Abstract
Abstract: :
Purpose: To study the pathogenesis of cataract in experimental diabetes using an animal model whose lens physiology is comparable to that of human lens. Mouse, which has low aldose reductase level in the lens, has been selected for these studies. Methods: CD-1 strain of mice, weighing 25-30 g, were used. Diabetes was induced by intraperitoneal injections of Streptozotocin. Diabetic status was assessed by hyperglycemia and the extent of polyuria, polydypsia and polyphagia. The diabetic mice were then divided into the following two groups: the first group was treated with 1% Pyruvate in food and water. The second group was left as untreated control. Development and progress of cataract was monitored by ophthalmoscopy and slit-lamp examination. In addition, lenses were dissected out between four to five weeks for biochemical studies. Results: Blood glucose of all Streptozotocin-treated mice was between 300 and 400 mg/dl. The animals also showed physiological signs of diabetes such as polyuria and polydypsia. Glycated proteins in the normal mice lenses was 1.45±1.35% of the total water-soluble proteins. In the untreated (control) diabetic group it was elevated to 8.9±1.07%. In the group treated with pyruvate in food and water it was 3.22±0.77%. Glutathione (GSH) levels were found to be 2.35±0.57 nmoles/mg lens weight in the normal ,1.17±0.09 nmoles/mg lens weight in diabetic and 2.23±0.29nmoles/mg lens weight in the group treated with pyruvate. Conclusion: The findings demonstrate that lens aldose reductase activity in this model is of minor significance in cataractogenesis. Factors such as oxidative stress and glycation are important contributors. This is evident by the observed protective effect of pyruvate, which is known to exert an antioxidant effect as well as an inhibitory effect against protein glycation, as demonstrated here, as well as previously.
Keywords: 338 cataract • 387 diabetes • 504 oxidation/oxidative or free radical damage