ArticlePloS one2013
ALDH2 genotype has no effect on salivary acetaldehyde without the presence of ethanol in the systemic circulation.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 23 citations in OpenAlex.
- Long-term exposure to the ethanol-derived metabolite acetaldehyde elevates structural genomic alterations but not base substitutions.Communications biology · 2026Article
- The Influence of the Oral Microbiome on Oral Cancer: A Literature Review and a New Approach.Biomolecules · 2023Review
- Salivary nitrate/nitrite and acetaldehyde in humans: potential combination effects in the upper gastrointestinal tract and possible consequences for the in vivo formation of N-nitroso compounds-a hypothesis.Archives of toxicology · 2022Article
- Local Acetaldehyde: Its Key Role in Alcohol-Related Oropharyngeal Cancer.Visceral medicine · 2020Review
- Systemic Adeno-Associated Virus-Mediated Gene Therapy Prevents the Multiorgan Disorders Associated with Aldehyde Dehydrogenase 2 Deficiency and Chronic Ethanol Ingestion.Human gene therapy · 2020Article
- Effects of Acute Alcohol Consumption on the Human Brain: Diffusional Kurtosis Imaging and Arterial Spin-Labeling Study.AJNR. American journal of neuroradiology · 2019Article
- Review
- Local Acetaldehyde-An Essential Role in Alcohol-Related Upper Gastrointestinal Tract Carcinogenesis.Cancers · 2018Review
- Polymorphisms in ADH1B and ALDH2 genes associated with the increased risk of gastric cancer in West Bengal, India.BMC cancer · 2017Article
- Activation of Human Salivary Aldehyde Dehydrogenase by Sulforaphane: Mechanism and Significance.PloS one · 2016Article
- Article
- Relationship between acetaldehyde concentration in mouth air and tongue coating volume.Journal of applied oral science : revista FOBArticle
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAcetaldehyde associated with alcoholic beverages was recently classified as carcinogenic (Group 1) to humans based on uniform epidemiological and biochemical evidence. ALDH2 (aldehyde dehydrogenase 2) deficient alcohol consumers are exposed to high concentrations of salivary acetaldehyde and have an increased risk of upper digestive tract cancer. However, this interaction is not seen among ALDH2 deficient non-drinkers or rare drinkers, regardless of their smoking status or consumption of edibles containing ethanol or acetaldehyde. Therefore, the aim of this study was to examine the effect of the ALDH2 genotype on the exposure to locally formed acetaldehyde via the saliva without ethanol ingestion.
methodsThe ALDH2 genotypes of 17 subjects were determined by PCR-RFLP. The subjects rinsed out their mouths with 5 ml of 40 vol% alcohol for 5 seconds. Salivary ethanol and acetaldehyde levels were measured by gas chromatography.
resultsAcetaldehyde reached mutagenic levels rapidly and the exposure continued for up to 20 minutes. The mean salivary acetaldehyde concentrations did not differ between ALDH2 genotypes.
conclusionsFor ALDH2 deficient subjects, an elevated exposure to endogenously formed acetaldehyde requires the presence of ethanol in the systemic circulation. IMPACT: Our findings provide a logical explanation for how there is an increased incidence of upper digestive tract cancers among ALDH2 deficient alcohol drinkers, but not among those ALDH2 deficient subjects who are locally exposed to acetaldehyde without bloodborne ethanol being delivered to the saliva. Thus, ALDH2 deficient alcohol drinkers provide a human model for increased local exposure to acetaldehyde derived from the salivary glands.
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