-T
AsO 2 "
MoO 4 "
WO 4 "
VO3=

Na 2 SeO 3
K 2 TeO 3
NaAsO 2
Na 2 MoO 4
Na 2 WO 4
NH 4 VO 3

CN"
++

Zn
Fe + +
Pb + +
Cd + +
Cu + +

Ag+

Cr +3
Hg ++

Frequency
Dosage
of cataract
(fimoles
element/rat) (percent)

KCN

0.15
0.15
0.30
0.30
0.30
0.30
0.30

100
0
0
0
0
0
0

ZnCl 2
FeCl2
Pb(C 2 H 3 O 2 ) 2
CdCl2
Cu(C 2 H 3 O 2 ) 2
AgNO 3
CrCl3
HgCl2

0.76
0.45
0.30
0.30
0.30
0.30
0.30
0.15

0
0
0
0
0
0
0
0

and distilled water ab libitum. The animal room was

light (12-hr fluorescent) and temperature (~72) controlled.
On days 5 through 9 postpartum, the suckling pups
received daily 0.05 ml subcutaneous injections of either: (1) saline (controls), (2) selenium or one of the
14 other ions shown in Table 1, or (3) selenium at
one site on the back, and, usually within 5 min, one
of the other ions at a separate site on the back. The
dosage of selenium given was 0.15 jtimoles Se per pup
per day, which averaged approximately 0.70 mg
Se/kg b.w. per day over the 5 days of the injections.
Other ions were given at one to five times the dosage
level of selenium on a molar basis (Table 1) depending on the toxicity of the element. All chemicals injected into the animals were labeled either "reagent
grade" or "chemically pure" except for potassium
tellurite (Sigma), which was not graded but was 98%
pure.
A single injection experiment was also performed
in which suckling pups received single 0.05-ml subcutaneous injections of selenium and cadmium only
on day 10 postpartum. One group of nine animals
received 0.42 /tmoles of selenium per pup, while a
second group of eight animals received 0.42 ^moles
selenium per pup at one injection site on the back
and 0.42 ^tmoles of cadmium per pup at another injection site on the back.
Oral Dosage Experiments

Four Sprague-Dawley derived, COB albino female

rats (Charles River, Wilmington, MA) with their litters of pups were housed as described above. On days
6 through 10 postpartum, the suckling pups received
daily 0.01 ml 0.5 M glucose solutions containing ei-

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Vol. 24

ther nothing (controls), or 0.11, 0.23, or 0.46 ^moles

Se, as Na2Se03, per pup per day. The solutions were
gently placed in the oral cavity with a micropipetter
(Labsystems, Helsinki, Finland). The animals readily
swallowed the solutions, and none dribbled out of
their mouths.
The eyes were dilated with a 1:1 solution of 10%
phenylephrine hydrochloride (Smith, Miller, and
Patch) and 1% atropine (Isopto Atropine, Alcon) and
examined with a photographic slit lamp (Zeiss, West
Germany). A numerical scoring system was used to
grade three areas of the lens. The central area of the
nucleus and the peripheral area surrounding the nucleus were scored:
0 = Clear;
1+ = Shadowy dust-like opacities, occasionally
with some very small, dense particles;
2+ = Definite opacity, but transmitted considerable light;
3+ = Almost total opacity, transmitted small
amount of light;
4+ = Totally opaque.
Swollen lenticular fibers were scored:
0
1+
2+
3+

=
=
=
=

Not visible;
Visible;
Pronounced;
Fibers seemed separated.

