Chronic administration of ethanol leads to an increased incidence of hepatocellular adenoma by promoting H-ras-mutated cells

Cancer Lett. 2011 Feb 28;301(2):161-7. doi: 10.1016/j.canlet.2010.11.010. Epub 2010 Dec 17.

Abstract

This study used tissue samples from male B6C3F1 mice treated with ethanol in drinking water (0%, 2.5%, or 5%) for 4 or 104 weeks. We tested whether chronic alcohol drinking promotes oxidative stress in the liver and characterized the mutation profile of spontaneous and ethanol-induced tumors. We show that ethanol does not cause detectable oxidative stress in the liver at any time point and acts by promoting H-ras mutated cells.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Adenoma, Liver Cell / chemically induced
  • Adenoma, Liver Cell / genetics*
  • Adenoma, Liver Cell / metabolism
  • Animals
  • Cell Proliferation / drug effects
  • Central Nervous System Depressants / administration & dosage
  • Central Nervous System Depressants / toxicity
  • DNA Damage
  • Dose-Response Relationship, Drug
  • Ethanol / administration & dosage
  • Ethanol / toxicity*
  • Gene Frequency
  • Hepatitis, Alcoholic / etiology
  • Hepatitis, Alcoholic / pathology
  • Immunohistochemistry
  • Liver / drug effects
  • Liver / metabolism
  • Liver / pathology
  • Liver Neoplasms, Experimental / chemically induced
  • Liver Neoplasms, Experimental / genetics*
  • Liver Neoplasms, Experimental / metabolism
  • Male
  • Mice
  • Mice, Inbred Strains
  • Mutagenesis / drug effects
  • Oxidative Stress / drug effects
  • Proliferating Cell Nuclear Antigen / analysis
  • Time Factors
  • beta Catenin / metabolism
  • ras Proteins / genetics*

Substances

  • Central Nervous System Depressants
  • Proliferating Cell Nuclear Antigen
  • beta Catenin
  • Ethanol
  • ras Proteins