Alcohol intoxication caused liver injury in association with increases in plasma endotoxin and hepatic lipid peroxidation. Alcohol administration via gavage at a dose of 6 g/kg to 129/Sv mice induced hepatic TNF-α production in Kupffer cells as demonstrated by measuring protein levels, immunohistochemical localization, and mRNA expression. The present study was undertaken to determine the mediators of acute alcohol-induced TNF-α production using a mouse model of acute alcohol hepatotoxicity. However, a cause-and-effect relationship between these factors has not been fully defined. Both oxidative stress and endotoxin have been implicated in the process of alcohol-induced TNF-α production. Tumor necrosis factor-α (TNF-α) production is a critical factor in the pathogenesis of alcoholic liver injury.
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