Redox biology and gastric carcinogenesis: the role of Helicobacter pylori.
Redox biology and gastric carcinogenesis: the role of Helicobacter pylori.
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DOI：
10.1179/174329211x12968219310756
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发表时间：
2011
期刊：
影响因子：
--
通讯作者：
Yoshikawa T
中科院分区：
文献类型：
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作者：
Handa O;Naito Y;Yoshikawa T
几乎一半的世界人口感染幽门螺杆菌（H。pylori）。这种细菌增加了人类胃中活性氧（ROS）和活性氮（RNS）的产生，据报道，这对胃炎症和癌变有影响。然而，H.幽门螺杆菌引起胃癌的发生目前尚不清楚。虽然ROS/RNS产生的主要来源可能是宿主中性粒细胞，但H.幽门自身产生O2·−。此外，其细胞毒素可诱导胃上皮细胞产生ROS，影响细胞内信号转导，从而导致胃癌的发生。胃粘膜上皮细胞产生过多的活性氧可引起DNA损伤，从而可能参与胃癌的发生。了解H.幽门诱导的癌变对于开发新的抗胃癌策略是重要的。
Almost half the world's population is infected by Helicobacter pylori (H. pylori). This bacterium increases the production of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in human stomach, and this has been reported to impact upon gastric inflammation and carcinogenesis. However, the precise mechanism by which H. pylori induces gastric carcinogenesis is presently unclear. Although the main source of ROS/RNS production is possibly the host neutrophil, H. pylori itself produces O2•−. Furthermore, its cytotoxin induces ROS production by gastric epithelial cells, which might affect intracellular signal transduction, resulting in gastric carcinogenesis. Excessive ROS production in gastric epithelial cells can cause DNA damage and thus might be involved in gastric carcinogenesis. Understanding the molecular mechanism of H. pylori-induced carcinogenesis is important for developing new strategies against gastric cancer.