Suppression by superoxide dismutase of immune-complex--induced pulmonary alveolitis and dermal inflammation.

The possible role of oxygen metabolic products in immune-complex--induced injury of rat lung and of dermal blood vessels has been probed with the use of two inhibitors, superoxide dismutase (SOD) and catalase. With the use of the reversed passive Arthus reaction in the skin, local administration of SOD, but not of catalase, blocked the early phase of the tissue injury, as quantitated by the leakage of homologous albumin. The early phases of immune-complex--induced injury of the lung were completely blocked by the parenteral (intraperitoneal) administration of SOD. Except at very high doses, SOD did not interfere with chemotactic-factor--induced release of lysosomal enzymes from rat neutrophils. These data suggest that oxygen metabolic products such as O(2-) may play an important role in the early phases of damage produced in rat alveolar walls and dermal vasculature by the deposition of immune complexes.