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Amelioration of oxidative stress with ensuing inflammation contributes to chemoprevention of H. pylori-associated gastric carcinogenesis.

Authors
Park, S; Kim, WS; Choi, UJ; Han, SU; Kim, YS; Kim, YB; Chung, MH; Nam, KT; Kim, DY; Cho, SW; Hahm, KB
Citation
Antioxidants & redox signaling, 6(3):549-560, 2004
Journal Title
Antioxidants & redox signaling
ISSN
1523-08641557-7716
Abstract
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.
MeSH terms
AnimalsAntigens, Bacterial/geneticsBacterial Proteins/geneticsDeoxyguanosine/metabolismGastritis/microbiologyGenomic IslandsHelicobacter pylori/*metabolismHumansMembrane Glycoproteins/metabolismModels, BiologicalNADPH Oxidase/metabolismNitric Oxide Synthase/metabolismNitric Oxide Synthase Type IIOxidants/metabolismOxidation-Reduction*Oxidative StressReactive Nitrogen SpeciesReactive Oxygen SpeciesReceptors, Cell Surface/metabolismStomach Neoplasms/*microbiology/*pathologyTime FactorsToll-Like Receptors
DOI
10.1089/152308604773934305
PMID
15130281
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Surgery
Journal Papers > School of Medicine / Graduate School of Medicine > Pathology
Journal Papers > School of Medicine / Graduate School of Medicine > Gastroenterology
AJOU Authors
한, 상욱김, 영배조, 성원함, 기백
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