Previous studies in rodents have suggested a possible association between inflammation and liver injury for several drugs associated with human IADRs, including chlorpromazine (Buchweitz et al., 2002) , ranitidine , diclofenac (Deng et al., 2006) , trovafloxacin (Shaw et al., 2007) , sulindac (Zou et al., 2009b) , and halothane (Dugan et al., 2010) . The results of the present study expand these findings and demonstrate that a nonhepatotoxic dose of AMD is rendered hepatotoxic when acute inflammation is triggered by LPS administration. Acute increases in serum markers for hepatocellular and cholestatic injury were found in rats cotreated with AMD/LPS. These resemble the clinical hepatic chemistry changes in human idiosyncrasy during AMD therapy (Rätz Bravo et al., 2005) . The midzonal and bridging necrosis and infiltration of inflammatory cells in AMD/LPS are also consistent with some of the histological changes found in human patients (Babatin et al., 2008; Rätz Bravo et al., 2005) . However, the histological characteristics in people with AMD-induced liver injury were variable. Different patterns of hepatocellular necrosis, such as midzonal, centrilobular, bridging, and panlobular, have been reported (Lewis et al., 1989) . Genetic differences, concurrent medications, and even different origins of inflammation might account for these varied responses; nevertheless, the AMD/LPS interaction model in rats mimics important aspects of AMD-induced IADRs in human patients.