| First Author | Chen X | Year | 2018 |
| Journal | Arch Biochem Biophys | Volume | 657 |
| Pages | 65-73 | PubMed ID | 30222954 |
| Mgi Jnum | J:266984 | Mgi Id | MGI:6237475 |
| Doi | 10.1016/j.abb.2018.09.012 | Citation | Chen X, et al. (2018) Nicotine enhances alcoholic fatty liver in mice: Role of CYP2A5. Arch Biochem Biophys 657:65-73 |
| abstractText | Tobacco and alcohol are often co-abused. Nicotine can enhance alcoholic fatty liver, and CYP2A6 (CYP2A5 in mice), a major metabolism enzyme for nicotine, can be induced by alcohol. CYP2A5 knockout (cyp2a5(-/-)) mice and their littermates (cyp2a5(+/+)) were used to test whether CYP2A5 has an effect on nicotine-enhanced alcoholic fatty liver. The results showed that alcoholic fatty liver was enhanced by nicotine in cyp2a5(+/+) mice but not in the cyp2a5(-/-) mice. Combination of ethanol and nicotine increased serum triglyceride in cyp2a5(+/+) mice but not in the cyp2a5(-/-) mice. Cotinine, a major metabolite of nicotine, also enhanced alcoholic fatty liver, which was also observed in cyp2a5(+/+) mice but not in the cyp2a5(-/-) mice. Nitrotyrosine and malondialdehyde (MDA), markers of oxidative/nitrosative stress, were induced by alcohol and were further increased by nicotine and cotinine in cyp2a5(+/+) mice but not in the cyp2a5(-/-) mice. Reactive oxygen species (ROS) production during microsomal metabolism of nicotine and cotinine was increased in microsomes from cyp2a5(+/+) mice but not in microsomes from cyp2a5(-/-) mice. These results suggest that nicotine enhances alcoholic fatty liver in a CYP2A5-dependent manner, which is related to ROS produced during the process of CYP2A5-dependent nicotine metabolism. |
