Inhibition by uric acid of free radicals that damage biological molecules.

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 2,2'-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, alpha-tocopherol had little effect on damage to biological molecules. Lipid peroxidation by the lipophilic free radical generator 2,2'-azobis(2,4-dimethylvaleronitrile) (AMVN) was little inhibited by uric acid, but not by alpha-tocopherol. Copper-induced lipid peroxidation was inhibited by uric acid and alpha-tocopherol. NADPH- and ADP-Fe(3+)-dependent microsomal lipid peroxidation was efficiently inhibited by alpha-tocopherol, but not by uric acid. Uric acid seems to scavenge free radicals in hydrophilic conditions to inhibit lipid peroxidation on the lipid-aqueous boundary, and the antioxidation is only little in lipophilic conditions.