title: Amelioration of oxidative stress with ensuing inflammation contributes to chemoprevention of H. pylori-associated gastric carcinogenesis.
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.
authors.affiliation: Genomic Research Center for Gastroenterology, Ajou University School of Medicine, Suwon, Korea.
authors.forename: Soojin
authors.initials: S
authors.lastname: Park
authors.forename: Won Seok
authors.initials: WS
authors.lastname: Kim
authors.forename: Un Jung
authors.initials: UJ
authors.lastname: Choi
authors.forename: Sang Uk
authors.initials: SU
authors.lastname: Han
authors.forename: Yong Seok
authors.initials: YS
authors.lastname: Kim
authors.forename: Young Bae
authors.initials: YB
authors.lastname: Kim
authors.forename: Myung Hee
authors.initials: MH
authors.lastname: Chung
authors.forename: Ki-Tak
authors.initials: KT
authors.lastname: Nam
authors.forename: Dae Yong
authors.initials: DY
authors.lastname: Kim
authors.forename: Sung Won
authors.initials: SW
authors.lastname: Cho
authors.forename: Ki-Baik
authors.initials: KB
authors.lastname: Hahm
mesh_terms: D000818:Animals; D000942:Antigens, Bacterial / Q000235:genetics; D001426:Bacterial Proteins / Q000235:genetics; D003849:Deoxyguanosine / Q000378:metabolism; D005756:Gastritis / Q000382:microbiology; D044404:Genomic Islands; D016480:Helicobacter pylori / Q000378:metabolism*; D006801:Humans; D008562:Membrane Glycoproteins / Q000378:metabolism; D008954:Models, Biological; D019255:NADPH Oxidases / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II; D016877:Oxidants / Q000378:metabolism; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D026361:Reactive Nitrogen Species; D017382:Reactive Oxygen Species; D011956:Receptors, Cell Surface / Q000378:metabolism; D013274:Stomach Neoplasms / Q000382:microbiology* / Q000473:pathology*; D013997:Time Factors; D051193:Toll-Like Receptors
chemical_list: D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D008562:Membrane Glycoproteins; D016877:Oxidants; D026361:Reactive Nitrogen Species; D017382:Reactive Oxygen Species; D011956:Receptors, Cell Surface; D051193:Toll-Like Receptors; C080866:cagA protein, Helicobacter pylori; C496319:NOS2 protein, human; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; D019255:NADPH Oxidases; D003849:Deoxyguanosine