Type 2 diabetes mellitus (DM), characterized by decreased insulin secretion, hypoinsulinemia and/or insulin resistance, accounts for 90% of all cases of DM. Oxidative stress is considered as an essential prerequisite for the pathogenesis of this disease. On one hand, current theory of oxidative stress is associated with autooxidation of glucose, which leads to the reactive ketoaldehydes formation, on the other hand it intensifies non-enzymatic glycation of proteins. The increase in reactive oxygen species (ROS) production and a decline in the activity of antioxidants is not only a result of hyperglycemia, but also of hyperinsulinemia and decreased tissue sensitivity to insulin. Because of a significant role of (ROS) in the pathogenesis of chronic diabetic complications, efforts should be made to diminish their toxic effects. Scientific research revealed that the best method for the prevention and treatment of diabetic complications was a long-term compensation of diabetes. To obtain optimal glycemia is crucial, since hyperglycemia is the main source of oxidative stress in patients with diabetes mellitus.