The lens cortex was checked for vacuoles and

changes in density, but it was not assigned a numerical score.
At the termination of the experiment, the lenses
were dissected from enucleated eyes, weighed and
analyzed for selenium by a fluorometric method.21
This method involved wet digestion of the lenses in
a boiling mixture of nitric, sulfuric, and perchloric
acids, complexation with 2, 3 diaminonapthalene reagent, and fluorescence determination.
Results
Cataractogenesis by Selenium

Injections of 0.15 ^moles of selenium as sodium

selenite on days 5-9 postpartum caused bilateral nuclear cataracts to form in all animals. Slit-lamp examination showed that central nuclear area to be very
opaque (3+ to 4+), and this area was often lobed or
angular in shape (Fig. 1 A). The area surrounding the
central opacity was spherical and showed diffuse
opacity (1+ to 2+). This peripheral nuclear area usually showed the same degree of density throughout,
but occasionally there were 4+ particles scattered in
it. At the margin between the peripheral nuclear area
and the lens cortex, a spoke-like pattern of swollen

No. 4

5ELENITE AND TRACE ELEMENTS IN CATARACT / Shearer er al.

419

lens fibers was seen, and these swollen fibers appeared

to meet at the Y suture. At this dosage level of selenium, the cortex of the lenses containing nuclear
cataracts did not have opacities, but differences in
refraction appearing as dense rings were observed in
the outer cortex. The lenses of control animals receiving saline were clear.
Oral administration of selenium also caused cataract formation (Fig. IB). On day 6 to 10 postpartum,
these rats received selenium in 0.01 ml of 0.5 M glucose solution that was placed in the oral cavity of the
animals. At levels of 0.23 jumoles Se and above, all
animals developed bilateral nuclear cataracts (Table
2). The cataracts formed were similar in appearance
and severity (Table 2) to those described above for
rats receiving selenium by injection. Also note that
the dosage level of selenium needed to cause cataracts
when given orally (0.23 /^moles/rat) was similar to
that needed to cause cataracts by injection (0.15
Mmoles/rat).
Lack of Cataractogenesis by Other Trace Minerals

Fourteen other ions were tested for their ability to

produce cataracts at the dosage levels shown in Table
1 using the same experimental protocol that produced
cataractogenesis with injected selenite. Careful examination with the slit lamp revealed no significant
opacities or vacuoles in the animals (Table 1). Three
of the ten animals receiving 0.76 yumoles of zinc
showed very mild opacities scoring 1 +, but these were
not observed in a repeat experiment.
Protection Against Selenium-induced Cataract by
Other Trace Elements

Injections of trace elements along with selenium

influenced the frequency of selenium-induced cataract. Tellurium was minimally effective in protecting
against selenium-induced cataract since 80% of the
animals receiving tellurium injections along with selenium injections developed cataracts (Table 3). The
20% of the animals that were cataract free had no
evidence of cataract as seen by careful examination
with the slit lamp. Copper and cadmium were moderately effective in prevention of selenium-induced
cataract since only 56% and 40%, respectively, of the
selenium animals receiving these trace minerals developed cataract. Arsenic, cyanide, and silver ions
were very effective since only 20 to 25% of the animals
receiving these elements along with selenium developed cataracts. The cataracts that did develop in
rats receiving both selenium and competing ions had
the typical features of selenium-induced cataract
(Fig. 1C).

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Fig. 1. Slit-lamp photographs of eyes of rats with selenium-induced cataract. A, Approximately 3 weeks after suckling rat pup
received subcutaneous injections of 0.15 umoles Se on days 5-9
postpartum. The central nucleus was opaque and the peripheral
nucleus showed diffuse opacity (asterisk). B, Nuclear cataract in
lens of animal receiving oral selenium, C, Eye of rat receiving
simultaneous injections of selenium and copper.

