The production of superoxide free radical, O2-, by metabolically activated phagocytes results in damage to the phagocyte which is manifested by the premature death of the cell in vitro. The cytotoxic agent appears to be formed by the reaction of superoxide with hydrogen peroxide, and is thought to be hydroxyl radical or a secondary radical thereof. In vivo two animal models of induced inflammation also appear to be largely dependent on superoxide production by phagocytes for the development of tissue damage manifested as oedema. Intravenously administered superoxide dismutase shows anti-inflammatory activity in these models, but only when so derivatized that it can remain in the circulation for longer periods of time. Catalase, or a catalase derivative, on the other hand, shows no anti-inflammatory activity in vivo.
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