In rats, AMD is deethylated by cytochromes P450 (CYPs) 3A4, 1A1, 2D1, and 2C11 in the liver (Elsherbiny et al., 2008) . DEA, the major metabolite, is three-to fivefold more toxic than AMD to cultured HepG2 cells (Waldhauser et al., 2006) and to primary rat hepatocytes (Gross et al., 1989) . In our treatment of Hepa1c1c7 cells, a similar trend was observed (Fig. 8) . The administration of LPS affects the expression and activities of CYPs in rats (Sewer et al., 1997) . This raised the possibility that LPS might potentiate the toxicity of AMD by increasing its metabolism to DEA. To evaluate this, serum and liver concentrations of AMD and DEA were measured with LC/ MS/MS. The average serum concentration of DEA in AMDtreated rats was 128 ng/ml, which is about 1/10 of the serum AMD concentration. This ratio is commonly seen in the serum after an intravenous loading dose of AMD, both in people (Ha et al., 2005) and rats (Shayeganpour et al., 2008) . Neither the serum nor the liver concentration of AMD or DEA was affected by LPS cotreatment, suggesting that neither AMD accumulation nor DEA generation was affected by LPS.