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在无胃酸萎缩性胃炎中,乙醇衍生的微生物产生致癌乙醛。

Ethanol-derived microbial production of carcinogenic acetaldehyde in achlorhydric atrophic gastritis.

作者信息

Väkeväinen S, Mentula S, Nuutinen H, Salmela K S, Jousimies-Somer H, Färkkilä M, Salaspuro M

机构信息

Research Unit of Substance Abuse Medicine, Biomedicum Helsinki, University of Helsinki, Finland.

出版信息

Scand J Gastroenterol. 2002 Jun;37(6):648-55. doi: 10.1080/00365520212500.

Abstract

BACKGROUND

Acetaldehyde is a local carcinogen in the digestive tract in humans. Atrophic gastritis leads to microbial colonization of the stomach, which could enhance microbial production of acetaldehyde from ethanol. The aim of the study was to study microbial ethanol metabolism and acetaldehyde production in the stomach of achlorhydric atrophic gastritis patients.

METHODS

For the in vivo study, glucose or ethanol was infused via a nasogastric tube to the stomach of seven achlorhydric atrophic gastritis patients and five healthy controls. Gastric juice samples for ethanol and acetaldehyde determinations and microbial analysis were obtained at 30 and 60 min after the infusions. For the in vitro study, gastric juice samples from 14 atrophic gastritis patients and 16 controls were obtained during gastroscopy, whereafter the samples were incubated for 2 h with 1% ethanol at 37 degrees C and acetaldehyde was determined.

RESULTS

Minor endogenous ethanol and acetaldehyde concentrations were detected after glucose infusion in the gastric juice of four atrophic gastritis patients. After ethanol infusion, the mean intragastric acetaldehyde level of the atrophic gastritis patients was 4.5-fold at 30 min and 6.5-fold at 60 min compared to controls. In vitro, the difference between the study groups was even higher, 7.6-fold. A vast selection of oral bacterial species and some Enterobacteriaceae and yeasts were presented in the gastric juice of atrophic gastritis patients.

CONCLUSIONS

Microbial ethanol metabolism leads to high intragastric acetaldehyde levels after ethanol drinking in achlorhydric atrophic gastritis patients. This could be one of the factors responsible for enhanced gastric cancer risk among atrophic gastritis patients.

摘要

背景

乙醛是人类消化道中的一种局部致癌物。萎缩性胃炎会导致胃部微生物定植,这可能会增强微生物将乙醇转化为乙醛的能力。本研究的目的是探讨无酸萎缩性胃炎患者胃内的微生物乙醇代谢及乙醛生成情况。

方法

在体内研究中,通过鼻胃管向7例无酸萎缩性胃炎患者和5例健康对照者的胃内输注葡萄糖或乙醇。输注后30分钟和60分钟采集胃液样本,用于测定乙醇和乙醛含量以及进行微生物分析。在体外研究中,在胃镜检查期间采集14例萎缩性胃炎患者和16例对照者的胃液样本,然后将样本在37℃下与1%乙醇孵育2小时,测定乙醛含量。

结果

在4例萎缩性胃炎患者的胃液中,输注葡萄糖后检测到少量内源性乙醇和乙醛浓度。输注乙醇后,萎缩性胃炎患者胃内乙醛的平均水平在30分钟时是对照组的4.5倍,在60分钟时是对照组的6.5倍。在体外,研究组之间的差异甚至更大,为7.6倍。萎缩性胃炎患者的胃液中存在大量口腔细菌种类以及一些肠杆菌科细菌和酵母菌。

结论

无酸萎缩性胃炎患者饮酒后,微生物乙醇代谢会导致胃内乙醛水平升高。这可能是萎缩性胃炎患者胃癌风险增加的因素之一。

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