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)

The effect of (1-benzoyl-1H-indazol-3-yl)oxylacetate L-Lysine (bendazac-lysine) on some enzymatic activities involved in the metabolism of reduced glutathione (GSH) was studied in the rabbit lens during developing cataract induced by a single dose of X-rays (2000 rads). The specific activities of glutathione reductase (G.R.), glutathione peroxidase (GSH.Px) and glutathione S-transferase (GSHS-tr.) do not change following irradiation and treatment with bendazac-lysine. The activity of the same enzymes expressed as a function of water soluble proteins (WSP) per lens significantly decreases (P less than 0.01) as compared to controls in the irradiated lens not treated with bendazac-lysine (ILNTB) at the 8th week, whereas no significant decrease as compared to controls is observed in the irradiated lens treated with bendazac-lysine (ILTB). In the ILNTB the specific activity of glucose-6-phosphate dehydrogenase (G6PDH) is reduced by 10% after 0.3 weeks and by 29% after 12 weeks. In the ILTB the specific activity of G6PDH is reduced by 8% after 0.3 weeks and by 14.5% after 12 weeks. The specific activity of superoxide dismutase (SOD) in the ILNTB is reduced by 19% after 0.3 weeks and reached 31% after 12 weeks. In the ILTB the specific activity of SOD is reduced by 11% after 0.3 weeks and 19.8% after 12 weeks. The mechanism of protective effect of bendazac-lysine on cataract is discussed.
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PMID:Effects of bendazac L-lysine salt on some metabolic enzymes of glutathione in the rabbit lens after X-irradiation. 361 May 98

The Italian island of Sardina occupies an important position on the map of glucose-6-phosphate dehydrogenase (G6PD)-deficiency distribution throughout the world, since in this region the condition is particularly frequent and severe (erythrocytes show only 0-7% of G6PD normal activity, while people result affect up to 35% depending on the district). In order to investigate the relationship between the deficiency of G6PD in erythrocytes and in lens, and cataractogenesis, we studied 2125 idiopathic cataractous and non-cataractous subjects, both G6PD-deficient and normal, males and females. Parameters investigated included incidence, distribution and type of cataracts, age at the moment of the first observation, geographical provenance, and G6PD activity in erythrocytes. Moreover, G6PD activity and glutathione (GSSG)-reducing activity was assessed in cataractous lenses obtained from deficient and normal individuals. G6PD deficiency was found to be significantly more frequent in males of the age-group 40-49 years (P = 0.025), while the frequency of G6PD deficiency was decisively lower in the older age-groups. In females, mainly heterozygotes, no evidence of such a relation was found. Cataractous lenses obtained from male patients with no G6PD activity in erythrocytes showed undetectable levels of G6PD activity, and lowered, but not extinguished, levels of GSSG-reducing activity. Cataractous lenses from heterozygous females showed intermediate levels of G6PD activity and GSSG-reducing activity. A preliminary study of 182 diabetic, G6PD-deficient and non-deficient subjects, failed to demonstrate that Sardinian variants of G6PD deficiency provide protection against cataract formation in diabetic patients.
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PMID:The relationship between glucose-6-phosphate dehydrogenase deficiency and cataracts in Sardinia. An epidemiological and biochemical study. 633 98

Steroids that inhibit glucose-6-phosphate dehydrogenase (G6PD) were used to examine the correlation between the loss of GSSG-reducing activity and G6PD deficiency in the lens. The correlation was found to be nonlinear. In senile cataracts, which had lost 36% of NADPH-generating activity as compared to clear lenses, the estimated loss of GSSG reduction was only 20%. On the other hand, lenses with severe G6PD deficiency (i.e. 93% loss) retained at least 28% GSSG-reducing activity. The declined reducing activity, however, suggested a possible role of G6PD deficiency in cataract formation in young patients.
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PMID:GSSG-reducing activity in lenses deficient in glucose-6-phosphate dehydrogenase. 662 60

A study of diabetic and nondiabetic subjects was performed to evaluate the possible association of diabetes mellitus with cataract formation. Parameters investigated included cataract incidence and type model of diabetic therapy, degree of diabetic control, duration of glucose-6-phosphate dehydrogenase (G-6-PD) activity. Diabetes mellitus was found to be correlated with posterior subcapsular cataract formation, as was duration of diabetic disease. Race, degree of metabolic control, and age of onset of disease did not appear to be correlated with cataract formation. Oral hypoglycemic agent therapy was significantly associated with posterior subcapsular cataract formation. The African variant of G-6-PD deficiency appeared to protect against cataract formation in diabetic patients. The most important overall factor in cataractogenesis proved to be age. Posterior subcapsular cataracts were associated with corticosteroid therapy, presence of diabetes mellitus, and oral hypoglycemic agent therapy.
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PMID:The effect of diabetes mellitus and diabetic therapy on cataract formation. 723 95

