We investigated whether a mutation in the ATPase subunit-8 gene exerts effects on the course of endotoxemic acute liver failure in mice. Wildtype and ATP8 mutant mice were challenged with D-galactosamine and E. coli lipopolysaccharide and studied 6 hrs thereafter. Induction of endotoxemic liver failure provoked marked liver damage, a drop of total adenosine nucleotide level and an increased malondialdehyde production. In contrast, ATP levels in livers ATP8 mutants remained significantly higher. As a net result, ATP8 mutant mice showed lower transaminase release and better survival rate.