Lipid peroxidation stimulated by mercuric chloride and its relation to the toxicity.

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Abstract
The toxicity of HgCl2 in mice, measured in terms of the single dose 12-h LD50, was enhanced by prior exposure to a vitamin E-deficient diet and pretreatment with diethyl maleate and was diminished by pretreatment with N,N''-diphenyl-p-phenylenediamine. Lipid peroxidation as determined by measurement of the pentane content in expired gases of rats showed a dose-dependent increase 12 h after the s.c. injection of HgCl2. In the kidney of rats 12 h after a 4 mg/kg dose, formation of thiobarbituric acid (TBA)-reactive substances was greatly increased. Slight increases of pentane in expired gases and of TBA-reactive substances in the kidney of rats at earlier times after a 2-mg/kg dose were also seen compared to the control. After injection of HgCl2 (2 or 4 mg/kg), glutathione was decreased in the kidney at 12 h. The urinary excretions of alkaline phosphatase (ALP) and leucine aminopeptidase (LAP) were markedly increased 6 h after a 4-mg/kg dose, and at 2 mg/kg the excretion of LAP but not that of ALP, was elevated at 12 h. Lipid peroxidation was partly responsible for the acute toxic effect of HgCl2, which involved renal damage.