Abstract

Sequential reduction of oxygen along the univalent pathway leads to the generation of superoxide anion, hydrogen peroxide, hydroxyl radical, and water [1, 2]. These partially reduced oxygen intermediates have been implicated as important mediators in various models of ischemic, toxic and immune-mediated tissue injury including glomerular injury [3]. Reactive oxygen metabolites have been shown to affect several biological processes potentially important in glomerular diseases, and their role in both inflammatory as well as non-inflammatory glomerular diseases has recently been demonstrated [3]. Evidence for the importance of reactive oxygen metabolites in experimental models of glomerular disease is based largely on the protective effects of scavengers of reactive oxygen metabolites.

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