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)

Vitamin E is well accepted as nature's most effective lipid-soluble, chain-breaking antioxidant, protecting cell membranes from peroxidative damage. Free-radical-mediated pathology has been implicated in the development over time of degenerative diseases and conditions. This paper reviews the current research on the protective role and requirements for vitamin E and the other antioxidants in preventing or minimizing free-radical damage associated with specific diseases and lifestyle patterns and processes, including cancer, aging, circulatory conditions, arthritis, cataract, pollution, and strenuous exercise. While awaiting results of further human studies, research evidence suggests that an adequate intake of vitamin E and the other antioxidants can provide protection from the increasingly high free-radical concentrations caused by air pollutants and current lifestyle patterns.
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PMID:Protective role of vitamin E in biological systems. 201 17

We undertook a prospective study in senile cataract patients using systemic aspirin and systemic vitamin E. Vitamin E treated eyes did show less progression of PSC opacities extent and less new nuclear opacities during the follow-up, but overall vitamin E treated eyes did no better than the control group eyes. More eyes in systemic aspirin treated group maintained the initial vision and loss of vision in the aspirin group was also less marked. Aspirin also caused a significant less mean increase in cortical opacity extent, nuclear/opacity and density and PSC opacity extent and density as well as in ophthalmoscopically graded opacity extent and density. We suggest that aspirin is a potential drug which should be further evaluated in large double blind photodocumentated studies. The present data does not justify the recommendation that aspirin be prescribed for slowing down cataract progression. This must await large studies and confirmation.
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PMID:Systemic aspirin and systemic vitamin E in senile cataracts: cataract V. 263 49

The effect of vitamin E-containing liposome on experimental sugar cataract formation in vitro was investigated. The lenses of male Wistar rats aged 6 weeks were prepared by incubating with 55. 6 mM glucose with vitamin E-containing liposome (dipalmitoyl phosphatidylcholine: DPPC). We examined the formation of lens opacity and assayed vitamin E and its related compounds. Incubation with vitamin E-containing liposome prevented sugar cataract formation. In Addition, vitamin E concentration in lens was significantly elevated by incubation with vitamin E-containing liposome. In lenses of the high level glucose group incubated without vitamin E-containing liposome, lipid peroxide (LPO) content was increased, but in lenses of the high-level glucose group incubated with vitamin E-containing liposome the increase was significantly inhibited at each incubation time. Vitamin E had no effect either on the decrease of reduced glutathione (GSH) or the increase of sorbitol content in lens incubated with high level glucose medium. In conclusion vitamin E-containing liposome was transported from medium to lens well and was significantly effective in preventing experimental sugar cataract formation in vitro. The protective effects of vitamin E are probably caused not only by its antioxidative action.
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PMID:[Effect of vitamin E-containing liposome on experimental sugar cataract]. 275 Jun 6

Vitamin E (d-alpha-tocopherol) and aspirin were evaluated for their effects on the phase separation temperature, Tc, of calf lens cytoplasm. Vitamin E and aspirin were added to nuclear homogenate and the change in Tc was measured. Aspirin had no measurable effect on Tc. Vitamin E lowered Tc at a rate of -22 degrees C M-1 l-1. The results suggest that the effects of aspirin on cataract are unrelated to phase separation and that vitamin E may act on the phase separation in precataractous lens cells.
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PMID:Effect of aspirin and vitamin E on phase separation in calf lens homogenate. 361 40

Most of the estimated 40 million blind individuals in the world are in the older age groups. Data on blindness and visual impairment are primarily from blindness registries and prevalence surveys in different countries throughout the world. The quality of these data vary tremendously from one country to another, and comparability of the results from different studies is difficult. However, all studies indicate an increase in the prevalence of visual loss and blindness with increasing age. Cataract is the most prevalent eye disease in the world and is a major cause of visual loss in developing as well as in developed countries. Other major eye diseases in the elderly include age related macular degeneration, glaucoma, and diabetic retinopathy. A number of risk factors have been suggested for cataract, age related macular degeneration, and glaucoma, yet few have been well established. Certain factors for these conditions are similar, including age, hypertension, prolonged exposure to sunlight, and nutritional factors such as Vitamin E. Epidemiologic studies are needed to define the risk factors for these different eye diseases with the goal of decreasing risk of disease and possible disease prevention, as well as developing better estimates of the magnitude of the problems of visual loss and eye diseases in the elderly.
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PMID:Epidemiology of eye disease in the elderly. 365 39

We tried to counteract the appearance of galactosemic cataracts in weaned rats by high doses of vitamin E. Rats were fed a diet containing 33% galactose. Cataract development was monitored by biomicroscopy and by several biochemical parameters: K+/Na+ ratio, aldose reductase activity, level of protein and non-protein sulfhydryl (SH) groups. Vitamin E was given parenterally at a dose of 100 mg/kg/day. The K+/Na+ ratio drops after 15 days of galactosemia, while the level of the aldose reductase rises after only 5 days of treatment. The non-protein SH groups lens contents fall from the 5th day of treatment onwards, while protein SH groups are not affected. In short-term experiments vitamin E does not prevent biochemical changes caused by galactosemia. The oxidative insult does not seem to be primarily involved in galactose cataract.
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PMID:Changes of some biochemical parameters of the lens in galactose-treated weaned rats with and without vitamin E therapy. 392 May 97

