Before examining liver injury induced by chronic alcohol feeding, serum levels of alcohol were detected. After 4 weeks of ethanol feeding, serum levels of alcohol in cyp2a5−/− mice were similar to those in cyp2a5+/+ mice (Fig 1A). Consistently, expression of ADH and CYP2E1, two major alcohol metabolizing enzymes, was comparable in cyp2a5−/− and cyp2a5+/+ mice after ethanol feeding (Fig 1B and C). As expected, expression of CYP2A5 was induced in cyp2a5+/+ mice but not in cyp2a5−/− mice (Fig 1B); however, CYP2A5 has a minor role in ethanol metabolism compared with CYP2E1 (12). These results indicate that serum alcohol levels and hepatic expression of CYP2E1 are comparable in the cyp2a5−/− and cyp2a5+/+ mice. Thus, CYP2E1, a risk factor for alcoholic liver disease, won’t be a confounding factor in this model.
