Amelioration of Oxidative Stress with Ensuing Inflammation Contributes to Chemoprevention of H. pylori-Associated Gastric Carcinogenesis

Soojin Park, Won Seok Kim, Un Jung Choi, Sang Uk Han, Yong Seok Kim, Young Bae Kim, Myung Hee Chung, Ki Tak Nam, Dae Yong Kim, Sung Won Cho, Ki Baik Hahm

Research output: Contribution to journalReview articlepeer-review

33 Citations (Scopus)


The gastric inflammatory response provoked by Helicobacter pylori (H. pylori) consists of infiltrations by neutrophils, lymphocytes, and macrophages, resulting in varying degrees of epithelial cell damage. H. pylori-associated inflammation not only activates various oxidant-producing enzymes such as NADPH oxidase and inducible nitric oxide synthase, but also lowers the antioxidant ascorbic acid in the stomach. Reactive oxygen metabolites and nitrogen metabolites generated by these enzymes react with each other to generate new or more potent reactive species. The specific types of cellular damage resulting from reactive oxygen metabolites include lipid peroxidation, protein oxidation, and oxidative DNA damage. All of these oxidative products can result in biochemical changes leading to cancer. A positive association has been demonstrated between H. pylori infection and gastric adenocarcinoma with increased oxidative stress. Therefore, appropriate treatment to reduce oxidative stress would be expected to prevent subsequent gastric carcinogenesis through lessening of H. pylori-associated inflammation. This review will provide evidence that antiinflammatory regimens can decrease the development of tumors and the amelioration of gastric inflammation might lead to chemoprevention strategies by the attenuation of oxidative stress.

Original languageEnglish
Pages (from-to)549-560
Number of pages12
JournalAntioxidants and Redox Signaling
Issue number3
Publication statusPublished - 2004 Jun

All Science Journal Classification (ASJC) codes

  • Physiology
  • Biochemistry
  • Molecular Biology
  • Clinical Biochemistry
  • Cell Biology


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