吸烟与饮酒对于胃肠癌进展的作用
2009/07/30
目的：探讨吸烟与饮酒对于胃肠癌进展的作用及相关机制。
背景：吸烟和酒精是多种癌症包括胃肠道癌症的主要危险因素。烟草烟雾中包含许多致突变和致癌的化合物，包括多环碳水化合物、亚硝胺和尼古丁等。而酒精本身只有较弱的致癌潜能，但酒精的第一个代谢产物乙醛是一个较强的致突变和致癌的物质。
总结:吸烟可以增加饮酒后代谢产物乙醛的负荷，饮酒可以增加烟草中各种前致癌原物质的激活，其机制是通过在上消化道和肝脏粘膜中诱导细胞色素P450-2E1依赖的微粒体生物转化系统的代谢活性增加引起的。
（张永明编译 刘国梁审校）
Methods Mol Biol. 2009;472:217-241
Contribution of alcohol and tobacco use in gastrointestinal cancer development
Seitz HK, Cho CH.
Department of Medicine, Center of Alcohol Research, Liver Disease and Nutrition, Salem Medical Center, University of Heidelberg, Heidelberg, Germany.
Tobacco smoke and alcohol are major risk factors for a variety of cancer sites, including those of the gastrointestinal tract. Tobacco smoke contains a great number of mutagenic and carcinogenic compounds, including polycyclic carbohydrates, nitrosamines, and nicotine, while ethanol per se has only weak carcinogenic potential, but its first metabolite, acetaldehyde, is a mutagen and carcinogen, since it forms stable adducts with DNA. The possibility of proto-oncogene mutation in gastrointestinal mucosa cells may be associated with tobacco smoking-induced cancers through the formation of unfavorable DNA adducts. Individuals with defective DNA repair mechanisms and unfavorable genetic make-up for carcinogen metabolism may be at increased risk for gastrointestinal cancers. Individuals with a high production rate of acetaldehyde from ethanol also have an increased cancer risk when they drink chronically. These include individuals with a genetically determined increased acetaldehyde production due to alcohol dehydrogenase polymorphism and those with a decreased detoxification of acetaldehyde due to acetaldehyde dehydrogenase mutation. In addition, oral bacterial overgrowth due to poor oral hygiene also increases salivary acetaldehyde. Dietary deficiencies such as a lack of folate, riboflavine, and zinc may also contribute to the increase cancer risk in the alcoholic patient. It is of considerable importance that smoking and drinking act synergistically. Smoking increases the acetaldehyde burden following alcohol consumption and drinking enhances the activation of various procarcinogens present in tobacco smoke due to increased metabolic activation by an induced cytochrome P450-2E1-dependent microsomal biotransformation system in the mucosa of the upper digestive tract and the liver.
PMID: 19107435 [PubMed - indexed for MELINE]
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吸烟和婴儿猝死综合征
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环境吸烟与主动吸烟对哮喘与鼻炎的发生和结局的影响
