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Redox biology and gastric carcinogenesis: the role of Helicobacter pylori.

Abstract
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.
AuthorsOsamu Handa, Yuji Naito, Toshikazu Yoshikawa
JournalRedox report : communications in free radical research (Redox Rep) Vol. 16 Issue 1 Pg. 1-7 ( 2011) ISSN: 1743-2928 [Electronic] England
PMID21605492 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
Chemical References
  • Bacterial Proteins
  • Reactive Nitrogen Species
  • Reactive Oxygen Species
  • Superoxides
  • Catalase
  • Nitric Oxide Synthase Type II
Topics
  • Bacterial Proteins (metabolism)
  • Catalase (metabolism)
  • Electron Transport
  • Epithelial Cells (immunology, microbiology)
  • Gastric Mucosa (immunology, microbiology, physiopathology)
  • Gastritis (immunology, microbiology)
  • Helicobacter Infections (immunology, microbiology)
  • Helicobacter pylori (enzymology, immunology, pathogenicity)
  • Humans
  • Immune Evasion
  • Neutrophils (immunology, microbiology)
  • Nitric Oxide Synthase Type II (metabolism)
  • Oxidation-Reduction
  • Oxidative Stress
  • Reactive Nitrogen Species (metabolism)
  • Reactive Oxygen Species (metabolism)
  • Stomach Neoplasms (immunology, microbiology, physiopathology)
  • Superoxides (metabolism)

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