Degree Name

MS (Master of Science)

Program

Biology

Date of Award

12-2018

Committee Chair or Co-Chairs

Dr. Yongke Lu

Committee Members

Dr. Allan Forsman, Dr. Jonathan Peterson, Dr. Jim Stewart

Abstract

Excessive alcohol consumption is the primary contributing factor in the development of alcoholic liver diseases (ALD). Nicotine contained in tobacco is a major addictive alkaloid, which enhances the effects of ALDs. The major enzyme involved in nicotine metabolism is cytochrome P450 2A5 (CYP2A5) which is produced in the liver. Alcohol can stimulate the CYP2A5 enzyme. We utilized cyp2a5-/- knockout mice in this research to examine the effects of CYP2A5.

The cyp2a5-/- mice and wild-type (WT) mice were fed liquid ethanol diet with or without nicotine to induce ALD. Nicotine enhancing effects on ALD were observed in WT mice but not in cyp2a5-/- mice. Oxidative stress was stimulated by alcohol and further increased by nicotine in WT mice but not in cyp2a5-/-mice. Microsomal ROS production during microsomal metabolism of nicotine was increased in WT mice but not in cyp2a5-/-mice. These results suggest that nicotine enhances ALD is CYP2A5 dependent.

Document Type

Thesis - Open Access

Copyright

Copyright by the authors.

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