Previous work has shown that dietary exposure of rats to non-toxic levels of chlordecone (10 parts per million) for 15 days and a subsequent intraperitoneal injection of a low, non-toxic dose of CCl4 results in a dramatic potentiation of hepatotoxicity and lethality greater than that observed after a high dose (2.5 ml/kg body weight) of CCl4 alone. This remarkable amplification of CCl4 toxicity is due to the failure of the hepatocellular regenerative and hepatolobular repair mechanisms. Polyamines are known to be important for liver regeneration and the progressive phase of hepatotoxicity and lethality observed after the combination treatment might be related to the extent of suppressed polyamine metabolism in the liver. In the study polyamines and related enzymes were estimated in the livers of rats treated with either chlordecone and CCl4 or CCl4 alone.