Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0086543 (cataract)
 29,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Endogenous oxidative damage to proteins, lipids, and DNA is thought to be an important etiologic factor in aging and the development of chronic diseases such as cancer, atherosclerosis, and cataract formation. The pathology associated with these diseases is likely to occur only after the production of reactive oxygen species has exceeded the body's or cell's capacity to protect itself and effectively repair oxidative damage. Vitamin C, vitamin E, and beta-carotene, often referred to as "antioxidant vitamins," have been suggested to limit oxidative damage in humans, thereby lowering the risk of certain chronic diseases. However, epidemiological studies and clinical trials examining the efficacy of antioxidant vitamins, either individually or in combination, to affect disease outcome rarely address possible underlying mechanisms. Thus, in these studies it is often assumed that antioxidant vitamins act by lowering oxidative damage, but evidence in support of this contention is not provided. Therefore, in this review, we examine the scientific evidence that supplementation of humans with vitamin C, vitamin E, or beta-carotene lowers in vivo oxidative damage to lipids, proteins, or DNA based on the measurement of oxidative biomarkers, not disease outcome. With the only exception of supplemental vitamin E, and possibly vitamin C, being able to significantly lower lipid oxidative damage in both smokers and nonsmokers, the current evidence is insufficient to conclude that antioxidant vitamin supplementation materially reduces oxidative damage in humans.
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PMID:Can antioxidant vitamins materially reduce oxidative damage in humans? 1023 49

Oxidative damage occurring in the lenses of patients with senile cataract may be due to partially reduced forms of oxygen. We assayed the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), glutathione reductase (GSH-Red), and glucose-6-phosphate dehydrogenase (G6PD) in rat lenses at different ages (1, 4, and 24 months), and also evaluated lens glutathione (GSH) levels and the effects of chronic administration of vitamin E and sodium ascorbate. We observed a significant age-related decrease in GSH-Px, GSH-Red and G6PD activities, but no age-related change in SOD activity. Chronic treatment with both vitamin E and sodium ascorbate failed to restore enzymatic activities to the levels of younger rats. An age-related reduction in GSH content was also observed; however, chronic administration of vitamin E, but not of sodium ascorbate, restored GSH levels to those of younger rats.
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PMID:Antioxidant systems in rat lens as a function of age: effect of chronic administration of vitamin E and ascorbate. 1033 41

The preventive effect of topical vitamin E-containing liposome instillation on the progression of galactose cataract was compared between 5-week- and 12-week-old Wistar rats fed a 25% galactose diet. Vitamin E-containing liposomes [LP(+VE)] and vitamin E-free liposomes [LP(-VE)] were prepared with dipalmitoylphosphatidylcholine and dioleoylphosphatidylcholine (7:3 w/w). Twice daily instillation of either LP(-VE) or LP(-VE) into both eyes of 5-week-old rats fed the galactose diet for 18 days (5WGR) and 12-week-old rats fed the galactose diet for 7 weeks (12WGR) at which time some vacuoles appeared in the lens cortical equator, was conducted for a period of 4 and 9 weeks, respectively. The severity of cataracts at the end of instillation was similar in 5WGR and 12WGR. Instillation of LP(+VE), but not LP(-VE), retarded cataract progression in 5WGR and 12WGR. In 12WGR, LP(-VE) instillation caused a transient retardation of the progression. In lenses of 5WGR and 12WGR, decreases in vitamin E and reduced glutathione contents and increases in lipid peroxide, galactitol, and water contents occurred at the onset of instillation. For 5WGR, a decrease in lens reduced glutathione content and increases in lens vitamin E, lipid peroxide, galactitol, and water contents occurred at the end of instillation. For 12WGR, decreases in lens reduced glutathione and vitamin E contents and increases in lens lipid peroxide, galactitol, and water contents occurred at the end of instillation. In sera of 5WGR and 12WGR, vitamin E concentration decreased at the onset of instillation increased at the end in 5WGR and was unchanged in 12WGR. In 5WGR, instillation of LP(+VE), but not LP(-VE), for 4 weeks prevented these changes except the changes in lens galactitol and water contents and serum vitamin E concentration. In 12WGR, instillation of LP(+VE), but not LP(-VE), for 9 weeks prevented these changes except the changes in lens galactitol and water contents and serum vitamin E concentration. These results indicate that topically instilled LP(+VE) can retard cataract progression in 5WGR and 12WGR, mainly by the antioxidative action of vitamin E contained in the instilled liposomes.
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PMID:Preventive effect of topical vitamin E-containing liposome instillation on the progression of galactose cataract. Comparison between 5-week- and 12-week-old rats fed a 25% galactose diet. 1037 38

