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慢性乙醇给药通过促进 H-ras 突变细胞导致肝细胞腺瘤发生率增加。

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

机构信息

Department of Environmental Sciences and Engineering, University of North Carolina, Chapel Hill, 27599-7431, United States.

出版信息

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

DOI:10.1016/j.canlet.2010.11.010
PMID:21168264
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3035933/
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.

摘要

本研究使用雄性 B6C3F1 小鼠的组织样本，这些小鼠在饮用水中接受乙醇处理（0%、2.5%或 5%）4 或 104 周。我们检测了慢性饮酒是否会促进肝脏中的氧化应激，并描述了自发性和乙醇诱导肿瘤的突变谱。结果表明，乙醇在任何时间点都不会引起肝脏中可检测到的氧化应激，而是通过促进 H-ras 突变细胞起作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/903d/3035933/ba9da260f1cf/nihms259525f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/903d/3035933/409be4b6ab41/nihms259525f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/903d/3035933/ba9da260f1cf/nihms259525f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/903d/3035933/409be4b6ab41/nihms259525f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/903d/3035933/ba9da260f1cf/nihms259525f2.jpg

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