Author(s): Armstrong D, Browne R
It is almost impossible to read through a medical journal, or even the newspaper and not encounter an article that deals with oxidative stress, or with antioxidant involvement in a disease process. Indeed, free radicals, their reactive intermediates, low molecular weight aldehyde byproducts derived from lipid peroxidation and antioxidant status are important measurements we can utilize to provide a more comprehensive understanding of pathologic mechanisms (1–8). All subcellular organelles normally generate superoxide (O2·-), hydrogen peroxide and a variety of free radicals ie; hydroyl (OH·), perhydroxy(HO2·), carbon and nitrogen centered. It has been estimated that 10 billion of these radicals are produced daily via autoxidation and metabolic reactions. In cellular injury, increased amounts of O2·- radicals and peroxides can arise from the mitochondrial electron-transport system during hypoxia and following reperfusion, they can arise primarily through the activation of NADPH oxidase in phagocyte plasma membranes or from platelet derived endoperoxides of arachidonic acid, from the conversion of xanthine dehydrogenase to xanthine oxidase in tissue and from the generation of OH· radicals in iron-catalyzed reactions involving hemoproteins (9). The most current review by Chaudiere covers theoretical and factual site-specific formation and damage (10).
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