[Superoxide-dismutase and superoxide-radical-release in rheumatoid arthritis (author's transl)]

Abstract

Polymorphonuclear leukocytes (PMNs) release superoxide anion (O-2) when they are exposed to a phagocytic stimulus. Intracellularly the copper-containing enzyme superoxide dismutase (SOD) protects against the toxic effects of O-2. To investigate the role of O-2 and SOD in the inflammatory process we determined the O-2 release and SOD content in PMNs. In PMNs of children with rheumatoid arthritis the SOD activity was diminished compared to healthy controls. Upon stimulation with opsonized zymosan PMNs obtained from children with rheumatoid arthritis generated greater amounts of superoxide anion than control cells. The "SOD deficiency" in PMNs of children with rheumatoid arthritis may promote this extreme release of the toxic superoxide radical inducing the damage of the connective tissue. The involvement of superoxide dismutase and superoxide anion in inflammatory process may induce further studies, leading hopefully to an appropriate understanding or even to new principles in the treatment of the rheumatoid arthritis.