Open AccessDifferent Effects of Carbon Tetrachloride on Carcinogen–induced Hepatocellular Carcinoma and Normal Liver of the Rat: Lowered Lipid Feroxidation and Accelerated Necrosis in Cancer
Author(s) -
Lertprasertsuke Nirush,
Shinoda Masayuki,
Takekoshi Susumu,
Tsutsumi Yutaka,
Yamamoto Yorihiro,
Niki Etsuo,
Watanabe Keiichi
Publication year - 1991
Publication title -
japanese journal of cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 0910-5050
DOI - 10.1111/j.1349-7006.1991.tb01879.x
Subject(s) - polyunsaturated fatty acid , carbon tetrachloride , lipid peroxidation , chemistry , hepatocellular carcinoma , endocrinology , fatty acid , medicine , necrosis , vitamin e , biochemistry , antioxidant , biology , organic chemistry
To investigate molecular responses to lipid peroxidative stimuli in neoplastic cells, lipid peroxidation was induced in liver of rats bearing 3′‐methyl‐4‐dimethylaminoazobenzene‐induced hepatocellular carcinoma by injecting a high dose of carbon tetrachloride (CCL 4 ), a strong lipoperoxidative reagent. Normal rat livers with or without CCl 4 treatment served as controls. CCL 4 , administration markedly provoked fatty metamorphosis, visualized by oil red O staining, in normal livers while minimal fatty changes were seen in hepatocellular carcinomas, where necrosis was often observed instead. After CCl 4 treatment, the thiobarbituric acid values (representing levels of lipid peroxides in the tissue) were increased two–fold in the untreated normal liver, but were unchanged in the cancer tissue. Levels of vitamin C, an acutely reactive antioxidant, measured by high‐performance liquid chromatography were not influenced by the CCL 4 injection in the cancer tissue whereas a significant decrease was evident in normal livers. The total fatty acid content, measured by gas chromatography, was significantly lower in the cancer tissue than in the normal liver while the ratio of polyunsaturated fatty acids (PUFAs) in total fatty acids was little changed. Resistance of hepatocellular cancer cells to fatty metamorphosis and their susceptibility to necrosis induced by free radicals may be due to the paucity of the target PUFAs in their cell membrane fraction, resulting in low levels of lipid peroxides. Peroxidation of PUFAs might act as a “shock absorber” against free radical‐induced toxic cell death in normal cells.