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Cytochrome P450s and Alcoholic Liver Disease.

Yongke Lu1,2, Arthur I Cederbaum3

  • 1Department of Health Sciences, College of Public Health, East Tennessee State University Johanson City, TN37614, United States.

Current Pharmaceutical Design
|April 12, 2018
PubMed
Summary

Alcoholic liver disease (ALD) involves ethanol metabolism. While Cytochrome P450 2E1 (CYP2E1) contributes to ALD, the related CYP2A5 enzyme protects against it, offering new insights into disease development.

Keywords:
Alcohol inductionCYP2A5CYP2A6CYP2E1FGF21HIF-1αLPSMAPKNrf2PPARαTNFαalcoholic liver diseaseantioxidantsautophagycoumarin 7-hydroxylaseinteractionsliver fibrosisnicotinepyrazolereactive oxygen species.

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Area of Science:

  • Hepatology
  • Biochemistry
  • Toxicology

Background:

  • Alcohol consumption is a primary cause of Alcoholic Liver Disease (ALD).
  • Early theories linked ALD to malnutrition from alcohol metabolism via alcohol dehydrogenase (ADH).
  • The discovery of the microsomal ethanol oxidizing system (MEOS), primarily cytochrome P450 enzymes (CYP), revised understanding of alcohol's hepatic effects.

Purpose of the Study:

  • To review the complex roles of Cytochrome P450 2E1 (CYP2E1) and Cytochrome P450 2A5 (CYP2A5) in Alcoholic Liver Disease (ALD).
  • To investigate the recently discovered alcohol induction of CYP2A6 and its mouse analog CYP2A5.
  • To elucidate the protective function of CYP2A5 against ALD development, contrasting with CYP2E1's role.

Main Methods:

  • Review of existing literature on ethanol metabolism and liver disease.
  • Analysis of experimental findings regarding CYP2E1 and CYP2A5 induction by alcohol.
  • Examination of the mechanistic relationship between CYP2E1, CYP2A5, and ALD pathogenesis in mouse models.

Main Results:

  • Cytochrome P450 2E1 (CYP2E1) is a significant reactive oxygen species (ROS) generator implicated in ALD.
  • Alcohol also induces human CYP2A6 and its mouse homolog CYP2A5.
  • CYP2A5 induction by alcohol in mice is dependent on CYP2E1, and CYP2A5 demonstrates a protective effect against ALD.

Conclusions:

  • The understanding of ALD pathogenesis is evolving beyond initial malnutrition hypotheses.
  • CYP2E1 is a key contributor to ALD, while CYP2A5 exhibits a protective role.
  • The interplay between CYP2E1, CYP2A5, and ALD is a critical area for future research and therapeutic strategies.