The most effective trace element studied for prevention of selenium-induced cataract was mercuric
ion (Table 3). At dosage levels equal to selenite, mer-

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Vol. 24

INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE / April 1983

Table 2. Influence of oral selenite on cataractogenesis

Dosage fomoles Se/rat)
Parameter

0.0

0.11

0.23

0.46

96 2(10)*
0

91 2(10)
0

96 2 (9)
0

69 6 (7)
30

Frequency of cataract
Animals
Percent

0/10
0

0/10
0

10/10
100

7/7
100

Cataract opacity score

Central nucleus
Peripheral nucleus
Swollen fibers

Clear (10)
Clear(10)
Absent

Clear (10)
Clear (10)
Absent

3.5 0.2 (9)

1.3 0.2 (9)
1.8 0.3 (9)

Hypermature (6)
Hypermature (6)
Hypermature (6)

Body weight (g)

Mortality (%)

* Mean SE (number of animals) on day 27 post partum.

cury was totally effective in preventing selenium-induced cataract formation. Further titration of the
mercury dosage to half the molar level of selenium
(0.075 /imoles Hg per rat) still prevented cataract formation in 70% of the animals receiving selenium.
Zinc, iron, lead, chromium, molybdenum, tungstate, and vanadium had no influence on the frequency of selenium-induced cataract (Table 4). This
occurred despite the fact that the levels of these trace
minerals administered were two to five times the dosage level of selenium.
The data in Table 5 show the influence of protective trace minerals on the severity of selenium-induced cataract. Selenium alone caused very dense
cataract formation in the nucleus, resulting in an average nuclear score of 3.9. The peripheral nucleus was
only mildly involved, with an average score of 1.1.
Swollen fibers scored an average of 1.9 (pronounced).
The protective ions tellurium, copper, cadmium, arsenic, cyanide, and silver all tended to reduce the
severity of selenium-induced cataracts (Table 5).
Opacity scores in the central nucleus, peripheral nucleus, or swollen fibers tended to be lower in animals
receiving these ions along with selenium. The selenium plus mercury group could not be scored because

mercury completely protected against cataract formation.

Similar to the frequency studies, the nonprotective
trace minerals zinc, iron, chromium, molybdenum,
tungsten, vanadium, and lead were ineffective in reducing the severity of selenium-induced cataract.
Scores in the central and peripheral nuclear areas of
these cataracts were similar to the animals receiving
only selenium, while the scores for the presence of
swollen fibers were actually increased in the groups
receiving lead and zinc. Tungstate may have potentiated the severity of selenium-induced cataracts since
cortical opacities were observed.
Neither selenium nor selenium plus the other protective ions caused any changes in the weights of
lenses measured at the termination of the multiple
injection experiments (Table 6). The average concentration of selenium in the lenses of control rats was
0.53 ppm Se (Table 6). In rats receiving selenium
injections alone, lens selenium concentrations were
0.63 ppm Se, and this value was not statistically different from controls. Likewise, there were no obvious
changes in the concentrations of selenium measured
in the lenses of animals receiving selenium plus other
trace minerals.
Table 4. Trace minerals not protective against
Se-induced cataract

Table 3. Trace elements protective against

se-inaucea cataract

Trace mineral

Trace mineral
Frequency oj cataract

Freque,ncyof
cataract

Group

Dosage (\imoles
element/rat)

Form

Animals

Percent

Group

Dosage (^moles
element/rat)

Form

Animals

Percent

Se
Se + Te
Se + Cu
Se + Cd
Se + As
Se + CN
Se + Ag
Se + Hg

0.15
0.15
0.30
0.30
0.30
0.30
0.30
0.15

SeO 3 =
TeO 3 =
Cu + +
Cd + +
AsO 2 "
Cn"
Ag+
Hg + +

44/44
8/10

100
80
56
40
25
25
20
0

Se
Se + Zn
Se + Fe
Se + Pb
Se + Cr
Se + Mo
Se + W
Se + V

0.15
0.76
0.45
0.30
0.30
0.30
0.30
0.30

SeO 3 =
Zn + +
Fe + +
Pb + +
Cr +3
Mo<V
WO 4 "
Vo 3 -

44/44
11/11
10/10
10/10
10/10
10/10
10/10

100
100
100
100
100
100
100
100

5/9

4/10
2/8
2/8

2/10
0/10

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No. 4

SELENITE AND TRACE ELEMENTS IN CATARACT / Shearer er al.

