ABSTRACT
For a number of years following the recognition that cellular metabolism can generate free radicals and other oxygen-derived oxidants, elevated oxidative status was viewed only as a potential cause of cellular damage. The antioxidant enzymes known as the superoxide dismutases (SOD), together with catalase and glutathione peroxidase, were viewed as essential, protective "housekeeping" enzymes, designed to effectively scavenge and eliminate their toxic substrates. One notable exception to this general concept was the realization that phagocytes produce superoxide radical not as a toxic by-product but rather as weapon in their war against invading microbes (1). Thus, in this limited context, superoxide production could be viewed as desirable or positive, even though its cellular action was still that of cytotoxicity directed against both the ingested microbe and the ingesting phagocyte. Extracellular superoxide dismutase, for example, was found capable of preventing the phagocytosis-induced death of the neutrophil (2).