Lens cells can synthesize, degrade, and remodel lipids. Endogenous lipid synthesis, in conjunction with uptake of exogenous cholesterol and certain fatty acids, leads to the formation of a plasma membrane that is especially rich in sphingomyelin, cholesterol, and long-chain saturated fatty acids. As a result of this unusual lipid composition, lens membranes have very low fluidity, which is restricted even further by lipid-protein interactions. The composition and metabolism of membrane lipids may affect the formation of various types of cataracts. Diets rich in vegetable oils offer some protection against the formation of osmotic cataracts and the hereditary cataract of the RCS rat, although the mechanism of this effect is not clear. Vitamin E also protects against the formation of several types of cataract in vivo and in vitro, suggesting that lipid peroxidation may play a role in cataractogenesis. Certain drugs which inhibit lipid synthesis or degradation are cataractogenic, and a deficiency in cataractogenic, and a deficiency in phosphatidylserine is associated with a loss of Na+/K+ ATPase activity in several types of cataract. Human senile cataracts show a marked loss of protein-lipid interactions, although the overall lipid composition is normal. This loss of protein-lipid interactions may be related to oxidative damage to membrane-associated proteins. Interestingly, the decrease in the fluidity of lens membranes with age would counteract the formation of aqueous pores in the membrane, which can result from the oxidative cross-linking of membrane-associated proteins. Certain pathways of lipid metabolism seem to have regulatory functions. Among these are phosphatidylinositol turnover, phosphatidylethanolamine methylation, and arachidonic acid metabolism. All of these pathways function in the lens. Phosphatidylinositol turnover is correlated with the rate of lens epithelial cell division, while phosphatidylethanolamine methylation seems to be related to the initiation of lens fiber cell formation. Both pathways are associated with the release and metabolism of arachidonic acid in other cell types. While it is not known whether phosphatidylinositol turnover or phosphatidylethanolamine methylation result in the release of arachidonic acid in the lens, recent work has shown that lens cells from a variety of species can metabolize arachidonic acid by both the cyclooxygenase and lipoxygenase pathways. The possible physiological significance of these metabolites to the lens is yet to be determined.
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PMID:Lens lipids. 639 28

Kinetic studies on the aldose reductase protein (AR2) have shown that it does not behave as a classical enzyme in relation to ring aldose sugars. These results have been confirmed by X-ray crystallography studies, which have pinpointed binding sites for pharmacological "aklose reductase inhibitors" (ARIs). As with non-enzymic glycation reactions, there is probably a free-radical element involved derived from monosaccharide autoxidation. In the case of AR2, there is free radical oxidation of NADPH by autoxidising monosaccharides, enhanced in the presence of the NADPH-binding protein. Whatever the behaviour of AR2, many studies have showed that sorbitol production is not an initiating aetiological factor in the development of diabetic complications in humans. Vitamin E (alpha-tocopherol), other antioxidants and high fat diets can delay or prevent cataract in diabetic animals even though sorbitol and fructose levels are not modified; vitamin C acts as an AR1 in humans. Protein post-translational modification by glyc-oxidation or other events is probably the key factor in the aetiology of diabetic complications. There is now no need to invoke AR2 in xylitol biosynthesis. Xylitol can be produced in the lens from glucose, via a pathway involving the enzymes myo-inositol-oxygen oxidoreductase, D-glucuronate reductase. L-gulonate NAD(+)-3-oxidoreductase and L-iditol-NAD(+)-5-oxidoreductase, all of which have recently been found in bovine and rat lens. This chapter investigates the molecular events underlying AR2 and its binding and kinetics. Induction of the protein by osmotic response elements is discussed, with detailed analysis of recent in vitro and in vivo experiments on numerous ARIs. These have a number of actions in the cell which are not specific, and which do not involve them binding to AR2. These include peroxy-radical scavenging and recently discovered effects of metal ion chelation. In controlled experiments, it has been found that incubation of rat lens homogenate with glucose and the copper chelator o-phenanthroline abolishes production of sorbitol. Taken together, these results suggest AR2 is a vestigial NADPH-binding protein, perhaps similar in function to a number of non-mammalian crystallins which have been recruited into the lens. There is mounting evidence for the binding of reactive aldehyde moieties to the protein, and the involvement of AR2 either as a 'housekeeping' protein, or in a free-radial-mediated 'catalytic' role. Interfering with the NADPH binding and flux levels--possibly involving free radicals and metal ions--has a deleterious effect. We have yet to determine whether aldose reductase is the black sheep of the aldehyde reductase family, or whether it is a skeleton in the cupboard, waiting to be clothed in the flesh of new revelations in the interactions between proteins, metal ions and redox metabolites.
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PMID:Aldose reductase: a window to the treatment of diabetic complications? 969 97

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

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


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