Journal
INFLAMMATION RESEARCH
Volume 59, Issue 12, Pages 997-1003Publisher
SPRINGER BASEL AG
DOI: 10.1007/s00011-010-0245-x
Keywords
Oxidative stress; Leucocytes; Infection; NO
Categories
Funding
- Japan Society for the Promotion of Science [21390184, 22590705]
- Ministry of Education, Culture, Sports, Science and Technology, Japan
- Japan Science and Technology Agency
- Grants-in-Aid for Scientific Research [21390184, 22590705] Funding Source: KAKEN
Ask authors/readers for more resources
Reactive oxygen species (ROS) and reactive nitrogen species (RNS) have been reported to impact gastric inflammation and carcinogenesis. However, the precise mechanism by which Helicobacter pylori induces gastric carcinogenesis is presently unclear. This review focuses on H. pylori-induced ROS/RNS production in the host stomach, and its relationship with gastric carcinogenesis. Activated neutrophils are the main source of ROS/RNS production in the H. pylori-infected stomach, but H. pylori itself also produces ROS. In addition, extensive recent studies have revealed that H. pylori-induced ROS production in gastric epithelial cells might affect gastric epithelial cell signal transduction, resulting in gastric carcinogenesis. Excessive ROS/RNS production in the stomach can damage DNA in gastric epithelial cells, implying its involvement in gastric carcinogenesis. Understanding the molecular mechanism behind H. pylori-induced ROS, and its involvement in gastric carcinogenesis, is important for developing new strategies for gastric cancer chemoprevention.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available