The DOI matches its Crossref record; 37 of the 37 references it cites were found in a registry or an index.
Increased salivary acetaldehyde levels in heavy drinkers and smokers: a microbiological approach to oral cavity cancer
Abstract
The pathogenetic mechanisms behind alcohol-associated carcinogenesis in the upper digestive tract remain unclear, as alcohol is not carcinogenic. However, there is increasing evidence that a major part of the tumour-promoting action of alcohol might be mediated via its first, toxic and carcinogenic metabolite acetaldehyde. Acetaldehyde is produced from ethanol in the epithelia by mucosal alcohol dehydrogenases, but much higher levels derive from microbial oxidation of ethanol by the oral microflora. In this study we investigated factors that might alter the composition and quantities of the oral microflora and, consequently, influence microbial acetaldehyde production. Information about dental health, smoking habits, alcohol consumption and other factors was obtained by a questionnaire from 326 volunteers with varying social backgrounds and health status, e.g. oral cavity malignancy. Paraffin-induced saliva was collected and the microbial production of acetaldehyde from ethanol was measured. Smoking and heavy drinking were the strongest factors increasing microbial acetaldehyde production. Whether poor dental status may alter local acetaldehyde production from ethanol remained unanswered. Bacterial analysis revealed that mainly gram-positive aerobic bacteria and yeasts were associated with higher acetaldehyde production. Increased local microbial salivary acetaldehyde production due to ethanol among smokers and heavy drinkers could be a biological explanation for the observed synergistic carcinogenic action of alcohol and smoking on upper gastrointestinal tract cancer. It offers a new microbiological approach to ethanol-associated carcinogenesis at these anatomic sites.
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Cites
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Cited by
Fan, X., Alekseyenko, A. V., Wu, J., Peters, B. A., Jacobs, E. J., Gapstur, S. M., Purdue, M. P., Abnet, C. C., Stolzenberg-Solomon, R., Miller, G., et al. (2018) · Gut · doi:10.1136/gutjnl-2016-312580 · Cited by 702
Brooks, P. J., Enoch, M.-A., Goldman, D., Li, T.-K., & Yokoyama, A. (2009) · PLoS Medicine · doi:10.1371/journal.pmed.1000050 · Cited by 480
Light alcohol drinking and cancer: a meta-analysis
Bagnardi, V., Rota, M., Botteri, E., Tramacere, I., Islami, F., Fedirko, V., Scotti, L., Jenab, M., Turati, F., Pasquali, E., et al. (2013) · Annals of Oncology · doi:10.1093/annonc/mds337 · Cited by 424
Basuroy, S., Sheth, P., Mansbach, C. M., & Rao, R. K. (2005) · American Journal of Physiology-Gastrointestinal and Liver Physiology · doi:10.1152/ajpgi.00464.2004 · Cited by 134
The Human Microbiome in Relation to Cancer Risk: A Systematic Review of Epidemiologic Studies
Huybrechts, I., Zouiouich, S., Loobuyck, A., Vandenbulcke, Z., Vogtmann, E., Pisanu, S., Iguacel, I., Scalbert, A., Indave, I., Smelov, V., et al. (2020) · Cancer Epidemiology, Biomarkers & Prevention · doi:10.1158/1055-9965.epi-20-0288 · Cited by 80
Metadata
- Authors
- Homann, N., Tillonen, J., Meurman, J. H., Rintamaki, H., Lindqvist, C., Rautio, M., Jousimies-Somer, H., & Salaspuro, M.
- Venue
- Carcinogenesis
- Publisher
- Oxford University Press (OUP)
- Published
- 2000-04-01
- Volume
- 21
- Issue
- 4
- Pages
- 663-668
- ISSN
- 0143-3334 (ISSN-L)
- 1460-2180
- OpenAlex
- W2130785878
- Cited by
- 331
- References
- 37
- FWCI
- 10.98
- Type
- journal article
- Language
- en
- Open access
- closed
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- Homann, N., Tillonen, J., Meurman, J. H., Rintamaki, H., Lindqvist, C., Rautio, M., Jousimies-Somer, H., & Salaspuro, M. (2000). Increased salivary acetaldehyde levels in heavy drinkers and smokers: a microbiological approach to oral cavity cancer. Carcinogenesis. https://doi.org/10.1093/carcin/21.4.663
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