The mechanism of carbon tetrachloride (CCl 4 )-induced hepatotoxicity, especially necrosis and fatty liver, has long been a challenging subject of many researchers from variousˆelds over the past 50 years. Even though the mechanisms of tissue damages are diŠerent among chemicals and aŠected tissues, CCl 4 has played a role as a key substance of tissue injury. A number of studies have been conducted and various hypotheses have been raised. As a result, several important basic mechanisms of tissue damages have emerged, involving metabolic activation, reactive free radical metabolites, lipid peroxidation, covalent binding and disturbance of calcium homeostasis. Recent studies also revealed in‰am-mation and regeneration as important modiˆcation factors in the tissue injury. The author attempted to summarize the history of CCl 4 research with some emphasis on the experiments done by the author and his colleagues. Their studies with isolated perfused rat liver suggest that covalent binding of CCl 4 metabolites rather than lipid peroxidation has a signiˆcant role in the production of centrilobular necrosis following CCl 4 administration. Further studies are necessary to unveil detailed mechanisms of hepatocyte necrosis induced by CCl 4 .

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