ABSTRACT
The toxic effects of exogenous free radical compounds on biological tissues have been known for decades, but the extent to which endogenously generated oxygenderived free radicals play an important role in mediating tissue damage in many common pathophysiological conditions has only recently been appreciated. It is now recognized, for example, that reestablishment of normal levels of blood flow to ischemic organs can often increase the amount of tissue dysfunction present (Southern, 1988). This "reperfusion" injury is produced largely by hydroxyl radicals formed during the period of reperfusion. Studies have shown that this mechanism may account for tissue injury following ischemia-reperfusion in several vital organs, including the heart, kidney, brain, and intestines (Gaudeul and Duvelleroy, 1984; Baker et al., 1985; Domanska-Janik and Wideman, 1974; Granger et al., 1980). ln addition, oxygen-derived free radicals are thought to play a role in mediating tissue injury produced in response to neutrophils, fatty acids, arachidonic acid, hyperoxia, and in response to ionizing radiation (Smith et al., 1989b; Badwey et al. , 1984; Kontos and Hess, 1983; White et al ., 1989; Yau and Mencl, 1981).
