Abstract
The possibility of hepatic toxicity of trichloroethylene (TCE) related to the increase of lipid peroxide in the liver was investigated. Trichloroacetic acid (TCA) and dichloroacetic acid (DCA) were dominant metabolites of TCE in the liver, so that TCA was metabolized in vitro by microsomes and lipid peroxidation was measured as an oxygen uptake by the oxygen electrode method. The increase of lipid peroxidation with the metabolism of TCA and the TCA-induced lipid peroxidation was inhibited by mannitol, uric acid and flavin derivatives, but scarcely inhibited by superoxide dismutase and catalase. Moreover, non-enzymic DCA radical production induced by 2, 2'-azobis (2-amidinopropane) dihydrochloride was inhibited by radical scavengers and flavin derivatives. These results suggest that the active oxygen scarcely contributes to the lipid peroxidation with the metabolism of TCA and that the inhibitory effect of flavin derivatives depends on the affinity for DCA radical and lipid peroxide radical.
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