Superoxide and inflammation: a mechanism for the anti-inflammatory activity of superoxide dismutase

Several models of inflammation induced in laboratory animals were markedly inhibited by intravenous administration of the enzyme superoxide dismutase. In most cases, the enzyme required chemical modification to increase its circulating lifetime. In all cases, histological examination of the sites of the potential lesions revealed that treatment with superoxide dismutase prevented the accumulation of inflammatory cells. Experiments in vitro demonstrated the existence of a plasma factor which reacts with superoxide to become a potent chemotactic factor for neutrophils. The factor apparently serves to call increasing numbers of neutrophils to the inflammatory locus in response to the superoxide produced by the first cells to encounter the stimulus.