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PubMed2005

Prevention of cataract by pyruvate in experimentally diabetic mice.

Previous studies have demonstrated that administration of pyruvate prevents cataract formation in diabetic rats. It is known that the induction of cataractous process in this case is initiated by aldose reductase (AR) catalyzed synthesis and accumulation of excessive sorbitol in the lens fibres and epithelium and their consequent osmotic hydration. Synthesis of this and other polyols is competitively inhibited by pyruvate. The objective of the present investigations was hence to determine whether pyruvate would have a similar protective effect in species where cataract formation is relatively independent of sorbitol synthesis such as in humans where the lens AR activity is extremely low, especially with glucose as a substrate. The Km of AR for glucose is known to be very high. The possible protective effect of pyruvate in the low AR models was conceived on the basis of our previous findings suggesting that it can also exert substantial antiglycating as well as antioxidant effects. The present studies have hence been conducted with mice, a species known to be low in lens AR, similar to that in humans. As stipulated, pyruvate administration has indeed been found to offer a significant protection against development of diabetic cataract in this model also. The effect correlated with the inhibition of protein glycation as well as of oxidative stress. The latter was apparent by the prevention of the loss of glutathione known to be associated with diabetes. Although there was a small but noticeable increment in the sorbitol content of the diabetic lenses, this was osmotically insignificant. Even this increase was prevented by pyruvate. The magnitude of the elevation in the contents of glycated proteins and the depression in the level of glutathione were, on the contrary, highly pronounced, suggesting a more prominent role of the latter factors. In addition, the possibility of a direct metabolic support it could offer to the tissue is also imminent by its effect on the maintenance of ATP, as shown earlier. The present studies are therefore considered more relevant to the pathogenesis of cataract in human diabetics and its possible prevention by endogenous compounds with antiglycating and antioxidant properties. Inhibition of cataract formation by pyruvate in an animal model with low lens AR, similar to that in humans, has been shown for the first time.

Animals↗
PubMed1984

Short- and long-term endothelial cell loss associated with cataract extraction and intraocular lens implantation.

A group of 249 patients undergoing cataract extraction with intraocular lens implantation underwent specular microscopic endothelial cell photographs before surgery and eight weeks, one year, and two years after surgery. The intraocular lenses used were the Shearing posterior chamber lens and the transiridectomy clip lens after extracapsular cataract extraction and the Medallion iris suture lens after intracapsular cataract extraction. Thirty-seven patients who underwent cataract extraction without implantation served as controls. Eight weeks after surgery, there was no statistical difference between the groups with intraocular lenses and the groups without them. One year and two years after surgery, endothelial cell loss had occurred in all groups except the group who underwent extracapsular cataract extraction without intraocular lens implantation--a group in which the patients were younger. The long-term endothelial cell loss was greater after intracapsular cataract extraction and was greater in the presence of an implant. There was statistically more endothelial cell loss with the transiridectomy clip lens than with the posterior chamber lens eight weeks and one year after surgery; the patients with posterior chamber lenses had continued to have more endothelial cell loss during the second postoperative year.

Aged↗
PubMed1987

Cataract extraction in the diabetic eye after vitrectomy.

We examined 289 phakic, diabetic eyes for evidence of cataract formation after a successful vitrectomy. Of 289 eyes, 107 (37%) developed or had significant progression of a cataract over a follow-up period of 16 to 108 months. Postvitrectomy hemorrhage and vitreous lavage were associated with an increased rate of cataract formation. Of the 107 eyes, 33 (31%) subsequently had cataract extraction, with 24 eyes (73%) treated by extracapsular cataract extraction and nine eyes (27%) with intracapsular surgery. A posterior chamber lens was used in 11 of the 24 eyes that underwent extracapsular surgery. Of the 33 eyes, 31 (94%) had improved visual acuity after cataract extraction. Intraoperative and postoperative complications were minimal and did not result in permanent reduction of vision. Intraocular lenses were well tolerated in the 11 patients in whom they were used.

Cataract Extraction↗
PubMed1989

Lens opacity induced by lipid peroxidation products as a model of cataract associated with retinal disease.

