Increased salivary acetaldehyde levels in heavy drinkers and smokers:: a microbiological approach to oral cavity cancer
Increased salivary acetaldehyde levels in heavy drinkers and smokers:: a microbiological approach to oral cavity cancer
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DOI：
10.1093/carcin/21.4.663
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发表时间：
2000-04-01
期刊：
影响因子：
4.7
通讯作者：
Salaspuro, M
中科院分区：
文献类型：
--
作者：
Homann, N;Tillonen, J;Salaspuro, M
上消化道酒精相关致癌作用的发病机制尚不清楚，因为酒精不致癌。然而，越来越多的证据表明，酒精的肿瘤促进作用的主要部分可能是通过其第一个有毒和致癌的代谢产物乙醛介导的。乙醛是由粘膜乙醇脱氢酶在上皮细胞中的乙醇产生的，但是更高的水平来自于口腔微生物对乙醇的微生物氧化。在这项研究中，我们研究了可能改变口腔微生物群落的组成和数量的因素，从而影响微生物乙醛的产生。通过对326名具有不同社会背景和健康状况（如口腔恶性肿瘤）的志愿者进行问卷调查，获得有关牙齿健康、吸烟习惯、饮酒和其他因素的信息。收集石蜡诱导的唾液，并测量乙醇中乙醛的微生物生产。吸烟和大量饮酒是增加微生物乙醛产量的最强因素。牙齿状况不佳是否会改变乙醇产生的乙醛，这一点还没有答案。细菌分析表明，主要是革兰氏阳性好氧菌和酵母菌与较高的乙醛产生，增加局部微生物唾液乙醛的生产，由于酒精的吸烟者和酗酒者之间可以是一个生物学解释的酒精和吸烟对上消化道癌的协同致癌作用。它提供了一个新的微生物方法，乙醇相关的致癌作用在这些解剖部位。
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 Grampositive 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.