Antioxidants are compounds that inhibit oxidation. Oxidation may be a reaction which will produce free radicals, thereby resulting in chain reactions which will damage the cells of organisms. Antioxidants like thiols or vitamin C terminate these chain reactions.An antioxidant are often defined as: “any substance that, when present in low concentrations compared thereto of an oxidisable substrate, significantly delays or inhibits the oxidation of that substrate”.1 The physiological role of antioxidants, as this definition suggests, is to stop damage to cellular components arising as a consequence of chemical reactions involving free radicals. In recent years, a considerable body of evidence has developed supporting a key role for free of charge radicals in many fundamental cellular reactions and suggesting that oxidative stress could be important within the pathophysiology of common diseases including atherosclerosis, chronic kidney failure , and DM . The aim of this review is to think about mechanisms of radical formation within the body, the results of radical induced tissue damage, and therefore the function of antioxidant defence systems in health and disease.A radical are often defined as any molecular species capable of independent existence that contains an unpaired electron in an atomic orbital.2 The presence of an unpaired electron leads to certain common properties that are shared by most radicals. Radicals are weakly interested in a magnetic flux and are said to be paramagnetic. Many radicals are highly reactive and may either donate an electron to or extract an electron from other molecules, therefore behaving as oxidants or reductants. As a results of this high reactivity, most radicals have a really short half life (10−6 seconds or less) in biological systems, although some species may survive for for much longer .2 the foremost important free radicals in many disease states are oxygen derivatives, particularly superoxide and therefore the hydroxyl . Radical formation within the body occurs by several mechanisms, involving both endogenous and environmental factors (fig 1).