The cataractous lenses of patients with retinitis pigmentosa have been studied by electron microscopy. The posterior subcapsular opacities showed common ultrastructural features. Large areas of disruption of the lens fibre pattern were observed which showed an increase in the number of fibre membranes per unit area. In many regions an elaborate and regular folding of membranes was noted which produced complex 'figure-of-eight' and 'tramline' patterns, as well as membranous lamellar bodies. Masses of various size globules were also identified. It has been established that injection into the vitreous body of the rabbit eye of a suspension of liposomes prepared from phospholipids containing lipid peroxidation products induces the development of posterior subcapsular cataract. Such modelling of cataract is based on a type of clouding of the crystalline lens similar to that observed in cataract resulting from diffusion of toxic lipid peroxidation products from the retina to the lens through the vitreous body on degeneration of the photoreceptors. Saturated liposomes (prepared from beta-oleoyl-gamma-palmitoyl-L-alpha-phosphatidylcholine) do not cause clouding of the lens, which demonstrates the peroxide mechanism of the genesis of this form of cataract. Clouding of the lens is accompanied by accumulation of fluorescing lipid peroxidation products in the vitreous body, aqueous humor and the lens and also by a fall in the concentration of reduced glutathione in the lens. From the results it is concluded that lipid peroxidation may initiate the development of cataract.

Adult↗
PubMed1976

Protein changes in the human lens during development of senile nuclear cataract.

Senile nuclear cataractous lenses were divided into three groups of increasing nuclear color. These groups were considered as successive stages in the development of senile nuclear cataract. The cortex and the nucleus of normal and cataractous lenses were separated into water-soluble, urea-soluble and urea-insoluble fractions. Fractionation on a Sephadex G-200 column of the water-soluble components revealed five protein fractions for both cortex and nucleus. Only minor quantitative differences in polypeptide chain composition were found by isoelectric focusing between corresponding protein fractions isolated from normal and cataractous lenses. The weight percentages of the water-soluble, urea-soluble, and urea-insoluble fractions of cortex and nucleus from the normal and cataractous lenses were determined. A decrease of the amounts of the water-soluble and urea-soluble fractions and a concomitant increase of the urea-insoluble fraction were observed in the nucleus as a function of cataract development. Lens wet weight and protein content did not change significantly. The carbohydrate content of the urea-soluble fractions increased, that of the urea-insoluble fraction decreased. A striking decrease of the phospholipid content in the urea-insoluble fraction was found.

Aged↗
PubMed1983

Early development of selenium-induced cataract: slit lamp evaluation.

The purpose of our research was to document early lenticular changes preceding cataract formation in rats receiving an elevated dose of selenium. The following stages were observed after selenium injection: Stage 1 (13-24 hr post-injection), formation of posterior equatorial subcapsular cataract (PESC); Stage 2 (24-72 hr), decline of the PESC, development of a prominent 'washer' shaped change in the refraction of the cortex, and first appearance of swollen fibers around the nucleus; Stage 3 (three to five days), appearance of bilateral dense central nuclear cataracts and further development of perinuclear swollen fibers; Stage 4 (five to 10 days), some nuclear cataracts became more opaque and/or angular. The results are consistent with the hypothesis that the initial site of action of selenium in nuclear cataract formation is not in the lens nucleus. Rather, selenium causes early changes outside the nucleus, which are followed by nuclear cataracts.

Animals↗
PubMed1983

Sugar cataracts in Mongolian gerbil (Meriones unguiculatus).

Mongolian gerbils (Meriones unguiculatus) given a 50% galactose diet developed cataracts similar to those produced in rats maintained on the same diet. This report describes the various stages through which the cataracts progressed. The first sign of a cataract appeared 24 hr after feeding gerbils on the high galactose diet. The pace of cataract maturation was observed to be about twice of that in rats, although the blood galactose levels were similar in the two species. Aldose reductase activity in the gerbil lens was also about twice of that in the rat lens. In conformity with this, dulcitol accumulated to a higher level in gerbil lens during the early phase of cataractogenesis. The data are, therefore, in accordance with the concept that excessive accumulation of polyol in the lens initiates cataract development. The gerbil thus appears to be another suitable model for the study of sugar cataracts.

Aldehyde Reductase↗
PubMed1985

Modelling cortical cataractogenesis VII: Effects of vitamin E treatment on galactose-induced cataracts.

The possibility that vitamin E or other antioxidants might prevent cataracts was tested by incubating rat lenses in vitro in galactose-enriched medium or by treating rats fed a diet containing 50% galactose (w/w). The vitamin E was added to the medium at 2.4 microM, and to the diet at a level of 5 g kg-1 diet. In vitro, lenses incubated with 55.6 mM galactose underwent globular degeneration, which was partially prevented by addition of vitamin E (2.4 microM). Even in such vitamin E-protected lenses, which appeared clear, many small globules could be seen in the region of interdigitation at the 'corners' where hexagonal cells intersected. In vivo, in dietary experiments, a dense nuclear opacity of the lens was observed after approximately 5 weeks; unlike diabetic cataracts, this was not prevented by the addition of vitamin E to the diet. The extensive globular degeneration observed was typical of that found in long-term (21-week diabetic) cataracts. Although no significant difference in cataract incidence was observed, the extent of damage in vitamin E-treated rat lenses appeared to be less. The difference in effectiveness of vitamin E in galactose-induced cataracts, as compared to diabetic cataracts, is tentatively ascribed to (1) the more severe osmotic stress expected from the products of the aldose reductase pathway for galactose and (2) the greater depletion of reduced pyridine nucleotides (NADPH + NADH) expected of galactose as compared to glucose.

