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Query: UMLS:C0086543 (cataract)
 29,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rat lenses with experimentally induced cataract (either by naphthalene or by streptozotocin) were analyzed biochemically. Both noxae had some effects in common. Water-soluble protein and aldose reductase activity decreased, and glucose-6-phosphate dehydrogenase, phosphofructokinase and glutathione reductase activity increased. A specific effect of streptozotocin was the rise in glucose, fructose and sorbitol. A specific effect of naphthalene was increased amounts of water-insoluble protein.
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PMID:Alterations of lens metabolism with experimentally induced cataract in rats. 297 80

In this study we have investigated the oxidative metabolism of red blood cells (RBC), plasma, serum, aqueous humor, and lens of healthy subjects and of age-matched cataractous patients with and without diabetes. Reduced and oxidized glutathione (GSH GSSG) levels in RBC were similar among the three groups. Plasma levels of GSSG were higher in diabetics than in cataractous and control subjects. No differences in plasma content of GSH were noted among the three groups. The activity of the enzyme glucose-6-phosphate dehydrogenase was significantly diminished in diabetic patients. Controls and cataractous patients showed similar levels of malondialdehyde (MDA). Although not significant the MDA content in RBC from diabetics was elevated. No differences in plasma levels of vitamin E were noted among the three groups. The biological liquid oxidant activity of serum in diabetic patients was significantly higher than in controls and cataractous patients. GSH levels in aqueous humor were similar in diabetic and nondiabetic cataractous patients. The content of GSSG in aqueous humor was highest in diabetic patients. Control clear lenses showed low levels of MDA. The MDA levels in cataractous lenses from nondiabetic patients were significantly higher than those of controls. In diabetic patients the content of MDA in the lens was approximately twice as high as the cataractous values. Our results seem to demonstrate that oxidative damage could play a role in the pathogenesis of cataract in diabetes.
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PMID:Systemic human diseases as oxidative risk factors in cataractogenesis. I. Diabetes. 318 3

The activities of lactate dehydrogenase (LDH), glucose 6-phosphate dehydrogenase (G6PD) and glyceraldehyde 3-phosphate dehydrogenase (GAPD) in two zones of the epithelium of the lens of 6- and 27-month-old rats were measured using quantitative cytochemical methods. In both age groups, the epithelium in the equatorial zone showed the highest enzymatic activity. LDH activity was similar in young and old rats in both areas. G6PD and GAPD activities in the central area were similar in both age groups, but their activity was markedly lower in the equatorial zone in old rats compared to young ones. This decrease in G6PD and GAPD activities may play a role in cataract formation.
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PMID:Quantitative cytochemistry of enzymes in the epithelium of ageing rat lenses. 323 91

The relationship between biochemical markers of antioxidant status and senile cataract was examined in 112 subjects aged 40 to 70 years. Seventy-seven of these subjects had a cataract in at least one lens. Antioxidant status was measured using erythrocyte superoxide dismutase, glutathione peroxidase, and glucose-6-phosphate dehydrogenase activity, and indexes that included these enzymes plus plasma levels of vitamin E, vitamin C, and carotenoids. Subjects were grouped by level (low, moderate, or high) of the enzymes and antioxidant indexes. Results suggest that subjects with high levels of at least two of the three vitamins (vitamin E, vitamin C, or carotenoids) are at reduced risk of cataract relative to subjects with low levels of one or more of these vitamins (odds ratio, 0.2). The erythrocyte enzymes, either individually or in combination, did not appear to differ between subjects with and without cataract.
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PMID:Antioxidant status in persons with and without senile cataract. 334 51

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

1. Cataracts were developed by incubating rabbit lenses for 22hr. at 37 degrees in a culture medium containing tyrosine and tyrosinase (EC 1.10.3.1). 2. A 45% diminution in the content of GSH and significant inhibition of glucose 6-phosphate dehydrogenase (EC 1.1.1.49) activity were observed in the cataractous lenses compared with controls. 3. GSSG accumulated in both cataractous and control lenses. Significant amounts of GSSG were transported outward from the cataractous lenses and small amounts from control lenses. 4. Transport of GSSG from rabbit lens incubated in a diffusate of plasma from a naphthalene-fed rabbit was also observed. 5. GSSG was found in the aqueous humour obtained between 2 and 24hr. after feeding of naphthalene to rabbits; subsequently the GSSG in the aqueous humour decreased to almost undetectable amounts in 48hr.; in controls, GSSG was not detectable. 6. A possible mechanism of formation of experimental and senile cataract is briefly discussed.
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PMID:Cataract produced by tyrosinase and tyrosine systems in rabbitens in vitro. 497 83

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

This review examines the hypothesis that oxidative stress is an initiating factor for the development of maturity onset cataract and describes the events leading to lens opacification. Data are reviewed that indicate that extensive oxidation of lens protein and lipid is associated with human cataract found in older individuals whereas little oxidation (and only in membrane components) is found in control subjects of similar age. A significant proportion of lenses and aqueous humor taken from cataract patients have elevated H2O2 levels. Because H2O2, at concentrations found in cataract, can cause lens opacification and produces a pattern of oxidation similar to that found in cataract, it is concluded that H2O2 is the major oxidant involved in cataract formation. This viewpoint is further supported by experiments showing that cataract formation in organ culture caused by photochemically generated superoxide radical, H2O2, and hydroxyl radical is completely prevented by the addition of a GSH peroxidase mimic. The damage caused by oxidative stress does not appear to be reversible and there is an inverse relationship between the stress period and the time required for loss of transparency and degeneration of biochemical parameters such as ATP, GPD, nonprotein thiol, and hydration. After exposure to oxidative stress, the redox set point of the single layer of the lens epithelial cells (but not the remainder of the lens) quickly changes, going from a strongly reducing to an oxidizing environment. Almost concurrent with this change is extensive damage to DNA and membrane pump systems, followed by loss of epithelial cell viability and death by necrotic and apoptotic mechanisms. The data suggest that the epithelial cell layer is the initial site of attack by oxidative stress and that involvement of the lens fibers follows, leading to cortical cataract.
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PMID:Oxidative stress-induced cataract: mechanism of action. 767 10


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