Age-related cataract and age-related macular degeneration (AMD) are important public health problems. Approximately 50% of the 30 to 50 million cases of blindness worldwide result from unoperated cataract. In the US and other developed countries AMD is the leading cause of blindness, but age-related cataract remains the leading cause of visual disability. Age-related cataract and AMD represent an enormous economic burden. In the United States more than 1.3 million cataract extractions are performed annually at a cost of approximately $3.5 billion. Much of the experimental research on the etiology of cataract and AMD has focused on the role of nutritional antioxidants (vitamin C, vitamin E, and carotenoids). Evidence from epidemiologic studies support a role for nutritional antioxidants in delaying the onset of these age-related vision disorders. Although it is not yet possible to conclude that antioxidant nutrients have a role in prevention of cataract or AMD, a summary of the epidemiologic evidence suggests that it is prudent to consume diets high in vitamins C and E and carotenoids, particularly the xanthophylls, as insurance against the development of cataract and AMD.
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PMID:The potential preventive effects of vitamins for cataract and age-related macular degeneration. 1038 28

We attempted to clarify the pattern of cataract development in 12-month-old rats fed a 25% galactose diet and to assess the relation of cataract development with osmotic stress and oxidative damage. In lenses of 12-month-old male Wistar rats fed a 25% galactose diet over an 8-month period, suture accentuation appeared at 6 months of galactose feeding and then opacities developed from the anterior subcapsular cortex toward the posterior subcapsular cortex, reaching the nuclear region at 8 months of galactose feeding. Increases in lens galactitol and lipid peroxide contents and a decrease in lens reduced glutathione content occurred at 4, 6 and 8 months of galactose feeding. The increase in lens lipid peroxide content and the decrease in lens reduced glutathione content were accelerated with an increase in feeding period, while the increase in lens galactitol content was decelerated. An increase in lens water content and a decrease in lens protein content occurred at 6 and 8 months of galactose feeding. The lens vitamin E content increased at 6 months of galactose feeding and this increase was concomitant with increases in serum vitamin E and total cholesterol concentrations. The serum lipid peroxide concentration increased at 4 and 6 months of galactose feeding. The present results indicate that in lenses of 12-month-old rats fed a 25% galactose diet, suture accentuation appears initially and then opacities develop from the anterior subcapsular cortex toward the posterior subcapsular cortex, finally reaching the nuclear region. These results also suggest that in the galactosemic aged rats, osmotic stress would mainly contribute to cataract formation, while oxidative damage could be linked to both cataract formation and progression, although an increase in lens vitamin E content occurs during the cataract development.
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PMID:Cataract development in 12-month-old rats fed a 25% galactose diet and its relation to osmotic stress and oxidative damage. 1042 Jan 16

The activity of Na+,K+ATPase, gamma-glutamyltranspeptidase, ceruloplasmin, total antioxidative activity of water-soluble antioxidants, the contents of vitamins C and E, free amino-nitrogen and peroxide resistance of erythrocytes were determined at the blood's plasma of healthy persons (120 persons) and suffered from aged cataract (437 persons) of three aged groups (up to 40 years, 40-60 years and elder then 60 years). We have shown, that changes, which has been connected with cataractogenesis and age dependent changes are not equal. The lowering of activity of Na+,K(+)-ATPase, gamma-glutamyltranspeptidase and level of vitamin E was expressed less during the ageing, then during the development of lenses opacification. The increase of activity of oxidase during the cataractogenesis is less significant, then age depended inhibition of this enzyme. The opposite tendency (the lowering of activity at the patients with cataract is more expressed, then compensatory activations of these parameters at the persons of the corresponding age with transparent lenses) was revealed for total antioxidative activity of water-soluble antioxidants.
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PMID:[Biochemical blood parameters in people with a normal crystalline lens and in cataracts]. 1044 69