Animals↗
PubMed1985

Biosynthesis of proteoglycans by lens epithelial cells of cataractous mouse (Nakano strain).

The capsules (with epithelial cells attached) of lenses from normal and cataractous mice (Nakano strain) were biosynthetically labeled in vitro with radioactive precursors. The labeled macromolecules were chromatographed on a Sepharose CL-4B column and analyzed by specific enzyme digestion. The incorporation of [3H]-proline and [3H]-glucosamine into macromolecules was comparable in the cataract and normal capsules, while that of [35S]-sulfate was reduced by 60% in the cataract capsules, indicating that the proteoglycan synthesis was specifically decreased in the cataract lens. Glycosaminoglycan analyses showed an increased synthesis of hyaluronic acid and decreased synthesis of heparan sulfate in the cataract capsules. It is possible that the alterations in the synthetic level and glycosaminoglycan components of proteoglycan affect the permeabilities of macromolecules to lens capsule and lead to cataract in Nakano mouse lens.

Animals↗
PubMed1990

Association of hereditary cataracts in strain 13/N guinea-pigs with mutation of the gene for zeta-crystallin.

Congenital nuclear cataracts transmitted by an autosomal dominant gene are present in a line of strain 13/N guinea-pigs. Studies on the lens proteins from these animals demonstrate changes in both the composition and structure of the crystallins relative to normal controls. The most prominent difference is in the zeta-crystallin, a taxon-specific crystallin which has been shown to be related to the alcohol dehydrogenases. In animals homozygous for the cataract phenotype the normal zeta-crystallin polypeptide is absent from the lens. Quantitation is difficult in the cataractous lenses from heterozygotes because of protein changes secondary to opacification: however in liver and kidney which have catalytic levels of the protein, the concentrations are approximately half that present in tissue from normal control animals. These findings suggest that in the cataractous animals a mutation has occurred in the gene for zeta-crystallin. In addition, a novel protein which is very similar to zeta-crystallin is synthesized only in the lenses of animals with cataract. This protein appears to be the product of the mutant gene for zeta-crystallin. These data support the hypothesis that this hereditary congenital cataract results from a specific mutation in the zeta-crystallin gene.

Animals↗
PubMed1988

The effect of dose fractionation on the frequency of ethylnitrosourea-induced dominant cataract and recessive specific locus mutations in germ cells of the mouse.

A combined dominant cataract-recessive specific locus mutation experiment for fractionated exposure to ethylnitrosourea (2 X 80 mg/kg, 24-h fractionation interval) was designed to determine if lower doses of ethylnitrosourea are more effective in inducing dominant cataract mutations as suggested by previous results. This observation was not confirmed by the present experiment. The extensive, statistically more reliable specific locus results indicate an additive effect of fractionated ethylnitrosourea treatment. A saturable repair system for ethylnitrosourea-induced DNA damage has been previously documented (Karran et al., 1979; Sega et al., 1986; Van Zeeland et al., 1985). Two parameters inherent to a saturable system, the minimal time required for the saturated system to recover and the minimal dose to saturate the system are important, and results of experiments employing a fractionation exposure protocol must be interpreted relative to these two parameters. Longer fractionation intervals or smaller doses result in a reduced mutagenic effect. Due to the inherently lower experimental variability of the specific locus mutation assay as compared to the dominant cataract assay, the specific locus assay is the test of choice to determine factors affecting the mammalian germ cell mutation rate. The dominant cataract test requires a larger investment of experimental resources to achieve a comparable degree of accuracy. The dominant cataract mutation test is important in assessing the mutation rate to dominant alleles in germ cells of mammals. Due to the immediate expression of the mutant phenotype in newly occurring dominant mutations, a dominant mutation assay screens a genetically relevant endpoint in an assessment of the mutagenic hazard for man in mouse experiments. A multi-endpoint design screening specific locus, dominant cataract, and biochemical mutational endpoints (Ehling et al., 1985) allows a systematic comparison of mutagenic results for different classes of mutations in the same animals.

