We investigated the possible role of reactive oxygen species (ROS) on renal function in experimental diabetes.
Materials and methods: Seven groups of male rats were studied. Group I consisted of control animals. Diabetes was induced (by streptozotocin) in the animals in the other groups and they received either insulin or vitamin E (300 or 600 mg/kg), both insulin and vitamin E, or no treatment for 4 weeks. At the end of the study, blood pressure was measured and parameters of kidney function and oxidative stress were evaluated in serum and kidney tissue samples.
Results: Diabetic animals had higher blood pressures; increased serum glucose, urea, creatinine, cyclic guanosine monophosphate (cGMP); increased kidney tissue levels of malondialdehyde and inducible nitric oxide synthetase (iNOS); and reduced serum glutathione peroxidase when compared with control animals. Blood glucose levels in diabetic animals were controlled by insulin and not by any dose of vitamin E alone. However, all other measured parameters improved towards control levels with either insulin or vitamin E in either dose. An additive beneficial effect was observed on the levels of iNOS and cGMP when both forms of treatment were used in diabetic animals.
Conclusions: We conclude that ROS may play an important role in diabetes-induced nephropathy in this rat model. Vitamin E supplementation in addition to insulin can have additive protective effects against deterioration of renal function in this model.