ABSTRACT
Diabetes is a chronic condition, produces little or no insulin, and usually develops in childhood or early childhood. Hyperglycemia triggers the generation of reactive oxygen species (ROS) and autoxidation of glucose leading to domination ofthe condition of oxidative stress. It also causes tissue damage through different mechanisms, including increased intracellular formation of advanced glycation end products (AGEs), increased expression of the receptor for AGEs, and activation of protein kinase C isoforms. Glucose can cause multiple secondary complications through a variety of pathways, which are appearing to lead to oxidative stress. Oxidative stress is an imbalance between radical engendering and scavenging systems. Overproduction of free radicals and a defect in antioxidant protection involved pathogenesis of diabetes. ROS level elevation in diabetes may be due to decrease in destruction or/and increase in the production by superoxide dismutase (SOD), glutathione peroxidase (GSHPx) antioxidants, and catalase (CAT—enzymatic/nonenzymatic). Oxidative stress causes cell damage both directly and indirectly through the activation of different pathways. Hyperglycemia promotes autoxidation of glucose to form free radicals. The generation of free radicals beyond the scavenging abilities of endogenous antioxidant defenses results in macro- and microvascular dysfunctions. Vitamin E is converted to tocopheroxyl radicals after acting 78as a free radical scavenger, which means the regeneration of vitamin E is required to prevent unwanted tocopheroxyl-mediated oxidative process. Vitamin E regeneration system is composed of ascorbic acid, reduced glutathione, and CoQ10.
