Preservation of the antioxidant status in chemically-induced diabetes mellitus by melatonin

Oxidant stress is believed to be enhanced in patients with diabetes mellitu s, which may lead to endothelial dysfunction and the development of atheros clerosis. In diabetes, hyperglycemia drives non-enzymatic glycation and oxi dation of proteins and lipids which enhances the formation of advanced glyc ation end products (AGEs), which may be involved in the pathogenesis of dia betic vascular disease. The macrovascular complications of diabetes seem to be due to enhanced cellular oxidant stress by the interaction of AGEs with their receptor. It would be worthwhile to devise methods to reduce this ox idant stress. In alloxan-induced diabetic rats lipid peroxidation products were increased, while levels of nitric oxide glutathione peroxidase and sup eroxide dismutase were reduced. Melatonin restored these biochemical abnorm alities to normalcy independent of hyperglycemia. This model can be used to study the role of oxidant stress in the development of macrovascular compl ications in diabetes mellitus.