Three independent case-control studies with similar methodologies were conducted in India, the United States and Italy to investigate risk factors by cataract type. Their common objectives were to evaluate risk factors for each cataract type, giving priority to nutritional factors, and to determine whether risk factors differed among cataract types. Data included self-reporting of food frequencies and various biochemical determinations. A higher body mass index was the only nutritional factor found by more than one study to be associated with cataract, being less frequent in cases than in controls. Blood nutritional status from one study showed that a high antioxidant index decreased risk for at least one cataract type, high glucose-6-phosphate dehydrogenase values increased risk for at least one cataract type, a high albumin globulin ratio decreased risk for mixed cataract, and high iron levels decreased risk for cortical cataract. Only one of the three studies found that a high nutritional status, high dietary antioxidant index, and use of multiple vitamin supplements decreased risk for cataract. Findings from these studies suggest socioeconomic and nutritional components to cataract risk, although not consistently across studies or cataract types. Differences between studies may be due to differences in populations and/or data collection methods. Because reducing cataract risk would have major implications for a large segment of the population, clinical trials seem appropriate to confirm and evaluate the potentially modifiable risk factors suggested by these studies.
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PMID:Recent epidemiologic studies on nutrition and cataract in India, Italy and the United States. 826 67

Royal College of Surgeons (RCS) rats have hereditary retinal degeneration in association with posterior subcapsular opacities. Cataract formation is thought to be correlated with an increase in lipid peroxidation products in the vitreous (Zigler and Hess, 1985). In order to examine the possibility that parallel changes in enzyme activity are occurring within the lens, we analysed the activity of four key enzymes and the crystallin protein profile. We compared RCS rat lenses at three different stages of cataract formation to clear lenses of the nonpigmented RCS rat, lenses from pigmented RCS rat and to normal (Fisher) rat. Our data shows that concomitant with the appearance of the RCS cataract, the ratio of the crystallins beta 1, beta H and gamma to the total lens protein was reduced. The crystallin profile of a clear RCS lens was similar to that of a normal (Fisher) lens. No significant difference in the activity of the enzymes hexokinase and glucose-6-phosphate dehydrogenase (G6PD) was found among the lenses, however the activity of glutathione reductase and aldolase was reduced in the cataractous lenses.
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PMID:Enzyme activities and crystallin profiles of clear and cataractous lenses of the RCS rat. 840 88

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

Metabolic changes in the rabbit lens have been studied by means of nuclear magnetic resonance spectroscopy. These changes have been induced by prolonged topical treatment with dexamethasone. Our results demonstrate an increase in sorbitol, sorbitol-3-phosphate, fructose-3-phosphate, glycerol-3-phosphate and glucose-6-phosphate levels and a decrease in glutathione sulphate (GSH) and myo-inositol levels, in agreement with what was observed in lenses from streptozocin-diabetic rats before lens opacity. The hyperglycaemia can only partially explain all these observed biochemical variations. The lack of increase in the intermediates of pentose cycle, such as sedoheptulose-7-phosphate, seems to support the hypothesis of an inhibition of glucose-6-phosphate dehydrogenase by dexamethasone treatment. Finally dexamethasone treatment induces a decrease in GSH. The decreasing or the loss of GSH has been suggested as a possible pathogenic mechanism in the cataract formation.
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PMID:Metabolic changes in rabbit lens induced by treatment with dexamethasone. 1124 50

Cataracts have been attributed to oxidative injury in proteins and lipids. Primary defenses that directly protect the lens against oxidative damage include small molecule antioxidants (vitamin C, vitamin E, glutathione and carotenoids) and antioxidant enzymes (superoxide dismutase, catalase, and the glutathione enzyme systems - glutathione peroxidase, glutathione reductase and glucose-6-phosphate dehydrogenase). In humans, low plasmatic levels of vitamin C, vitamin E and carotenoids have been associated with a high risk of senile cataracts. Dogs are more prone to develop cataracts. A decrease in antioxidant defenses could be responsible for increased lens oxidation and cataract development. In this study we report the levels of erythrocytic enzymatic antioxidants (superoxide dismutase, catalase, glutathione peroxidase and glucose-6-phosphate dehydrogenase) and plasma vitamin C as well as malondialdehyde, in normal and cataractous English Cocker Spaniel dogs. Plasma vitamin C levels were consistently lower in cataractous dogs (20.17 &mgr;M +/- 8.2 &mgr;M) when compared with normal dogs (24.1 &mgr;M +/- 9.4 &mgr;M). These results indicate a possibly decreased synthesis in vitamin C, leading to lower aqueous humor levels of this vitamin. Considering that vitamin C levels in the aqueous humor may be responsible for lens antioxidant maintenance, and that these levels are obtained from plasma secretion through the ciliary epithelium, decreased plasma levels may indicate a decrease in the antioxidant capacity of the aqueous humor.
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PMID:Antioxidant profile of cataractous English Cocker Spaniels. 1139 47

Changes in glucose-6-phosphate dehydrogenase (G-6-PD), glutathione reductase (GSH-R), reduced glutathione (GSH), glutathione peroxidase (GSH-PO), transketolase (TK) and transaldolase (TA) were studied in lens and red blood cells (RBCs) to understand the possible biochemical mechanisms responsible for the development of senile cataract. The activity of G-6-PD was increased in lens, though not so in erythrocytes during cataractogenesis. A marked decrease was observed in GSH level and GSH-R activity in the lens and RBCs of the cataractous group. The activity of GSH-PO was remarkably high in lens but not in the erythrocytes during the maturity of cataract. The activity of TK decreased gradually in both the lens and erythrocytes. The activity of TA decreased in erythrocytes but increased in the lens with maturation of cataract.
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PMID:Changes in glutathione, glutathione-linked enzymes and hexose monophosphate shunt enzymes in senile cataract. 1525 23


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