It has recently been shown (1) that the release of superoxide (0 2-) produced by the one electron reduction of oxygen (2) is increased in human polymorphonuclear leukocytes during phagocytosis. Information on mononuclear phagocytes is lacking in this context. Since superoxide is potentially a microbicidal agent, and since the modes of killing employed by macrophages are still largely unknown, we have extended to those cells observations on superoxide release Our studies therefore compare OZ- production by mononuclear phagocytes from lung and peritoneum with polymorphonuclear leukocytes (PMN), in two species. Furthermore, the rate and extent of ingestion of particles, the metabolic responses of mononuclear phagocytes during ingestion, and the efficiency of bactericidal action have all been shown to be functions of the state of the cells. This is in turn a function of the prior treatment of the animal, e.g. administration of an eliciting agent, or infection with an organism such as Listeria monocytogenes to produce a macrophage "activated " by a lymphocyte-mediated phenomenon (3-7). To assess the possible role of superoxide in "activated"