Key role of local acetaldehyde in upper GI tract carcinogenesis.
Best Pract Res Clin Gastroenterol
; 31(5): 491-499, 2017 Oct.
Article
em En
| MEDLINE
| ID: mdl-29195668
ABSTRACT
Ethanol is neither genotoxic nor mutagenic. Its first metabolite acetaldehyde, however, is a powerful local carcinogen. Point mutation in ALDH2 gene proves the causal relationship between acetaldehyde and upper digestive tract cancer in humans. Salivary acetaldehyde concentration and exposure time are the two major and quantifiable factors regulating the degree of local acetaldehyde exposure in the ideal target organ, oropharynx. Instant microbial acetaldehyde formation from alcohol represents >70% of total ethanol associated acetaldehyde exposure in the mouth. In the oropharynx and achlorhydric stomach acetaldehyde is not metabolized to safe products, instead in the presence of alcohol it accumulates in saliva and gastric juice in mutagenic concentrations. A common denominator in alcohol, tobacco and food associated upper digestive tract carcinogenesis is acetaldehyde. Epidemiological studies on upper GI tract cancer are biased, since they miss information on acetaldehyde exposure derived from alcohol and acetaldehyde present in 'non-alcoholic' beverages and food.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Etanol
/
Neoplasias Gastrointestinais
/
Acetaldeído
Tipo de estudo:
Risk_factors_studies
Limite:
Humans
Idioma:
En
Revista:
Best Pract Res Clin Gastroenterol
Ano de publicação:
2017
Tipo de documento:
Article