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.
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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)
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Copyright | Copyright © 2010 Elsevier Ireland Ltd. All rights reserved. |
Chemical References |
- Central Nervous System Depressants
- Proliferating Cell Nuclear Antigen
- beta Catenin
- Ethanol
- ras Proteins
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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)
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