Calvert et al. formulated the hypothesis that carbon tetrachloride (CCl₄) acted on the central nervous system to produce and intensify sympathetic discharge which resulted in anoxic necrosis of the liver. Recknagel suggested that the essential feature of CCl₄ hepatotoxicity depended on the cleavage of it to CCl₃(free radical) and the peroxidative decomposition of cytoplasmic membrane structural lipids. And there are many reports which show the increase of adrenergic activity in hyperthyroidism. In this paper, the influence of thyroxine on the hepatotexicity of carbon tetrachloride was investigated in mice. The results obtained were summarized as follows; 1) Hepatic total lipid and lipid peroxide contents were slightly decreased by L-sodium thyroxine injection(4mg/kg/day for 4days or 6days), but hepatic glycogen content was significantly decreased. 2) Hepatic total lipid and lipid peroxide contents and serum lactic dehydrogenase activity were significantly increased by CCl₄ (4 ml/kg single dose or triple dose: 4ml/kg/day for 3days), but hepatic glycogen content was significantly decreased. 3) The increase of hepatic total lipid and lipid peroxide contents and serum lactic dehydrogenase activity induced by CCl₄ were significantly inhitited by the pretreatment of thyroxine. 4) The decrease of hepatic glycogen induced by CCl₄ was not affected by the pretreatment of thyroxine.