HIGH ACETALDEHYDE-LEVELS IN SALIVA AFTER ETHANOL-CONSUMPTION - METHODOLOGICAL ASPECTS AND PATHOGENETIC IMPLICATIONS

Chronic ethanol ingestion leads to an enhanced risk of upper gastroint estinal tract cancer, Although many hypotheses for the tumor promoting effect of alcohol exist, the pathogenetic mechanisms remain unclear s ince alcohol in itself is not carcinogenic, Acetaldehyde, the first me tabolite of ethanol, has been shown to have multiple mutagenic effects and to be carcinogenic to animals, Previous research has revealed tha t acetaldehyde can be formed from ethanol via microbial alcohol dehydr ogenase, Thus, at least part of the proposed tumorigenic effect of eth anol may be linked to local production of acetaldehyde from ethanol by oral microflora, In this study we demonstrate the production of marke d amounts of acetaldehyde in saliva after ingestion of moderate amount s of ethanol, Considerable inter individual variation in acetaldehyde production capacity is also shown. In vivo acetaldehyde production is significantly reduced after a 3-day use of an antiseptic mouthwash (ch lorhexidine), In vitro acetaldehyde production was shown to be linear in time, inhibited by 4-methylpyrazole and it could not be saturated u nder ethanol conditions that are relevant in vivo. There was a signifi cant positive correlation between salivary acetaldehyde production in vitro and in vivo. We conclude, that the microbial formation of acetal dehyde in saliva could be one explanation for the tumor promoting effe ct of ethanol on the upper gastrointestinal tract, Moreover, this may support the epidemiological finding, that poor oral hygiene is an inde pendent risk factor for oral cavity cancer.