The effect of vitamin E acetate (VEA) eye drops on naphthalene-induced cataract in rats was investigated by Scheimpflug image analysis. The control group was administered only naphthalene (1 g/kg), while the other group was additionally given 1% VEA eye drops into both eyes 5 times a day every day for 9 weeks from the start of naphthalene treatment. During those 9 weeks, the changes of the crystalline lens were documented by an anterior eye segment analysis system (EAS-1000, NIDEK) once a week in mydriasis (Mydrin-P, Santen Pharmaceutical Co., Ltd.). The characteristic density values of the anterior deeper cortex regions were measured. The light scattering intensity of lenses from VEA eye drop-treated animals was significantly lower than that of animals without VEA treatment. This difference was found 1 week, 4 weeks, and from 7 to 9 weeks after the start of naphthalene application. VEA eye drops may have the potential to delay the progression of naphthalene-induced cataract in rats.
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PMID:Effect of vitamin E eye drops on naphthalene-induced cataract in rats. 1046 73

Cataract is the leading cause of blindness in the world today, while age-related macular degeneration is responsible for the majority of new cases of visual impairment in the Western world. There is a growing body of evidence suggesting a role for antioxidant therapy to prevent the progression of these conditions. A 4-year prospective, randomised, controlled trial of an antioxidant versus placebo in a population of healthy volunteers aged 55-80 years at enrolment is described. This paper outlines the primary aims of the Vitamin E, Cataract and Age-related Macular Degeneration (VECAT) Study, the methodology, and the recruitment rates. Additional data on the toxicity and non-ocular effects of vitamin E will also be collected. Standardised clinical grading of macular and lens features, and comparison of serial macular photographs and digital lens photographs will form the basis for assessment of primary study outcomes. Information collected in this study will assist in the assessment of the potential value of antioxidants in preventing the enormous burden imposed on developed communities by age-related eye disease. In addition, important data on prevalence and progression rates of cataract and macular degeneration will be collected.
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PMID:Methodology of the VECAT study: vitamin E intervention in cataract and age-related maculopathy. 1048 74

In a random trial 50 patients with unilateral/ bilateral idiopathic immature senile cataract (cortical n = 25, nuclear n = 25) requiring surgery at least in one eye were included in the present study. Reduced glutathione (GSH), vitamin E, malondialdehyde (MDA) and glutathione peroxidase (GSH-Px) were studied in these patients receiving either vitamin E (n = 12 in each subgroup) or placebo (n = 13 in each group) for 30 days. A comparable increase of vitamin E in both types of lens homogenates of cataractous patients was observed in the study group. The level of GSH in cortical cataractous lenses in the study group was significantly raised (p < 0.001) whereas it was not increased significantly in nuclear cataractous lenses (p > 0.05) as compared to the placebo group. The percentage decrease in MDA levels was greater in cortical cataracts (38.07%) than in the nuclear type (27.94%). The activity of GSH-Px in cortical lenses was higher than that in the nuclear cataractous lens. The change in the size of lens opacity in cortical cataractous patients receiving vitamin E therapy was significantly decreased as compared to the placebo group. There may be a direct modulating effect of vitamin E on some GSH-related enzymes and the cortex of the lens might be protected more than the nucleus.
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PMID:Protective function of alpha-tocopherol against the process of cataractogenesis in humans. 1074 28

Although UVA radiation was considered to be benign as a factor that could contribute to cataract formation, the studies briefly summarized herein show that UVA may provide the more damaging radiant energy involved in the formation of human cataract. Of the UVA impinging onto the eye from sunlight, a sufficient dose does reach into the lens to enhance cataractous changes. The adverse physiological and biochemical effects on lens epithelial cells and their ability to differentiate into clear adult lenses include cell growth inhibition, cell membrane and cytoskeletal anomalies, and enzyme inactivation. Many of the damaging events are related to the excitation of sensitive UVA absorbing chromophores which generate singlet oxygen and free radicals. This process enhances lens oxidative stress. Some protection against this damage is provided by vitamin E and tea polyphenols. Thus, an imbalance between photooxidative stress, antioxidant protection, and repair processes would increase the potential to produce cataracts.
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PMID:Lens UVA photobiology. 1080 26


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