Radical scavenging action of tinoridine, a non-steroidal anti-inflammatory drug with a potent anti-peroxidative activity, was investigated. Tinoridine reduced a stable free radical, diphenyl-p-picryl-hydrazyl, in the molar ratio of about 1:2, indicating its free radical scavenging ability. Tinoridine inhibited the lipid peroxidation in rat liver microsomes induced by xanthine-xanthine oxidase system in the presence of ADP and Fe2+, in which hydroxyl radical (. OH) is formed. Tinoridine was demonstrated to be oxidized in the course of the lipid peroxidation by following the fluorescence derived from the oxidation product of tinoridine. It was also oxidized by the xanthine-xanthine oxidase system in the presence of Fe2+, but its oxidation was slow in the absence of Fe2+ and almost completely inhibited by catalase. Tinoridine was also oxidized by H2O2-Fe2+ system producing . OH (Fenton reaction), but it did not affect the reduction of cytochrome c caused by superoxide radical. These results indicate that tinoridine is able to scavenge . OH and the main active oxygen species responsible for the lipid peroxidation is . OH. The anti-peroxidative and . OH scavenging ability of tinoridine should contribute to its anti-inflammatory action.
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