The studies presented above provided trace minerals in daily injections over a 5-day period. In another experiment, similar to previous studies,2"5 we
found that a single injection of 0.42 /umoles Se on
day 10 postpartum caused cataract formation in 90%
of the injected animals, and the average opacity score
for the central nucleus was 4.0 0 (9). Cataracts were
generally observable as soon as the eyes opened (14
days postpartum). A second group of animals receiving a single injection of 0.42 jumoles of Cd along with
the single injection of 0.42 ^moles Se showed a markedly decreased frequency (38%) and severity of cataract (central nucleus opacity score: 1.3 0.33).

421

Table 5. Influence of protective trace elements on

severity of Se-induced cataract
Cataract opacity score

Group
Se
Se
Se
Se
Se
Se
Se
Se

+ Te
+ Cu
+ Cd
+ As
+ CN
+ Ag
+ Hg

Central nucleus

Peripheral
nucleus

3.9
2.9
2.2
3.6
2.0
2.0
4.0

1.1
0.8
0.6
0.3
0.3
1.0
0.0

0.04 (29)*
0.4 (8)
0.6 (5)
0.4 (4)
1.0(2)
1.0(2)
0.0 (2)
0

0.1
0.3
0.2
0.1
0.3
1.0
0.0

Swollen
fibers
.9 0.1
.6 0.2
.4 0.7
.3 0.3
.0 1.0
().8 0.3
.5 0.5
0

* Mean SE (number of animals with cataracts in a group).

Discussion
The data presented above emphasized two facets
of trace mineral-induced cataractogenesis: (1) compared to 14 other trace elements, selenium was a potent and extremely rapid promoter of cataracts; and
(2) the data also pointed out the rather dramatic influence trace element interactions can have on cataractogenesis.
Regarding the comparative strength of selenium
in promoting cataracts, we attempted to inject as
much of the other trace minerals so that dosage levels
were equimolar or greater than selenium, yet so as
not to exceed moderate toxicity levels of the elements.
Mercury and tellurium could be reasonably tolerated
only at levels equimolar to selenium. The animals in
the groups receiving zinc, iron, lead, silver, copper,
cyanide, arsenic, cadmium, chromium, molybdenum, tungsten, and vanadium received from two to
five times the dosage level of selenium. Despite these
higher dosages, none of the animals receiving these
elements alone showed any form of significant cataract at 27 days postpartum. On the other hand, 100%
of the animals receiving selenium developed very
dense bilateral nuclear cataracts that were visible as
soon as the eyes opened. It is possible that the other
elements could have produced cataracts under more
long-term exposure or after a longer latent period.
However, the data serve to emphasize how potent
selenium is in promoting cataract in a short period
of time.
Other investigators have reported that a single injection of selenium on day 10 postpartum will promote nuclear cataract formation in the rat, and that
the rabbit and guinea pig are also susceptible to this
cataract.2"4 Our present slit-lamp study revealed that
several other lenticular changes can be present along
with the obvious central nuclear opacity. A less dense
nuclear opacity was observed surrounding the central
nuclear cataract, and a single layer of a spoke-like
pattern of swollen lenticular fibers extended around

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the peripheral nuclear opacity to the Y suture. Transmission electron microscopy of lens fibers from selenium-induced cataracts showed no changes in the
apposition of one fiber to another, but rather extensive vacuolization of the cytoplasm within the fibers.10 Although the data presented in this report did
not show an increase in overall wet weight of selenium treated lenses (Table 6), other studies5 using
higher dosages of selenium showed a significant increase in the water content of hypermature cataracts.
Extensive vacuolization of the lens cortex was also
noted in a previous study where high doses of selenium were repeatedly injected over many days.1
These data may indicate that selenium cataract interferes with the normal functioning of the cation
pump, but this is speculation at the present time.
Another interesting feature of selenium-induced
cataracts is the fact that nuclear cataracts appear
within 3 to 4 days after selenium injection.4 Obviously, cells undergoing differentiation and appositional growth at the lens bow at the time of selenium
injection would not have sufficient time to migrate
Table 6. Selenium concentrations and wet weights
of lenses after multiple injections of protective
trace elements with selenite
Lens
Group
Control
Se
Se + Te
Se + Cu
Se + Cd
Se + As
Se + CN
Se +Ag
Se + Hg

