title: A critical role of gastric mucosal ascorbic acid in the progression of acute gastric mucosal lesions induced by compound 48/80 in rats.
abstract: OBJECTIVE
  To study the role of gastric mucosal ascorbic acid (AA) in the progression of acute gastric mucosal lesions induced by compound 48/80 (C48/80), a mast cell degranulator, in rats.
  
  
  METHODS
  C48/80 (0.75 mg/kg) was intraperitoneally injected to fasted Wistar rats. Oral administration of AA (10, 50 or 100 mg/kg) was performed 0.5 h after C48/80 treatment. Determinations for gastric mucosal lesion severity and blood flow, and assays for gastric mucosal total AA, reduced AA, oxidized AA, vitamin E, thiobarbituric acid reactive substances (TBARS), adherent mucus, nitrite/nitrate (NOx), non-protein SH (NPSH), and myeloperoxidase (MPO), and serum total AA, reduced AA, oxidized AA, and NOx were conducted 0.5 and 3 h after C48/80 treatment.
  
  
  RESULTS
  Gastric mucosal lesions occurred 0.5 h after C48/80 treatment and progressed at 3 h. Gastric mucosal blood flow decreased 0.5 h after C48/80 treatment but the decrease was recovered at 3 h. Gastric mucosal total AA, reduced AA, vitamin E, and adherent mucus concentrations decreased 3 h after C48/80 treatment. Gastric mucosal oxidized AA concentration remained unchanged after C48/80 treatment. Gastric mucosal NPSH concentration decreased 0.5 h after C48/80 treatment, but the decrease was recovered at 3 h. Gastric mucosal TBARS concentration and MPO activity increased 0.5 h after C48/80 treatment and further increased at 3 h. Serum total AA and reduced AA concentrations increased 0.5 h after C48/80 treatment and further increased at 3 h, while serum oxidized AA concentration increased at 0.5 h. Serum and gastric mucosal NOx concentrations increased 3 h after C48/80 treatment. AA administration to C48/80-treated rats at 0.5 h after the treatment prevented the gastric mucosal lesion progression and the changes in gastric mucosal total AA, reduced AA, vitamin E, adherent mucus, NOx, and TBARS concentrations and MPO activity and serum NOx concentration found at 3 h after the treatment dose-dependently. The AA administration to C48/80-treated rats caused further increases in serum total AA and reduced AA concentrations at 3 h after the treatment dose-dependently.
  
  
  CONCLUSIONS
  Gastric mucosal AA plays a critical role in the progression of C48/80-induced acute gastric mucosal lesions in rats.
authors.affiliation: Department of Internal Medicine, School of Medicine, Fujita Health University, Toyoake, Aichi 470-1192, Japan.
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Kamiya
authors.forename: Yoshiji
authors.initials: Y
authors.lastname: Ohta
authors.forename: Yoichiro
authors.initials: Y
authors.lastname: Imai
authors.forename: Tomiyasu
authors.initials: T
authors.lastname: Arisawa
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Nakano
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D001205:Ascorbic Acid / Q000097:blood*; D005753:Gastric Mucosa / Q000098:blood supply / Q000378:metabolism* / Q000473:pathology*; D005756:Gastritis / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology*; D008297:Male; D008833:Microcirculation / Q000187:drug effects / Q000502:physiology; D009093:Mucus / Q000378:metabolism; D009566:Nitrates / Q000378:metabolism; D009573:Nitrites / Q000378:metabolism; D010084:Oxidation-Reduction; D051381:Rats; D017208:Rats, Wistar; D012039:Regional Blood Flow / Q000187:drug effects / Q000502:physiology; D013438:Sulfhydryl Compounds / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D014810:Vitamin E / Q000494:pharmacology; D003189:p-Methoxy-N-methylphenethylamine
chemical_list: D000975:Antioxidants; D009566:Nitrates; D009573:Nitrites; D013438:Sulfhydryl Compounds; D017392:Thiobarbituric Acid Reactive Substances; D014810:Vitamin E; D003189:p-Methoxy-N-methylphenethylamine; D001205:Ascorbic Acid