title: Helicobacter pylori-associated gastric pro- and antioxidant formation in Mongolian gerbils.
abstract: Helicobacter pylori colonized gastric mucosa is manifest in a significant neutrophil infiltration with an extensive level of oxyradical formation. Mongolian gerbil is one of the excellent models for H. pylori-infection. The present study was designed to investigate pro- and antioxidant formation in the stomach of H. pylori-positive gerbils. Fourteen male Mongolian gerbils (MGS/Sea) were orally inoculated with H. pylori (ATCC43504) (Hp group) and 15 gerbils were inoculated with the culture media (Control). H. pylori infection was confirmed by the serum anti-H. pylori IgG test. Each gerbil was evaluated 6 or 12 weeks after the inoculation. Neutrophil infiltration was assessed by the tissue MPO activity. Mucosal oxidative stress was evaluated by thiobarbituric acid-reactive substances (TBARS), total glutathione contents, glutathione peroxidase (GSHPx) activity and Cu-, Zn-superoxide dismutase (SOD) activity. In Hp group, the H. pylori was persistently infected until 12 weeks. The level of MPO activity was significantly higher in Hp group at 6 and 12 weeks. Although the levels of TBARS and total glutathione were within the same range as controls at 6 weeks, they were significantly increased at 12 weeks. However, GSHPx activity was significantly increased at 6 weeks, but became the same range with the controls at 12 weeks. SOD activity showed no significant increase in Hp group at 6 and 12 weeks. In conclusion, H. pylori inoculation induced gastric mucosal neutrophil activation and pro-oxidant formation and also increased total glutathione contents, one of the mucosal antioxidants in gerbils.
authors.affiliation: Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Suzuki
authors.forename: M
authors.initials: M
authors.lastname: Mori
authors.forename: K
authors.initials: K
authors.lastname: Seto
authors.forename: A
authors.initials: A
authors.lastname: Kai
authors.forename: C
authors.initials: C
authors.lastname: Kawaguchi
authors.forename: M
authors.initials: M
authors.lastname: Suzuki
authors.forename: M
authors.initials: M
authors.lastname: Suematsu
authors.forename: T
authors.initials: T
authors.lastname: Yoneta
authors.forename: S
authors.initials: S
authors.lastname: Miura
authors.forename: H
authors.initials: H
authors.lastname: Ishii
mesh_terms: D000818:Animals; D000907:Antibodies, Bacterial / Q000097:blood; D000975:Antioxidants / Q000378:metabolism*; D005753:Gastric Mucosa / Q000382:microbiology* / Q000502:physiology / Q000503:physiopathology; D005849:Gerbillinae; D005978:Glutathione / Q000378:metabolism; D019803:Glutathione Disulfide / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D016481:Helicobacter Infections / Q000503:physiopathology*; D016480:Helicobacter pylori / Q000502:physiology*; D007074:Immunoglobulin G / Q000097:blood; D008297:Male; D009504:Neutrophils / Q000502:physiology; D016877:Oxidants / Q000378:metabolism*; D009195:Peroxidase / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis; D013997:Time Factors
chemical_list: D000907:Antibodies, Bacterial; D000975:Antioxidants; D007074:Immunoglobulin G; D016877:Oxidants; D017392:Thiobarbituric Acid Reactive Substances; D009195:Peroxidase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005978:Glutathione; D019803:Glutathione Disulfide