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

Abstract

The toxicity of mercuric chloride (MC) in mice, measured in terms of the single dose lethal to 50 percent of the animals after 12 h, was enhanced by prior exposure to a vitamin E-deficient diet and by 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 subcutaneous injection of MC. In the kidney of rats 12 h after a 4 mg/kg dose of MC, 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 of MC were also seen compared to the control. After injection of MC (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 of MC, and at a dose of 2 mg/kg the excretion of LAP, but not that of ALP, was also elevated at 12 h after MC. These results indicate that lipid peroxidation may be partly responsible for the acute-toxic effect of MC, which involves renal damage.