LIPID-PEROXIDATION IN RATS ADMINISTRATED WITH MERCURIC-CHLORIDE

Parenteral administration of mercuric chloride (HgCl2) to rats enhance d lipid peroxidation in liver, kidney, lung, testis, and serum (but no t in heart, spleen, or muscle), as measured by the thiobarbituric acid reaction for malondialdehyde (MDA) in fresh tissue homogenates and bo dy fluids. After sc injection of HgCl2 (5 mg/kg body wt), MDA concentr ations in liver and kidney became significantly increased by 9 h and r eached peak values at 24 h. Dose-response studies were carried out wit h male albino rats of the Fisher-344 strain (body wt 170-280 g) inject ed with 1, 3, 5 mg Hg/kg as HgCl2 and sacrificed after 24 h. in time-r esponse studies, animals were administered 5 mg Hg/kg as HgCl2 and sac rificed after 3, 9, 18, 24, and 48 h. Studies in the authors' laborato ry have shown that (1) concentrations of MDA are increased in targets (liver, kidney, lung, and testis) of HgCl2-treated rats; (2) severity of hepatotoxicity and nephrotoxicity is generally consistent with the elevation of Hg and MDA concentrations, based upon the time-course and dose-effect relationships observed after administration of HgCl2 to r ats; and (3) concentrations of MDA are reduced in target tissues after pretreatment with antioxidants and chelators to HgCl2-treated rats. T he results of this study implicate that the lipid peroxidation is one of the molecular mechanisms for cell injury in acute HgCl2 poisoning.