Carcinogenesis, Vol 18, 1739-1743, Copyright © 1997 by Oxford University Press
N Homann, H Jousimies-Somer, K Jokelainen, R Heine and M Salaspuro
Chronic ethanol ingestion leads to an enhanced risk of upper
gastrointestinal tract cancer. Although many hypotheses for the tumor
promoting effect of alcohol exist, the pathogenetic mechanisms remain
unclear since alcohol in itself is not carcinogenic. Acetaldehyde, the
first metabolite of ethanol, has been shown to have multiple mutagenic
effects and to be carcinogenic to animals. Previous research has revealed
that acetaldehyde can be formed from ethanol via microbial alcohol
dehydrogenase. Thus, at least part of the proposed tumorigenic effect of
ethanol may be linked to local production of acetaldehyde from ethanol by
oral microflora. In this study we demonstrate the production of marked
amounts of acetaldehyde in saliva after ingestion of moderate amounts 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 (chlorhexidine). In
vitro acetaldehyde production was shown to be linear in time, inhibited by
4-methylpyrazole and it could not be saturated under ethanol conditions
that are relevant in vivo. There was a significant positive correlation
between salivary acetaldehyde production in vitro and in vivo. We conclude,
that the microbial formation of acetaldehyde in saliva could be one
explanation for the tumor promoting effect of ethanol on the upper
gastrointestinal tract. Moreover, this may support the epidemiological
finding, that poor oral hygiene is an independent risk factor for oral
cavity cancer.
ARTICLES
High acetaldehyde levels in saliva after ethanol consumption: methodological aspects and pathogenetic implications
Research Unit of Alcohol Diseases, University Central Hospital of Helsinki, Finland.
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