Abstract

Purpose . To identify differential changes in redox status underlying type 1 (T1DC) and type 2 (T2DC) diabetic cataract (DC) formation in rat. Material and methods. Rat models of type 1 and 2 diabetes were respectively induced, and cataract progression was examined weekly. At week eight the levels of reduced glutathione (GSH), oxidized glutathione (GSSG), nicotinamide adenine dinucleotide 2’-phosphate reduced tetrasodium salt (NADPH), and glucose-6-phosphate dehydrogenase (G6PD) activity were measured and compared with those in controls. Results. Cataracts were observed two more weeks earlier in type 1 than type 2 diabetic rats. Furthermore, cataracts were progressed more slowly in T2DC compared with those in T1DC. Lens GSH levels were decreased 4-fold and 2-fold in type 1 and type 2 diabetic rats, respectively, compared with levels in normal control rats. NADPH levels were showed 2.4-fold and 1.5-fold decreases in type 1 and 2 diabetic rats, respectively, compared with normal controls. Similar changes were found in the activity of G6PD. Conclusions . The results suggest that GSH and NADPH loss might be important pathological mechanisms in T1DC and T2DC formation. The «fast» progression of cataracts in type 1 diabetic rats might be due to the more severe oxidative stress than in type 2 diabetic rats.

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