The protective effects of vitamin E on urinary bladder apoptosis and oxidative stress in streptozotocin-induced diabetic rats.

OBJECTIVES: 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.

METHODS: 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.

RESULTS: 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.

CONCLUSIONS: Our study revealed that vitamin E decreases apoptosis and may be protective for uroepithelial cells of diabetic bladder.