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.
Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Adenoma, Liver Cell / chemically induced
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Adenoma, Liver Cell / genetics*
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Adenoma, Liver Cell / metabolism
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Animals
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Cell Proliferation / drug effects
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Central Nervous System Depressants / administration & dosage
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Central Nervous System Depressants / toxicity
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DNA Damage
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Dose-Response Relationship, Drug
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Ethanol / administration & dosage
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Ethanol / toxicity*
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Gene Frequency
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Hepatitis, Alcoholic / etiology
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Hepatitis, Alcoholic / pathology
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Immunohistochemistry
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Liver / drug effects
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Liver / metabolism
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Liver / pathology
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Liver Neoplasms, Experimental / chemically induced
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Liver Neoplasms, Experimental / genetics*
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Liver Neoplasms, Experimental / metabolism
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Male
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Mice
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Mice, Inbred Strains
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Mutagenesis / drug effects
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Oxidative Stress / drug effects
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Proliferating Cell Nuclear Antigen / analysis
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Time Factors
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beta Catenin / metabolism
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ras Proteins / genetics*
Substances
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Central Nervous System Depressants
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Proliferating Cell Nuclear Antigen
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beta Catenin
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Ethanol
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ras Proteins