The predominant oxidative microbicidal mechanism of peroxidase- containing phagocytic cells appears to involve respiration-initiated formation of HOCl; cellular death is associated with inactivation of essential transport proteins located in microbial plasma membrane, including (in bacteria) the F0F1-ATP synthase. The oxidants produced by phagocytic cells lacking functional peroxidases are more obscure, but evidence is accumulating to suggest that ONOOH and ·CO3-, formed by reaction of CO2 with ONOO-, may be important toxins. If so, phagosomal compartmentation constitutes an integral component of the microbicidal mechanisms, since ·CO3- should be effectively scavenged by antioxidants and ONOOH by CO2 in extracellular environments, but not within the phagosome. There is at present no compelling evidence for metal-mediated H2O2 microbicidal mechanisms in which the metal catalysts are derived from the host fluids, although intraphagosomal concentrations of this oxidant might reach sufficient levels in peroxide-free phagocytes to overwhelm endogenous protective systems.