Mechanisms of chloroform and carbon tetrachloride toxicity in primary cultured mouse hepatocytes.
作者： R J Ruch , J E Klaunig , N E Schultz , A B Askari , D A Lacher
DOI: 10.1289/EHP.8669301
关键词:
摘要: Mechanisms of chloroform (CHCl3) and carbon tetrachloride (CCl4) toxicity to primary cultured male B6C3F1 mouse hepatocytes were investigated. The cytotoxicity both CHCl3 CCl4 was dose- duration-dependent. Maximal hepatocyte toxicity, as determined by lactate dehydrogenase leakage into the culture medium, occurred with highest concentrations (5 mM) (2.5 used longest duration treatment (20 hr). approximately 16 times more toxic than hepatocytes. these compounds decreased adding mixed function oxidase system (MFOS) inhibitor, SKF-525A (25 microM) cultures. addition diethyl maleate (0.25 mM), which depletes intracellular glutathione (GSH)-potentiated toxicity. could also be antioxidants N,N'-diphenyl-p-phenylenediamine (DPPD) microM), alpha-tocopherol acetate (Vitamin E) (0.1 or superoxide dismutase (SOD) (100 U/mL) These results suggest that: in hepatocytes, are metabolized components MFOS; GSH plays a role detoxifying those metabolites; free radicals produced during metabolism CCl4; may important mediators two halomethanes.
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