By M. V. Singer, D. Brenner
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Extra info for Alcohol And the Gastrointestinal Tract: Special Issue: Digestive Diseases 2005
The application of a knockout mouse model conﬁrmed that free radicals generated by NADPH oxidase in Kupffer cells play a pivotal role in ethanol-induced liver injury. In NADPH oxidase-deﬁcient knockout mice fed intragastrically with ethanol for 4 weeks, neither did liver pathology evolve nor were free radicals detectable by electron spin resonance . In addition, Kono et al.  questioned the concept that CYP2E1 induced in hepatocytes by chronic ethanol ingestion is a major factor in alcoholinduced liver injury via the generation of free radicals.
Were not associated with higher acetaldehyde production. Microbial changes in the oral microﬂora of alcoholics have been less intensively described . Epidemiological studies have shown that heavy drinking is associated with poor oral hygiene. It has been suggested that this may lead to bacterial overgrowth, but so far no study has convincingly proved this hypothesis and no bacterial species have been associated with high alcohol consumption [48, 72]. As high salivary acetaldehyde production was observed only among heavy drinkers, enzyme induction might be an explanation for this ﬁnding.
Brewery workers are also Riedel/Goessler/Hörmann presumed to drink a larger amount of beer than the general population. In cohort studies of brewery workers in Dublin, Denmark and Sweden, a relatively small but statistically signiﬁcant increase in the risk of head and neck cancer was found compared with the general population [40–42]. Type of Alcoholic Beverages Ethanol is present in alcoholic beverages as a consequence of the fermentation of carbohydrates with yeast. Beside ethanol, beer, wine and spirits also contain volatile and non-volatile ﬂavor compounds.
Alcohol And the Gastrointestinal Tract: Special Issue: Digestive Diseases 2005 by M. V. Singer, D. Brenner