coumarin-7-hydroxylase and responsible for the metabolism of nicotine, drugs and procarcinogens such as aflatoxin B1 (AFB1) and nitrosamines (Camus-Randon et al., 1993; Kirby et al., 1994a,b; Felicia et al., 2000). The hepatotoxic compounds that up-regulate CYP2A5/2A6 are structurally unrelated and are not considered to be CYP inducers. The mechanism of CYP2A5/2A6 increased in different pathogenesis induced liver damage is still unclear. It has been proposed that the common mechanism in the CYP2A5-inducing conditions is a direct or indirect systemic effect elicited by toxicity or tissue damage, rather than the chemical itself (Camus-Randon et al., 1996; Salonpää et al., 1997). Lipid accumulation (hepatocytes steatosis) is generally the early stage of liver damages induced by various structurally unrelated chemicals. Studies focus on the expression of hepatic CYP2A5/2A6 in hepatocytes steatosis is limited at the moment.
