Dr. Lu Publishes on Nicotine and Alcohol Interaction in the Liver

Dr. Yongke Lu, Assistant Professor in the Department of Health Sciences of the East Tennessee State University College of Public Health, has published an article entitled “Nicotine enhances alcoholic fatty liver in mice: Role of CYP2A5” in the Archives of Biochemistry and Biophysics.  The article, written by Dr. Lu and members of his research laboratory, examines cytochrome P450 enzymes in the interaction between nicotine and alcohol in the liver and their association with fatty liver.     

Alcohol drinking and tobacco smoking are two major public health issues and alcohol and tobacco are often co-abused. Previously, Dr. Lu’s lab found that hepatic cytochrome P450 2A6 (CYP2A6) was elevated in alcoholic patients, and CYP2A5, mouse ortholog of human CYP2A6, was induced by alcohol feeding in mice. Interestingly, CYP2A5 and CYP2A6 are major enzymes for nicotine metabolism. Thus, alcohol drinking may speed up blood nicotine clearance and individuals must smoke more cigarettes to maintain blood nicotine levels.  

In this study, Dr. Lu and colleagues found that nicotine enhanced alcoholic fatty liver in a CYP2A5-dependent manner. Cotinine, a major metabolite of nicotine, also enhances alcoholic fatty liver, for which CYP2A5 also plays an important metabolic role.  Further study showed that free radicals generated during the process of nicotine metabolism may contribute to the nicotine-enhanced alcoholic fatty liver.

E-cigarettes, nicotine gum, and nicotine patches are extensively used as safe tobacco surrogates. However, in combination with alcohol, these surrogates might pose more severe issue of public health.

Archives of Biochemistry and Biophysics, a peer-reviewed medical journal published by Elsevier, publishes original articles and reviews in the developing areas of biochemistry and biophysics, including biological oxidations, free radical reactions, redox signaling, oxygenases, and cytochrome P450 reactions.