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The superoxide radical (O 2 ·̅), hydrogen peroxide (H 2 O 2 ) and nitric oxide (NO) are pleiotropic infl ammatory mediators which play an important role in infl ammatory joint diseases. They are overproduced during rheumatoid arthritis and its experimental model - adjuvantinduced arthritis in rodents - and may be detected both systemically and intra-articularly. Their secretion is up-regulated by proinfl ammatory cytokines such as IFN-γ, IL-12, IL-6 and TNF-α, and they are responsible for the destruction of joint tissue. In this work, the effect of superoxide dismutase (SOD) from a thermotolerant yeast strain, Kluyveromyces marxianus, on the production of proinfl ammatory cytokines, reactive oxygen and nitrogen species was studied. Mice received three intraperitoneal injections of yeast SOD at a dose of 10 mg/ kg body weight (30,000 U/kg) on consecutive days starting on the day after arthritic induction. On days 3, 8 and 14 post induction peritoneal macrophages were isolated and both spontaneous and stimulated production of reactive oxygen and nitrogen metabolites were measured. Early in arthritic development yeast SOD treatment did not infl uence the O2·̅ production, but on day 14 both spontaneous and PMA-induced secretion were dramatically reduced. Spontaneous H 2 O 2  release was inhibited on day 14, while PMA-stimulated production was decreased from the beginning of the arthritic development. Yeast SOD treatment effectively suppressed the spontaneous and recombinant mouse IFN-γ + LPS induced release of NO as well. Serum levels of proinfl ammatory cytokines, IL-12, IFN-γ, IL-6 and TNF-α, were also signifi cantly reduced. The obtained results show some of the mechanisms of action of SOD in reducing the severity of arthritic infl ammation. Besides direct inhibition of joint tissue destruction exogenous SOD substantially limits the existing positive feedback between secretion of reactive oxygen species and infl ammatory cytokine production.

Effect of Yeast Superoxide Dismutase Treatment on Some Mediators of Infl ammation during Adjuvant-Induced Arthritis in Mice