Diabetes mellitus (DM) complications were attributed to deposition of glycosylation products on the interstitial tissue proteins and blood vessel walls, forming irreversible advanced glycosylation end products (AGEs) (1). In diabetic retinopathy, deposition of AGEs and plasma proteins in basement membranes resulted in retinal capillary closure, retinal hemorrhages and micro-aneurysms (2). AGEs altered the expression of certain genes that affect cellular growth, differentiation, inflammation and angiogenesis, which are the basis of ischemic and proliferative diabetic retinopathy (3). Moreover, hyperglycemia stimulated inducible nitric oxide synthetase enzyme (iNOs) and nitric oxide (NO) synthesis (4, 5). NO and iNOS modulated the proinflammatory and profibrotic pathways in the progression of diabetic nephropathy (6). Additionally, endogenous antioxidant enzymes such as serum catalase, glutathione peroxidase (GPx) and increased glutathione reductase (GR) were reported to decrease in chronic hyperglycemia (7). A synergistic relation between AGEs and serum antioxidant enzymes was suggested (8). This study sought to determine the potential prophylactic and antioxidant effects of aminoguanidine in experimentally induced diabetes. Four groups of Wistar rats, each composed of ten rats, were used. Two groups served as control. In group 3, diabetes was induced by a single intraperitoneal injection of streptozotocin (65 mg kg -1 ).In group 4, diabetes was induced and treated with aminoguanidine (100 mg kg -1 daily) orally for 3 months. Levels of serum glucose, glutathione peroxidase, glutathione reductase and erythrocytes catalase were analyzed on day 90 of the experiment. Retinal and kidney specimens were examined histopathologically after sacrifice of the animals. A significant antioxidant effect of aminoguanidine and its prophylactic role in diabetic retinopathy and nephropathy were observed in experimental animals.