second hit contributes to the progressive development of non-alcoholic steatohepatitis (NASH), liver fibrosis, cirrhosis, and even hepatocellular carcinoma from SS (Bugianesi et al., 2002). Excessive fatty acids (FA) deposition and its peroxidation in hepatocytes are considered to be the major factors causing cytotoxicity and exacerbated hepatopathology. According to the reported data of our lab and others, 18-carbon FA is the most abundant in hepatic FA composition and accumulated badly in the HFD-induced liver, especially in Nrf2 deleted animals (Zhukova et al., 2014; Wang X. et al., 2016). CYP2A5 and Nrf2 expression were both induced by 18-carbon FA treatment in mouse primary hepatocytes (Cui et al., 2016). Nevertheless, the role of 18-carbon FA in inducing CYP2A6 in human hepatoma cell line has never been reported.
