To clarify the antioxidative role of uric acid, its ability to scavenge carbon-centered and peroxyl radicals and its inhibitory effect on lipid peroxidation induced by various model systems were examined. Uric acid efficiently scavenged carbon-centered and peroxyl radicals derived from the hydrophilic free radical generator 2,2ø-azobis-(2-amidinopropane)-dihydrochloride (AAPH). All damage to biological molecules, including protein, DNA and lipids induced by AAPH, was strongly prevented by uric acid. In contrast, a-tocopherol had little effect on damage to biological molecules. Lipid peroxidation by the lipophilic free radical generator 2,2ø-azobis(2,4-dimethylvaleronitrile) (AMVN) was little inhibited by uric acid, but not by a-tocopherol. Copper-induced lipid peroxidation was inhibited by uric acid and a-tocopherol. NADPH-and ADP-Fe 3π -dependent microsomal lipid peroxidation was efficiently inhibited by a-tocopherol, but not by uric acid. Uric acid seems to scavenge free radicals in hydrophilic conditions to inhibit lipid peroxidation on the lipidaqueous boundary, and the antioxidation is only little in lipophilic conditions.
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