The influence of aluminium (Al) chloride on toxic responses to cadmium (Cd) chloride of hepatocytes isolated from fed rats were investigated. Hepatocytes exposed to 50-200 microM Al took up the Al-ion more efficiently when the cells were simultaneously incubated with 50 microM Cd for 60 min. Aluminium (50-200 microM) could not prevent the release of about 50% of lactate dehydrogenase (LDH) from cells due to 50 microM Cd. Aluminium itself increased LDH leakage only to a moderate extent, indicating the low toxicity of Al to hepatocytes. Cadmium diminished the total hepatocellular thiols (protein + non-protein) and, even more pronounced, the acid soluble thiols after 60 min of incubation. However, this response to Cd was inhibited by simultaneous exposure to 50-200 microM Al in an Al concentration-dependent manner. Concomitantly, the Cd-dependent lipid peroxidation (LPO; measured as thiobarbituric acid reactants) at 60 min was decreased by Al, which itself did not enhance basal LPO in hepatocytes. These data show that Al partly protects hepatocytes from Cd-induced depletion of acid soluble thiols (i.e. reduced glutathione) and from stimulation of LPO. However, Al did not prevent the Cd-induced damage of the cell membrane.