Abstract

Parenteral administration of methyl mercuric chloride (MMC, CH3HgCl) to rats enhanced lipid peroxidation in liver of rats, as measured by the thiobarbituric acid reaction for malondialdehyde (MDA) in fresh tissue homogenates. After sc injection of CH3HgCl (5 mg/kg body wt), MDA concentration in liver became significantly increased at 24 h and further increased at 48 h. Dose-response studies were carried out with male albino rats of the Fisher-344 strain (body wt 170-280 g) injected with 3 or 5 mg Hg/kg as CH3HgCl and sacrificed after 24 h. In time-response studies, animals were administered 5 mg Hg/kg as CH3HgCl and sacrificed after 24 and 48 h. Studies in the authors' laboratory have shown that (1) mercury is accumulated in liver; (2) concentration of MDA is increased in liver of CH3HgCl-treated rats; (3) severity of hepatotoxicity is generally proportional to the elevation of MDA concentration, based upon the dose-effect relationships observed after administration of CH3HgCl to rats. The results of this study implicate that the lipid peroxidation is one of the molecular mechanisms for cell injury in acute CH3HgCl poisoning.

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