Role of Kupffer cells, endotoxin and free radicals in hepatotoxicity due to prolonged alcohol consumption: studies in female and male rats

The Journal of Nutrition
R G ThurmanR P Mason

Abstract

Alcohol ingestion results in increases in the release of endotoxin from gut bacteria or membrane permeability of the gut to endotoxin, or both. Female rats are more sensitive to these changes. Elevated levels of endotoxin activate Kupffer cells to release substances such as eicosanoids, tumor necrosis factor-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 that lead to tissue damage in oxygen-poor pericentral regions of the liver lobule.

References

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Citations

Mar 3, 1999·Hepatology : Official Journal of the American Association for the Study of Liver Diseases·R F StachlewitzR G Thurman
Dec 21, 2018·World Journal of Gastroenterology : WJG·Arantza Lamas-PazFrancisco Javier Cubero
Jun 7, 2012·Inflammation Research : Official Journal of the European Histamine Research Society ... [et Al.]·Eric G LeeRandle M Gallucci
Jan 1, 2010·Digestive Diseases·Gavin E Arteel
Aug 13, 2013·Clinical Pharmacology and Therapeutics·H Li, W Jia
Apr 28, 2012·American Journal of Physiology. Gastrointestinal and Liver Physiology·Francisco Javier Cubero, Natalia Nieto

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