Effects of Leukocyte-Derived Oxidants on Sarcolemmal NA,K,ATP-ASE and Calcium Transport

Abstract

The mitochondrial electron transport chain is capable of reducing oxygen directly to water. However, 5 % of the oxygen consumption of tissues proceed by a univalent pathway in which superoxide anion, hydrogen peroxide and hydroxyl radicals are produced (for review, Thompson & Hess, 1986). Although hydroxyl radicals are very reactive, and therefore harmful, the cell is equipped with enzymes to metabolize superoxide anion and hydrogen peroxide to water, thereby bypassing the formation of hydroxyl radicals. These are superoxide dismutase, catalase and glutathione peroxidase, serving as part of physiological defense mechanisms (Thompson & Hess, 1986). Therefore, these intermediates of oxygen reduction play a pathogenic role only when their production is increased and/or when the cellular defense is reduced. Evidence has accumulated implicating oxy radical generation as an important factor in tissue injury caused by ischemia-reperfusion (Bolli, 1988; Burton, 1988; Kako et al., 1988, for reviews). Although the exact source of free radicals has not been settled, recent studies with spin resonance spectroscopy suggested it to be the endothelial cell (Zweier et al., 1988).

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