Abstract

Metabolites of oxygen-free radicals generated by polymorphonuclear leukocytes and macrophages are believed to inflict the initial tissue damage in acute inflammations. Of the various oxygen products, hydroxyl radicals are known to be potent toxic agents, and their generation depends largely on the presence of free iron. Treatment of experimental uveitis in Lewis rats with an iron chelator, deferoxamine mesylate, resulted in marked reduction in choroidal inflammation and suppression of retinal damage. These findings suggest that in experimental uveitis the severity of ocular inflammation and tissue damage may be mediated by the iron-catalyzed generation of hydroxyl radicals, and deferoxamine may thus serve as an anti-inflammatory agent.

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