Combination of vitamin E and folic acid ameliorate oxidative stress and apoptosis in diabetic rat uterus.

Abstract

This study was designed to assess oxidative damage and cell apoptosis in the uterus of rats with streptozotocin (STZ)-induced diabetes. The role of vitamin E (VE) and/or folic acid (FA) in the protection from such damage was also evaluated. The treatments were performed for 4 weeks on six groups of rats: 1) normal control 2) diabetic control 3) diabetic rats receiving olive oil as a vehicle (without VE) 4) diabetic rats treated with VE (200 mg/kg) in olive oil 5) diabetic rats treated with FA (25 mg/kg) and 6) diabetic rats treated with VE+FA (200 and 25 mg/kg, respectively). We measured the malondialdehyde level (MDA), glutathione content (GSH) and the activity of GSH peroxidase (GPx), GSH reductase (GR) and catalase. Changes in caspase-3 activity were quantified in uterine tissue to assess the rate of apoptosis. In the rat uterine tissues, MDA content and caspase-3 activity were significantly elevated, while GPx, GR and CAT activities and the GSH level were significantly decreased in the diabetic control compared with those in normal rats (p<0.05). The combination of the vitamins (VE+FA) restored uterine GSH content and enzymatic activities of GPx, GR and CAT and reduced the MDA level (p<0.05). A prominent reduction in apoptosis of uterine cells was detected in diabetic rats treated with two vitamins (p<0.05). Overall, VE alone, not FA, produced results similar to those of the VE+FA combination. Thus, in the uterine tissue of diabetic rats, diabetes complications (that are caused by oxidative damage and apoptosis induction) can be prevented by the systemic administration of VE and FA.