Adenosine triphosphatase activity of streptozotocin-induced diabetic rat brain microsomes. Effect of vitamin E.

Hyperglycemia causes protein glycosylation, oxidation and alterations in enzyme activities, which are the underlying causes of diabetic complications. This study was undertaken to test the role of vitamin E treatment on Ca2+-ATPase activity, protein glycosylation and lipid peroxidation in the brain of streptozotocin (STZ)-induced diabetic rats. Male rats weighing about 250-300 g were rendered diabetic by a single STZ injection of 50 mg/kg via the tail vein. Both the diabetic and non-diabetic rats were fed a vitamin E supplemented diet (500 IU/kg/day). Ca2+-ATPase activity was significantly reduced at week 10 of diabetes compared to the control group (p < 0.05), with 0.225+/-0.021 U/I (mean +/- S.E.M.) in the control group and 0.072 +/- 0.008 U/l (mean +/- S.E.M.) in the diabetic group. Vitamin E treatment prevented the enzyme activity from decreasing. The activities observed were 0.226 +/- 0.020 U/l and 0.172 +/- 0.011 U/I (mean +/- S.E.M.) in the vitamin E-treated control and diabetic group, respectively. STZ-induced diabetes resulted in an increased protein glycosylation and lipid peroxidation. Vitamin E treatment led to a significant inhibition in blood glucose, protein glycosylation and lipid peroxidation, which in turn prevented abnormal activity of the enzyme in the brain. This study indicates that vitamin E supplementation may reduce complications of diabetes in the brain.

Determination of Ca2+-atpase activity in streptozotocin-induced diabetic rat liver.

Microsomal Ca2+-ATPase activity was studied in control and streptozotocin (STZ)-induced diabetic rat livers. Male rats were rendered diabetic by injection of STZ (45 mg/kg body weight) via the tail vein. Diabetic rats at 1, 4, 8, 10 or 15 wk and control rats were sacrificed. Liver tissues were obtained for the isolation of Ca2+-ATPase. Ca2+-ATPase activity was determined spectrophotometrically and lipid peroxidation [measured as tiobarbituric acid reactive substances (TBARS)] in liver tissues was determined spectrofluorometrically. Total calcium was measured by atomic absorption spectrophotometry. Blood glucose levels of the diabetic animals were >500 mg/dl at 4, 8, 10 and 15 wk of diabetes. Ca2+-ATPase activity was significantly decreased at all weeks of diabetes compared to control group (p<0.001). Ca2+-ATPase activity of control rats was 0.193 +/- 0.015 U/I whereas activity was 0.130 +/- 0.015 U/I at 15 wk of diabetes. The difference in calcium levels of diabetic rat livers was not significantly different compared to control group. On the other hand TBARS were elevated by 67% at 15 wk of diabetes. The decrease in enzyme activity may have been caused by elevated TBARS levels observed in liver tissue sindicative of increased lipid peroxidation.