The acute phase response to chemically-induced organ damage involves inflammation and the production of LTs.The liver ordinarily takes up metabolites and excretes into bile cysteinyl LTs, but the effect of hepatic injury on theses processes is unknown. The hepatic uptake and biliary excretion of LTC4 was studied in male rats after exposure to eiter STZ, estadiol, or LPS/galactosamine respectively. Biliry excetion of 3H-LTC4 was similar to normal control rats in three models of acute liver injury.