iabetes mellitus is a multi-factorial disease in which increased oxidative stress plays an important pathogenic role. The term oxidative stress has been coined to represent a shift towards the pro-oxidant in the Pro-oxidant/Antioxidant balance that can occur as a result of an increase in oxidative metabolism. Chemical compounds capable of generating potential toxic oxygen species referred as pro-oxidants and compounds scavenging them are referred as antioxidants. Biochemical defects related to all diabetic complications may arise from overproduction of reactive oxygen species/nitrogen species. Free radicals arise from radiation, environmental chemicals, cigarette smoke, and various other environmental sources. A free radical is an atom or molecule that has one or more unpaired electrons, its tendency to acquire an electron from other anion for e.g.) hydroxyl radical, singlet oxygen, hydrogen peroxide, chlorine halogen radicals. When free radicals are overloaded, the antioxidants are not able to compete them and that leads to cell injury causing molecules to lose their structure and functions. ROS(reactive oxygen species) induced by elevation of glucose and free fatty acid levels, directly damage DNA, proteins , lipids, decrease insulin mRNA, cytosolic ATP, mitochondria, calcium influx into cytosol, and causes apoptosis.
They also directly induce damage to tissues by activating number of stress sensitive signaling pathways (NFkB, P38 mitogen activated protein kinase, NH2 terminal junk kinase, protein kinase, stress activated protein kinase, hexosamines etc… Oxidative stress participates not only in beta cell dysfunction and insulin resistance but also in the genesis of late complications of diabetes. Oxidative stress /nitrosative stress also inducts formation of advanced glycation end products (AGE). Effect of advanced glycation end products on vascular structures is important in the pathogenesis of diabetic micro and macro vascular complications. Oxidative stress involves altering mitochondrial function, ion channel alteration, and abnormal growth factor signaling.