Oxyradical Mediated Tissue Injury

Since the beginning of this century, phagocytes have been recognized for their critical role in the inflammatory response. In addition to their functions in host defense, phagocytes (neutrophils, monocytes, and maerophages) can mediate tissue injury through a variety of mechanisms (3). Traditionally, attention has been focused on the potential for leukocytic lysosomal proteases to damage tissue. In recent years, it has been recognized that lysosomal enzymes cannot completely account for the tissue-damaging effects of phagocytes. Recent studies have provided compelling evidence that oxygen-derived free radicals are important mediators of tissue injury. Free radicals are atoms or molecules that possess unpaired electrons. Through a variety of reactions, oxygen free radicals can participate in the generation of additional reactive oxygen-derived metabolites. The focus of this article will be how phagocytes, particularly polymorphonuclear leukocytes (PMN), generate these substances. We will examine the in vitro and in vivo evidence that oxygen radicals and their metabolites are important mediators of tissue injury.