title: Effect of oral vitamin E administration on acute gastric mucosal lesion progression in rats treated with compound 48/80, a mast cell degranulator.
abstract: The effect of oral vitamin E administration on acute gastric mucosal lesion progression was examined in rats treated once with compound 48/80 (C48/80) (0.75 mg/kg, i.p.) in comparison with that of subcutaneously administered superoxide dismutase (SOD) plus catalase (CAT). Vitamin E (50, 100 or 250 mg/kg) administered at 0.5 h after C48/80 treatment reduced progressive gastric mucosal lesions at 3 h after the treatment dose-dependently, like SOD plus CAT administered at the same time point. The gastric mucosa of C48/80-treated rats had decreased Se-glutathione peroxidase activity and vitamin E, ascorbic acid, and hexosamine contents and increased myeloperoxidase and xanthine oxidase activities and thiobarbituric acid reactive substances content at 3 h after the treatment. Administered vitamin E attenuated all these changes found at 3 h after C48/80 treatment dose-dependently, like administered SOD plus CAT. C48/80-treated rats administered with vitamin E (100 or 250 mg/kg) had higher gastric mucosal vitamin E content than C48/80-untreated rats. Neither administered vitamin E nor SOD plus CAT had any effect on the increases in serum serotonin and histamine concentrations and the decrease in gastric mucosal blood flow found at 3 h after C48/80 treatment. In the gastric mucosa of C48/80-untreated rats administered with vitamin E, thiobarbituric acid reactive substances content decreased with an increase in vitamin E content. These results indicate that orally administered vitamin E prevents acute gastric mucosal lesion progression in C48/80-treated rats possibly by suppressing oxidative stress, neutrophil infiltration, and mucus depletion in the gastric mucosa like administered SOD plus CAT.
authors.affiliation: Department of Chemistry, School of Medicine, Fujita Health University, Toyoake, Aichi, Japan. yohta@fujita-hu.ac.jp
authors.forename: Yoshiji
authors.initials: Y
authors.lastname: Ohta
authors.forename: Takashi
authors.initials: T
authors.lastname: Kobayashi
authors.forename: Yoichiro
authors.initials: Y
authors.lastname: Imai
authors.forename: Kazuo
authors.initials: K
authors.lastname: Inui
authors.forename: Junji
authors.initials: J
authors.lastname: Yoshino
authors.forename: Saburo
authors.initials: S
authors.lastname: Nakazawa
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001205:Ascorbic Acid / Q000494:pharmacology; D002374:Catalase / Q000494:pharmacology; D003594:Cytoplasmic Granules / Q000187:drug effects; D018450:Disease Progression; D004305:Dose-Response Relationship, Drug; D005753:Gastric Mucosa / Q000098:blood supply / Q000473:pathology*; D005979:Glutathione Peroxidase / Q000378:metabolism; D006595:Hexosamines / Q000494:pharmacology; D006632:Histamine / Q000097:blood; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D008407:Mast Cells / Q000187:drug effects / Q000648:ultrastructure; D020556:Neutrophil Infiltration; D009195:Peroxidase / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012039:Regional Blood Flow / Q000187:drug effects; D012701:Serotonin / Q000097:blood; D013276:Stomach Ulcer / Q000139:chemically induced / Q000473:pathology / Q000517:prevention & control*; D013482:Superoxide Dismutase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D014810:Vitamin E / Q000494:pharmacology*; D014969:Xanthine Oxidase / Q000378:metabolism; D003189:p-Methoxy-N-methylphenethylamine / Q000494:pharmacology*
chemical_list: D000975:Antioxidants; D006595:Hexosamines; D017392:Thiobarbituric Acid Reactive Substances; D014810:Vitamin E; D012701:Serotonin; D003189:p-Methoxy-N-methylphenethylamine; D006632:Histamine; D002374:Catalase; D009195:Peroxidase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D014969:Xanthine Oxidase; D001205:Ascorbic Acid