Wet weight (mg)

20
20
22
19
21
21
20
21
21

1 (3)*
1 (3)
1 (3)
2(3)
0(3)
1(3)
0(3)
1(3)
K3)

Selenium (ppm)
0.53
0.63
0.78
0.65
0.56
0.66
0.57
0.57
0.56

0.03
0.04
0.15
0.15
0.16
0.09
0.11
0.06
0.06

(3)
(3)
(3)
(3)
(3)
(3)
(3)
(2)
(3)

* Mean SE (n = pool of lenses). Each pool usually consisted of four

lenses that were collected 19-21 days after the last selenium injection.

422

INVESTIGATIVE OPHTHALMOLOGY 6 VISUAL SCIENCE / April 1983

into the nuclear region and form a cataract. Furthermore, studies using cataractous doses of selenium
tagged with 75Se indicate that there is very little 75Se
actually in the nuclear cataract.* These data indicate
that the site of action of selenium is extrinsic to the
nuclear cataract itself.
It should be noted that the ability of selenium to
induce cataract is dependent on the age of the animal.
After 18 days postpartum, selenium injections no longer cause permanent cataracts in rats.2 Why the sensitivity of the lens to selenium changes with time is
unknown, but investigations into this subject would
be useful since they may help pinpoint the biochemical basis for selenium-induced cataract.
Although the data in Table 6 showed no statistically significant increases in the selenium content of
lenses of animals receiving selenium injection, these
data should not be interpreted as showing that the
lens does not take up some selenium. Besides the
analytical variability in measuring small levels of selenium in the lens, the data may be misinterpreted
because selenium was measured almost 3 weeks after
the last selenium injection. Two other reports419 indicated that after a single injection of selenium, lens
selenium levels peak 6-24 hr postinjection, and
75
Se levels fall rapidly in the lens thereafter.* The
critical time period for cataract formation from selenium is probably within the first 3-4 days after injection. Future studies could test if some of the protective ions influence lens selenium levels at these
early time periods.
The biochemical mechanism of action of selenium
in cataract promotion may be related to the affinity
of selenite for sulfhydryl groups. Selenium in other
soft and hard tissues of the body is associated with
proteins, as selenoamino acids (ie, selenocysteine)
and as selenotrisulfides (R-S-Se-S-R).'' Selenotrisulfides are reduced further to selenopersulfides (R-SeH) by glutathione reductase and by excess reduced
glutathione, as is found in the lens. Selenite causes
the nonenzymatic oxidation of sulfhydryl groups to
form disulfides and selenotrisulfides.4'11 Two reports
described reduced levels of sulfhydryl groups in selenium-induced cataracts.4'5 It has been proposed that
selenite is cataractogenic by causing the formation of
cataractous disulfide linkages in lens proteins.5 However, we recently found that total lens disulfides were
not increased in selenite cataract. This does not exclude the possibility of disulfide formation in certain
classes of proteins or at specific anatomical sites.
The survey of 14 trace minerals in the present study
revealed six elements that offered significant protec-

* Shearer TR and Britton JL: Unpublished data.

