IMR Press / FBL / Volume 4 / Issue 5 / DOI: 10.2741/A478

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article
Mechanisms of alcohol-induced hepatotoxicity: studies in rats
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1 Laboratory of Hepatobiology and Toxicology, Department of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, NC
2 Department of Radiation Oncology, University of North Carolina at Chapel Hill, Chapel Hill, NC
3 Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC
4 Laboratory of Molecular Biophysics, NIEHS, NIH, Research Triangle Park, NC
Front. Biosci. (Landmark Ed) 1999, 4(5), 42–46; https://doi.org/10.2741/A478
Published: 15 July 1999
Abstract

Alcohol treatment results in increases in the release of endotoxin from gut bacteria and membrane permeability of the gut to endotoxin, or both. Females are more sensitive to these changes. Elevated levels of endotoxin activate Kupffer cells to release substances such as eicosanoids, TNF-alpha and free radicals. Prostaglandins increase oxygen uptake and most likely are responsible for the hypermetabolic state in the liver. The increase in oxygen demand leads to hypoxia in the liver, and on reperfusion, alpha-hydroxyethyl free radicals are formed which lead to tissue damage in oxygen-poor pericentral regions of the liver lobule.

Keywords
alcohol
liver
hypoxia
gender
free radicals
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