Abnormalities, Drug-Induced↗
PubMedDate not supplied

Cataracts induced by microwave and ionizing radiation.

Microwaves most commonly cause anterior and/or posterior subcapsular lenticular opacities in experimental animals and, as shown in epidemiologic studies and case reports, in human subjects. The formation of cataracts seems to be related directly to the power of the microwave and the duration of exposure. The mechanism of cataractogenesis includes deformation of heat-labile enzymes, such as glutathione peroxide, that ordinarily protect lens cell proteins and membrane lipids from oxidative damage. Oxidation of protein sulfhydryl groups and the formation of high-molecular-weight aggregates cause local variations in the orderly structure of the lens cells. An alternative mechanism is thermoelastic expansion through which pressure waves in the aqueous humor cause direct physical damage to the lens cells. Cataracts induced by ionizing radiation (e.g., X-rays and gamma rays) usually are observed in the posterior region of the lens, often in the form of a posterior subcapsular cataract. Increasing the dose of ionizing radiation causes increasing opacification of the lens, which appears after a decreasing latency period. Like cataract formation by microwaves, cataractogenesis induced by ionizing radiation is associated with damage to the lens cell membrane. Another possible mechanism is damage to lens cell DNA, with decreases in the production of protective enzymes and in sulfur-sulfur bond formation, and with altered protein concentrations. Until further definitive conclusions about the mechanisms of microwaves and ionizing radiation induced cataracts are reached, and alternative protective measures are found, one can only recommend mechanical shielding from these radiations to minimize the possibility of development of radiation-induced cataracts.

Animals↗
PubMed1986

Further experience of the mouse dominant cataract mutation test from an experiment with ethylnitrosourea.

6 mice with inherited cataracts and 1 new allele of microphthalmia were recovered from 923 progeny of untreated, outbred, PT stock females that had been mated to inbred C3H/HeH strain males, whose spermatogonia had been exposed to 250 mg/kg of ethylnitrosourea (ENU). The cataract phenotypes were quite variable in expression and 5/6 showed a similar range of phenotypes. 2 of the 6 mutant mice were daughters of the same ENU-treated C3H/HeH male and probably represent repeats of the same mutation. One mutation, designated lens opacity-4 (Lop-4), has been genetically mapped to the distal region of chromosome 2. The yield of 5 presumably independent cataract mutations from 923 F1 offspring is a little higher than that reported by others in similar but larger scale experiments. Approximately 3-5% of the F1 mice examined had cataracts, yet only 6/49 (12%) of these, in the experimental group, were inherited as simple Mendelian traits. We consider that this high frequency of false positives (88%), and the incomplete penetrance and variable expressivity of the cataract mutations that were found, pose serious problems that could undermine the objective nature of the dominant cataract mutation test. We suggest that further studies be made to evaluate whether the use of inbred strains would reduce the variability in the system and so make the test more objective. However, it seems likely that the high false positive rate will continue to be a serious drawback to this test system.

Animals↗
PubMed1986

Radioprotection against cataract formation by WR-77913 in gamma-irradiated rats.

Protection by WR-77913 against radiation-induced cataract formation in rats was observed following intraperitoneal (i.p.) administration of drug (1160 mg/kg) 15-30 min before exposure to 15.3 Gy of Cs-137 whole head irradiation. Control groups included irradiated, non-protected animals, and sham-irradiated aging controls. Protection was documented photographically and by analysis of eye lens constituents. All non-protected irradiated animals developed dense cataracts throughout the lens between 90-120 days post-irradiation, while WR-77913 protected animals developed minimal lens opacification through 200 days post-irradiation. No opacification in aging controls was seen. Lens protein analysis by Lowry assay and size exclusion HPLC showed radioprotected and aging control animals were similar in protein content, distribution of total and soluble protein, and degree of lens hydration. This contrasted significantly with cataractous lenses of non-protected animals. In cataractous lenses, the soluble protein concentration in the 25-43 K dalton range was approximately 10% of that found in radioprotected or aging control lenses. Hydration was substantially higher in cataractous lens. These results indicate that WR-77913 protects against lens opacification, protein insolubilization, and hydration in lenses of irradiated animals. Biodistribution studies with [S-35]-WR-77913 showed ocular uptake of drug within 15 minutes after i.p. injection, which remained relatively constant through 60 min. The relative order of drug concentration for individual eye components was: globe greater than total eye approximately equal to humor greater than lens. Although the mechanism of radioprotection observed remains to be elucidated, WR-77913 clearly prevents radiation-induced cataracts in rats. The potentially significant clinical use for this radioprotective compound is being investigated further.

