Aluminium (Al) chloride (10-200 microM) increased the Al content in hepatocytes isolated from fed male rats in a time- and concentration-dependent manner. After 60 min of incubation with 100 microM Al about 45% of cellular Al was found each in the mitochondrial and the postmitochondrial fraction of hepatocytes, whereas about 5% of Al sedimented with nuclei and cell debris. Concomitantly, the leakage of lactate dehydrogenase (LDH), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) increased in the presence of Al time- and concentration-dependently, but only to a moderate extent. Aluminium (10-200 microM) also accelerated the formation of lactate by hepatocytes. No significant differences were found in Al uptake and distribution and its effect on LDH leakage and lactate formation when the metal ion was given as AlCl3, Al(NO3)3 or Al(lactate)3. Al concentrations (AlCl3) exceeding 250 microM severely disturbed the determination of LDH, AST and lactate in a cell free system. The data suggest only a moderate toxicity of Al compounds to isolated hepatocytes, when given in amounts approximating (patho)physiological conditions.