0 F THE SYSTEMS that defend the host against invading microorganisms, the professional pha-gocytes(neutrophils, eosinophils, and mononuclear phagocytes) act in the most primitive fashion. Unlike cytotoxic lymphocytes and the complement system, which destroy their targets with a drop of poison,” 2 the professional phagocytes kill like Attila the Hun, deploying a battery of weapons that lay waste to both the targets and the nearby landscape with the subtlety of an artillery barrage. Among the most powerful of these weapons is a group of oxidizing agents that are produced by the phagocytes when they encounter invading microorganisms or other appropriate stimuli. These oxidants are reactive enough to destroy most biologic molecules and are responsible for much of the damage inflicted by phagocytes on both microorga-nisms and surrounding tissues at sites of infection or inflammation. In this article, I briefly review the nature of these oxidants, their mode of production, and their biologic effects, both good and bad.

THE REACTIVE OXIDANTS Reactive oxidants are produced from oxygen through a special metabolic pathway that, as far as is known, is unique to phagocytes. The consumption of oxygen through this pathway is initiated by the exposure of the cells to any one of a large number of stimuli, among the most effective of which are several that are likely to be present at sites of inflammation: opsonized microorganisms, 3 the complement fragment C5a, 4’5 leukotriene B4 (produced by stimulated phagocytes), 6’7 and N-formylated oligopeptides of bacterial origin4’8 that are actively secreted or are released by lysis of dead organisms. Activation of the pathway occurs within a few seconds after stimulation9’1#{176} and is characterized by an abrupt increase in oxygen uptake together with the onset of production of a series of compounds formed from this oxygen: superoxide(Ok), hydrogen peroxide (H2O2), and a number of additional oxygen-containing compounds, all of which are highly reactive. In addition, there is a large increase in the oxidation of glucose via the hexosemonophosphate