The Physiological and Biochemical Effects of Diabetes on the Balance between Oxidative Stress and Antioxidant Defense System

The number of reports on the effects of diabetes is still increasing because the diabetes is one of the major disease of industrialized and non-industrialized societies. Because at least 30 million people throughout the world suffer from diabetes, there is currently great interest in the potential contribution of increased oxidative stress to the pathogenesis of diabetes as well as its complications. Thus, the goal of this review was to explain the behaviors of the free radicals and antioxidant enzymes against diabetes. Hyperglycemia is a widely known cause of enhanced free radical concentrations and decreased antioxidant defense system, this mechanism may occur via at least four different routes: increased glycolysis; intercellular activation of sorbitol (polyol) pathway; auto-oxidation of glucose and non-enzymatic protein glycation. In addition, this overview not only to investigate the genesis of free radicals in hyper/hypo-insulinemia, but also to elucidate the inverse relationship between insulin action and free radicals. Increased free radicals in diabetes may be caused the pathogenesis of atherogenesis, atherosclerosis and the degeneration in the biological macromolecules; proteins and lipoproteins, and other degenerative disorders. Furthermore, this overview was extended to show the effect of streptozotocin on diabetes, antioxidant enzymes and oxidative stress. In general, the hypothesis was that, the imbalance of generation and scavenging of free radicals play an important role in determining tissue damage associated with diabetes. However, this argument is still ambiguous because of the difficulties of the direct observation of the active oxygen species in biological systems due to their short life time.