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幽门螺杆菌感染的人胃黏膜中氧化性DNA损伤增加。

Increased oxidative DNA damage in Helicobacter pylori-infected human gastric mucosa.

作者信息

Baik S C, Youn H S, Chung M H, Lee W K, Cho M J, Ko G H, Park C K, Kasai H, Rhee K H

机构信息

Department of Microbiology, Gyeongsang National University College of Medicine, Chinju, Kyung-Nam, Republic of Korea.

出版信息

Cancer Res. 1996 Mar 15;56(6):1279-82.

PMID:8640814
Abstract

Helicobacter pylori causes type B gastritis. It shows strong association with the development of gastric carcinoma. A plausible hypothesis for the missing link between H. pylori infection and gastric carcinogenesis involves oxygen free radical-induced DNA damage. To test this hypothesis, we compared the amount of 9-hydroxydeoxyguanosine, a marker for oxygen free radical-induced DNA damage, in the DNA of human gastric mucosa with and without H. pylori infection. Gastric antral biopsies were taken from pediatric patients and volunteers to select H. pylori-positive and H. pylori-negative specimens. The 8-hydroxydeoxyguanosine content of the gastric mucosal DNA was measured after H. pylori-positive and H. pylori-negative volunteers were identified. The increased level of oxidative DNA damage suggests the mechanistic link between H. pylori infection and gastric carcinoma.

摘要

幽门螺杆菌可导致B型胃炎。它与胃癌的发生密切相关。关于幽门螺杆菌感染与胃癌发生之间缺失环节的一个合理假说是,氧自由基诱导的DNA损伤。为验证这一假说,我们比较了幽门螺杆菌感染阳性和阴性的人胃黏膜DNA中9-羟基脱氧鸟苷(一种氧自由基诱导的DNA损伤标志物)的含量。从儿科患者和志愿者身上采集胃窦活检样本,以挑选出幽门螺杆菌阳性和阴性标本。在确定幽门螺杆菌阳性和阴性志愿者后,测量胃黏膜DNA中的8-羟基脱氧鸟苷含量。氧化DNA损伤水平的升高表明了幽门螺杆菌感染与胃癌之间的机制联系。

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