Investigation of the hepatotoxicity of a mixture of two halogen compounds--carbon tetrachloride (CT) and 1,2-dibromoethane (DBE) used in association, especially in agriculture--is reported. Their simultaneous administration in the rat potentiates the necrosis provoked by exposure to CT alone. This damage can be totally prevented by prior treatment with vitamin E, which raises the liver antioxidant level. Determination of the TBA-reacting substances released from the liver homogenates of animals treated with one or both substances also corroborates the importance of lipid peroxidation in the pathogenesis of this potentiation. Furthermore, no significant difference between poisoning by CT and CT + DBE is noted when liver GSH values are measured under the same experimental conditions. This finding rules out the possibility that potentiation is only the simply sum of the damage caused by the two compounds (lipid peroxidation due to a radical initiator for CT, depletion of GSH for DBE). It is thus something more than a mere combination of two mechanisms of action and further investigation is required to unravel its more complex pathogenesis.