作者: James E. Klaunig , Randall J. Ruch , Edith L.C. Lin
DOI: 10.1016/0041-008X(89)90153-1
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摘要: Chronic exposure to trichloroethylene (TCE) results in hepatocellular cancer mice but not rats. The induction of hepatic tumors by TCE appears be mediated through nongenotoxic or tumor promotion mechanisms. One cellular effect exhibited a number carcinogens and promoters is the inhibition gap junction intercellular communication. In present study, effects its metabolites, trichloracetic acid (TCA), trichloroethanol (TCEth), chloral hydrate (CH) on communication cultured B6C3F1 mouse F344 rat hepatocytes were assessed. TCA inhibited hepatocytes. TCEth CH had no hepatocyte either cells. both 24-hr-old freshly plated Both compounds produced greater cells when compared cultures. appeared require cytochrome P450 metabolism exhibit inhibitory dye coupling since treatment with SKF-525A prevented TCE. was unaffected SKF-525A. While species dependent may correlated different rates extent hepatocytes, inhibiting only suggests that other intrinsic factors male make this more susceptible These findings account, part, for observed difference susceptibility induced liver carcinogenesis.