Homann Nils
Department of Gastroenterology, Medical University of Luebeck, Germany.
Addict Biol. 2001 Sep;6(4):309-323. doi: 10.1080/13556210020077028.
Alcohol is, together with tobacco smoke, the main cause for upper GI tract cancer in industrialized countries. However, the tumour-promoting effects of alcohol intake are poorly understood and alcohol itself is not carcinogenic in the animal model. There is increasing evidence that alcohol metabolism, rather than the alcohol itself, generates carcinogenic and cell-toxic compounds. Acetaldehyde, first metabolite of ethanol, is highly toxic, mutagenic and carcinogenic. Polymorphisms in the genes coding for enzymes responsible for acetaldehyde accumulation and detoxification have been associated with an increased cancer risk. Acetaldehyde can also be produced in the mucosa and by the physiological microflora. This review summarizes the scientific evidence that alcohol intake leads to a local production of acetaldehyde. It describes the role of the oral microflora, the mucosa and the salivary glands in this process and shows that local acetaldehyde production from ethanol may contribute to the carcinogenesis of alcohol intake in the upper GI tract.
在工业化国家，酒精与烟草烟雾一样，是上消化道癌症的主要病因。然而，酒精摄入的促肿瘤作用尚未得到充分了解，并且在动物模型中酒精本身并无致癌性。越来越多的证据表明，是酒精代谢而非酒精本身产生了致癌和细胞毒性化合物。乙醛作为乙醇的首要代谢产物，具有高毒性、致突变性和致癌性。负责乙醛积累和解毒的酶的编码基因中的多态性与癌症风险增加有关。乙醛也可在黏膜中以及由生理微生物群产生。本综述总结了酒精摄入导致局部产生乙醛的科学证据。它描述了口腔微生物群、黏膜和唾液腺在此过程中的作用，并表明乙醇局部产生乙醛可能有助于上消化道酒精摄入致癌作用的发生。
