Abstract
To determine whether vitamin E has protective effects or not on streptozotocin-induced diabetic rats in diabetic urinary bladder dysfunction, with interrelationships between oxidative stress and apoptosis. Thirty-two Wistar albino male rats were divided into 4 groups. Group A (n = 8), control; group B (n = 8), diabetic control; group C (n = 8), control + vitamin E; and group D (n = 8), diabetic + vitamin E. Vitamin E was injected 40 mg/kg every other day intraperitoneally for 2 weeks. In the diabetic groups, diabetes was induced by a single intraperitoneal injection of 65 mg/kg of streptozotocin. Apoptosis studies were performed using apoptosis detection kit and the TUNEL (TdT-mediated dUTP nick-end labeling) technique. The levels of glucose, malondialdehyde (MDA), superoxide dismutase, catalase, and glutathione peroxidase were detected in hemolysate. It was observed that apoptosis number in urothelial cells of the bladder in diabetic rats increased significantly compared with control and decreased after vitamin E treatment. MDA levels of the diabetic group were significantly higher than those on the control and vitamin E groups. Diabetic + vitamin E group had significantly increased MDA levels compared with control group, although these values were lower than those in the diabetic group. All enzyme activities of the vitamin E group did not differ compared with the control group. In diabetic + vitamin E group, superoxide dismutase and glutathione peroxidase activities were similar to controls. Catalase activity of the diabetic + vitamin E group decreased significantly compared with control, although it was higher than that in the diabetic group. Our study revealed that vitamin E decreases apoptosis and may be protective for uroepithelial cells of diabetic bladder.
Published Version
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