title: Role of lipid peroxidation and antioxidants in gastric mucosal injury induced by the hypoxanthine-xanthine oxidase system in rats.
abstract: Free radical-induced gastric mucosal injury was caused by severe depletion of glutathione and alpha-tocopherol. Intravenous infusion of hypoxanthine (HX) via the jugular vein and local intra-arterial infusion of xanthine oxidase (XO) via the left gastric artery caused marked gastric mucosal injury in the antrum and the corpus. This study was performed to determine whether antioxidants in the gastric mucosa are mobilized during oxidative stress in the rat stomach. The level of thiobarbituric acid (TBA) reactive substance in the gastric mucosa was not significantly changed. The levels of total glutathione and alpha-tocopherol in the gastric mucosa significantly decreased. Total superoxide dismutase (Cu/Zn-and Mn-SOD) and glutathione peroxidase activities were not significantly changed. Administration of SOD reversed the glutathione level but not the alpha-tocopherol level in the gastric mucosa. To determine the role of glutathione and alpha-tocopherol in oxidative stress, the stomach was removed from a normal, alpha-tocopherol supplemented, and glutathione-depleted rat and used for experimentation. Frozen slices of the rat stomach were infused with HX-XO then examined histochemically using cold Schiff's reagent for signs of lipid peroxidation. It was found that the alpha-tocopherol supplemented stomach inhibited lipid peroxidation induced by HX-XO. Biochemical measurements and histochemical examination showed that the glutathione-depleted frozen tissue section and the homogenate had increased by lipid peroxidation induced by HX-XO. These findings suggested that alpha-tocopherol and glutathione may play a role in protecting the gastric mucosa against oxygen free radicals.
authors.affiliation: First Department of Internal Medicine, Kyoto Prefectural University of Medicine, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Yoshikawa
authors.forename: Y
authors.initials: Y
authors.lastname: Minamiyama
authors.forename: H
authors.initials: H
authors.lastname: Ichikawa
authors.forename: S
authors.initials: S
authors.lastname: Takahashi
authors.forename: Y
authors.initials: Y
authors.lastname: Naito
authors.forename: M
authors.initials: M
authors.lastname: Kondo
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D005609:Free Radicals / Q000378:metabolism; D005753:Gastric Mucosa / Q000187:drug effects / Q000293:injuries* / Q000378:metabolism*; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D006651:Histocytochemistry; D019271:Hypoxanthine / Q000633:toxicity; D015227:Lipid Peroxidation / Q000187:drug effects / Q000502:physiology*; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D014810:Vitamin E / Q000378:metabolism; D014969:Xanthine Oxidase / Q000633:toxicity
chemical_list: D000975:Antioxidants; D005609:Free Radicals; D017382:Reactive Oxygen Species; D017392:Thiobarbituric Acid Reactive Substances; D014810:Vitamin E; D019271:Hypoxanthine; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D014969:Xanthine Oxidase; D005978:Glutathione