title: Lipid peroxidation and glutathione metabolism in chronic pancreatitis.
abstract: In experimental models of pancreatitis lipid peroxidation products are increased possibly because of an enhanced generation of oxygen radicals. The purpose of this study was to determine whether lipid peroxidation products are increased in pancreatic tissue and serum of patients suffering from chronic or acute pancreatitis. In 20 patients undergoing operative treatment for chronic (n = 11) and acute pancreatitis (n = 9) the levels of malondialdehyde, conjugated dienes, and reduced and oxidized glutathione were determined in resected tissue samples. The excised tissue was examined and evaluated by light microscopy. Shortly before operation the serum concentrations of malondialdehyde, alpha-amylase, and lipase were measured. Pancreatic tissue from eight organ donors who had no abdominal trauma or pancreatic disease served as control. In chronic pancreatitis, conjugated dienes as well as malondialdehyde concentrations in the tissue were significantly elevated. Reduced glutathione was significantly decreased, suggesting glutathione depletion due to oxidative stress. In acute pancreatitis only the tissue and serum malondialdehyde levels were significantly high, whereas conjugated dienes remained within the normal range. Serum malondialdehyde levels correlated significantly with tissue concentrations (r = 0.76; p < 0.05) but not with the clinical course or the enzyme levels. In chronic pancreatitis, the increased tissue levels of lipid peroxidation products and the changes in glutathione metabolism suggest ongoing peroxidation of lipids due to an enhanced generation of oxygen radicals. In hemorrhagic necrotizing pancreatitis, however, oxygen radical-induced lipid peroxidation cannot be proven. Apparently, other pathomechanisms are involved in the development of the severe tissue damage.
authors.affiliation: Department of Surgery, University of Ulm, Germany.
authors.forename: M H
authors.initials: MH
authors.lastname: Schoenberg
authors.forename: M
authors.initials: M
authors.lastname: Büchler
authors.forename: C
authors.initials: C
authors.lastname: Pietrzyk
authors.forename: W
authors.initials: W
authors.lastname: Uhl
authors.forename: D
authors.initials: D
authors.lastname: Birk
authors.forename: S
authors.initials: S
authors.lastname: Eisele
authors.forename: M
authors.initials: M
authors.lastname: Marzinzig
authors.forename: H G
authors.initials: HG
authors.lastname: Beger
mesh_terms: D000208:Acute Disease; D000328:Adult; D002908:Chronic Disease; D005978:Glutathione / Q000097:blood / Q000378:metabolism*; D006470:Hemorrhage / Q000209:etiology; D006801:Humans; D015227:Lipid Peroxidation / Q000502:physiology*; D008875:Middle Aged; D009336:Necrosis; D010179:Pancreas / Q000378:metabolism*; D010195:Pancreatitis / Q000150:complications / Q000378:metabolism* / Q000473:pathology
chemical_list: D005978:Glutathione