Amifostine↗
PubMed1992

A guinea-pig hereditary cataract contains a splice-site deletion in a crystallin gene.

A congenital cataract present in guinea pigs provided a unique opportunity to study a hereditary lens disease at the molecular level. zeta-Crystallin, one of the most abundant guinea pig lens proteins, was found to be altered in the lens of cataractous animals. Several zeta-crystallin cDNA clones were isolated from a cataractous lens library and found to contain a 102-bp deletion towards the 3' end of the coding region. This deletion does not interfere with the reading frame but results in a protein 34 amino acids shorter. Sequence analysis of a normal genomic zeta-crystallin clone revealed that the missing 102-bp fragment corresponds to an entire exon (exon 7). PCR analysis of the genomic DNA isolated from cataractous animals showed that exon 7, though missing from the mRNA, is intact in the cataractous genome. Further sequence analysis of the zeta-crystallin gene disclosed a dinucleotide deletion of the universal AG at the acceptor splice-site of intron 6 of the mutant gene. The presence of this mutation results in the skipping of exon 7 during the mRNA processing which in turn results in the altered zeta-crystallin protein. This is the first time a genomic mutation in an enzyme/crystallin gene has been directly linked to a congenital cataract.

Animals↗
PubMed2005

Detecting cataract causing visual impairment using a nonmydriatic fundus camera.

PURPOSE: To assess the validity of a digital nonmydriatic fundus camera in detecting cataract as a cause of visual impairment. DESIGN: Diagnostic test comparison. METHODS: Photos of the anterior segment of 72 eyes were taken with a nonmydriatic fundus camera and assessed for cataract by two graders. Dilated biomicroscopy examination of the anterior segment of the same 72 eyes was then performed and cataract graded using the Wilmer scale. RESULTS: Grader 1 and 2 reported 90% and 94% sensitivity and 82% and 77% specificity, respectively, when the digital photos were compared with slit-lamp biomicroscopy in determining visually significant cataract. In addition, both graders showed similar substantial agreement between the digital photos and slit-lamp biomicroscopy when assessed for cataract (unweighted kappa 0.87 and 0.92, respectively, for graders 1 and 2). CONCLUSION: The nonmydriatic fundus camera may be an alternative method for screening for visually significant cataract in the community.

Cataract↗
PubMed2005

Pterygium, pinguecula, and 5-year incidence of cataract.

PURPOSE: To assess longitudinal associations between pterygium, pinguecula, and 5-year incident cataract. DESIGN: Population-based cohort study. METHODS: The Blue Mountains Eye Study examined 3,654 residents aged > or =49 years during 1992 to 1994 and reexamined 2,335 (75.1% of survivors) 5 years later. Slit-lamp examination recorded pterygium and pinguecula. Cataract was assessed using masked grading of lens photographs. Incidence was assessed in participants without cataract at baseline. Eye-specific data were analyzed using generalized estimating equation models, adjusting for age, sex, smoking, diabetes, and corticosteroid use. RESULTS: Pinguecula was associated with a borderline-significant, increased risk of developing cortical cataract (adjusted odds ratio, 1.3; 95% confidence interval, 1.0 to 1.7). We found no significant association between baseline pterygium and the incidence of cortical, nuclear, or posterior subcapsular cataract. CONCLUSIONS: Longitudinal data from the same study population provide weak support for cross-sectional associations between pinguecula and cortical cataract previously reported from our study.

Cataract↗
PubMed2004

Null genotype of glutathione S-transferase M1 is associated with senile cataract susceptibility in non-smoker females.

In the present study, we investigated whether the polymorphisms of glutathione S-transferase M1 (GSTM1) and T1 (GSTT1) genes are risk factors of cataract among Iranian population in a molecular epidemiological way. Blood samples from 150 subjects with cataract (72 male; 78 female) and 150 age- and sex-matched healthy persons were collected. Both patient and control groups were unrelated Iranian Muslims. Using PCR-based method, the genotypes were determined. The null GSTM1 genotype was associated with a 2.38-fold increase in the risk of developing cataract (OR=2.38; 95% CI=1.46-3.89; P = 0.0003). After stratification by sex of subjects, the association was apparent only among women (OR=3.20; 95% CI=1.58-6.52; P = 0.0007). The GSTT1 null genotype was associated with a 1.10-fold increased risk of developing cataract, but this association was not statistically significant. After stratification by sex of subjects, same results were obtained. Female patients with null genotype for GSTM1 and no history of smoking had a 3.45-fold increased cataract risk (P < 0.05), whereas females who were null for GSTM1 and having history of smoking were not at increased risk of cataract.

Aged↗