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

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.

• Authors: Emmanuelle Jeannot, Igor P Pogribny, Frederick A Beland, Ivan Rusyn
• Journal: Cancer letters (Cancer Lett) Vol. 301 Issue 2 Pg. 161-7 (Feb 28 2011) ISSN: 1872-7980 [Electronic] Ireland
• PMID: 21168264 (Publication Type: Journal Article, Research Support, N.I.H., Extramural)
• Copyright: Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.

Chemical References

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

Topics

• Adenoma, Liver Cell (chemically induced, genetics, metabolism)
• Animals
• Cell Proliferation (drug effects)
• Central Nervous System Depressants (administration & dosage, toxicity)
• DNA Damage
• Dose-Response Relationship, Drug
• Ethanol (administration & dosage, toxicity)
• Gene Frequency
• Hepatitis, Alcoholic (etiology, pathology)
• Immunohistochemistry
• Liver (drug effects, metabolism, pathology)
• Liver Neoplasms, Experimental (chemically induced, genetics, 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)