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Vol. 24

tion against selenium-induced cataract. Equimolar

amounts of mercury were totally effective in preventing selenium-induced cataracts, while silver, cyanide, arsenic, cadmium, and copper were partially
protective when injected at two times the level of
selenium. Interaction between mercury and selenium
in other soft tissues is reported to be due to the formation of mercury-selenium complexes that are
thought to be less toxic than the separate ionic species
of these elements.12 The binding constant for mercury
to sulfhydryl groups is high.21 Mercury may prevent
selenium cataracts by complexing with selenium or
by blocking uptake of selenium onto critical sulfhydryl groups.
Copper, silver, and cyanide are also known to form
complexes with selenium and to mutually alleviate
toxicity symptoms.12"14 Arsenite is known to increase
the secretion of selenium into bile, where the selenium is bound to protein and glutathione sulfhydryl
groups.15 Cadmium diverts selenium from low molecular weight complexes to high molecular weight
complexes.16 It should also be noted that with regard
to cadmium, the results with the single injection
model were similar to those for the multiple, 5-day
injection model. Common features of all the protective elements were that they either complex with selenium directly or altered the normal metabolism of
selenium.
Tellurium was interesting because it is the next
element below selenium in the periodic table, and it
may be metabolized by reductive pathways as is selenium.17 However, simultaneous injection of equimolar amounts of tellurium (0.15 ^moles/pup) prevented only 20% of selenium-induced cataracts. In
a separate experiment where no selenium was injected, animals were given a very toxic dose of 0.30
/imoles tellurium/pup. Three of the six surviving rats
developed only a very mild (1+) nuclear opacity.
Thus, tellurium was neither a good competitor of selenium for cataract prevention nor was tellurium very
effective in promoting cataract, again indicating the
potency of selenium in cataract formation even
among members of the same group in the periodic
table.
Per kilogram of body weight, the amounts of selenium and other trace elements administered in
these animal experiments was much higher than
those consumed by man.18 However, we feel that selenium-induced cataracts are a useful animal model
for a cataract formation for several reasons: (1) selenium-induced cataracts are a model of cataracts
caused by an oxidant stressor, in this case selenite
ion. (2) The data in the present communication are
the first demonstration that oral administration of
selenium was cataractogenic. The cataracts were sim-

No. 4

SELENITE AND TRACE ELEMENTS IN CATARACT / Sheorer er ol.

ilar to those produced by the injection model, and

the data indicate that this more physiologic route of
selenium ingestion was cataractogenic. (3) The protective ions Hg, Ag, CN, As, Cd, Cu, and Te may be
useful probes for studying the mechanism of action
of selenium and similar cataractic agents. (4) Future
experiments with this animal model might test the
interaction of selenium with subacute amounts of
other cataractogenic agents such as x-ray radiation
or altered blood sugars. Bhuyan19 recently reported
statistically significant increases in the selenium concentrations of human cataractous lenses. Also, we
wonder if continuous exposure to somewhat elevated
quantities of dietary selenium might be interactive
with other environmental agents and thereby predispose man to cataract.
Key words: selenite, trace elements, cataract, rat, slit lamp

7.
8.

9.
10.
11.

12.
13.

Acknowledgments
The authors wish to express appreciation to Dr. Earl
Palmer and Mr. Pat Wallace for help with the slit-lamp
biomicroscopy, and to Dr. Jack Fellman for helpful discussions.

14.
15.

References
16.
1. Shearer TR, McCormack DW, DeSart DJ, Britton JL, and
Lopez MT: Histological evaluation of selenium induced cataracts. Exp Eye Res 31:327, 1980.
2. Ostadalova I, Babicky A, and Obenberger J: Cataractogenic
and lethal effect of selenite in rats during postnatal ontogenesis.
Physiol Bohemoslov 28:393, 1979.
3. Bhuyan KC, Bhuyan DK, and Podos SM: Selenium-induced
cataract and its possible biochemical mechanism. In Selenium
in Biology and Medicine, Second International Symposium,
Spallholz JE, editor. Westport Conn. AVI Publishing, 1981.
4. Bunce GE and Hess JL: Biochemical changes associated with
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