title: [Studies on the influence of long-term doses of lipid peroxide generators on rat pancreas].
abstract: The role of oxygen derived free radicals or tissue lipid peroxides in the pathogenesis of chronic pancreatitis has not been established. To evaluate long-term effects of tissue lipid peroxides in the pathogenesis of chronic pancreatitis, we treated Wistar male rats with 2,2'-azo-bis-(2-amidino-propane) dihydrochloride (AAPH) and/or linoleic acid (LA) for 3 or 6 months. Rats were divided into eight groups. A: Saline-treated rats for 3 months as control, B: AAPH 40 mg/kgw intraperitoneally, twice a week for 3 months, C: LA 0.5 ml/kgw intraperitoneally, every other week for 3 months, D: AAPH and LA for 3 months, E: Saline-treated for 6 months, F: AAPH for 6 months, G: LA for 6 months, H: AAPH and LA for 6 months. The results were as follows: Lipid peroxide contents of the pancreas were elevated in groups: C, D, G and H. Histological examination revealed epithelial hyperplasia of large pancreatic ducts, vacuolization of ductal epithelium, intraepithelial neutrophilic infiltration, periductal mononuclear cell infiltration (ductulitis and peri-ductulitis), and sporadically in the lobules, destruction of acinar cells, neutrophilic infiltration and ductular proliferation in the same groups. These findings indicate that tissue damage was more severe in the pancreatic ducts than in the acinar cells, however no damage was seen in the endocrine pancreas. Vitamin E content of the pancreas was decreased in groups: B, C, D, F, G and H. Tissue glutathione peroxidase (GSH-Px) activity was increased in groups: D and H. Tissue catalase activity was increased in groups: D, G and H, but no change of superoxide dismutase (SOD) activity was seen in any of the groups. These results indicate that vitamin E may play the role of the main scavenger in the situation of a smaller dose of lipid peroxides, but when larger doses are administered, GSH-Px may play the main role as the scavenger in this experimental system.
authors.affiliation: First Department of Internal Medicine, Kochi Medical School.
authors.forename: T
authors.initials: T
authors.lastname: Nishioka
authors.forename: Y
authors.initials: Y
authors.lastname: Yamamoto
authors.forename: Y
authors.initials: Y
authors.lastname: Yamamoto
mesh_terms: D000578:Amidines / Q000009:adverse effects*; D000818:Animals; D002908:Chronic Disease; D016166:Free Radical Scavengers; D005609:Free Radicals; D005979:Glutathione Peroxidase / Q000502:physiology; D019787:Linoleic Acid; D008041:Linoleic Acids / Q000009:adverse effects*; D008054:Lipid Peroxides / Q000096:biosynthesis*; D008297:Male; D010179:Pancreas / Q000187:drug effects* / Q000378:metabolism; D010195:Pancreatitis / Q000378:metabolism / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar
chemical_list: D000578:Amidines; D016166:Free Radical Scavengers; D005609:Free Radicals; D008041:Linoleic Acids; D008054:Lipid Peroxides; C046728:2,2'-azobis(2-amidinopropane); D019787:Linoleic Acid; D005979:Glutathione Peroxidase