title: Increased expression of glutathione S-transferase-pi in the islets of patients with primary chronic pancreatitis but not secondary chronic pancreatitis.
abstract: The mechanism of tissue alteration in chronic pancreatitis (CP) is still unclear. Different hypotheses have been discussed, including increasing oxidant stress in the acinar cells, often as a result of exposure to xenobiotics. To evaluate the role of oxidative stress in CP, the authors investigated the expression of the drug-metabolizing phase II enzyme, glutathione S-transferase-pi (GST-pi), in the pancreatic tissue of patients with CP and compared it with the healthy pancreatic tissue from age-matched donors. Pancreatic tissue from patients with secondary CP resulting from ductal obstruction by pancreatic cancer (PC) was also examined. The percentage of cells immunoreacting with anti-GST-pi was counted within 15 randomly selected islets in each slide of the three groups. In all specimens, ductal and ductular cells, and in PC, cancer cells, expressed GST-pi in a moderate intensity. Acinar cells did not stain. Various numbers of islet cells in each of the three groups were stained strongly. More islet cells expressed GST-pi in CP (42%) than in healthy pancreatic tissue (16%, p < 0.001) or PC (17%, p < 0.001). Our results imply an important role of islet cells in the metabolism of substances, which are the substrate for GST-pi, and lend support to the hypothesis of oxidative stress as the cause of CP.
authors.affiliation: UNMC Eppley Cancer Center, University of Nebraska Medical Center, Omaha 68198-6805, USA.
authors.forename: A B
authors.initials: AB
authors.lastname: Ulrich
authors.forename: B M
authors.initials: BM
authors.lastname: Schmied
authors.forename: H
authors.initials: H
authors.lastname: Matsuzaki
authors.forename: T A
authors.initials: TA
authors.lastname: Lawson
authors.forename: H
authors.initials: H
authors.lastname: Friess
authors.forename: A
authors.initials: A
authors.lastname: Andrén-Sandberg
authors.forename: M W
authors.initials: MW
authors.lastname: Büchler
authors.forename: P M
authors.initials: PM
authors.lastname: Pour
mesh_terms: D000911:Antibodies, Monoclonal; D002908:Chronic Disease; D005260:Female; D005982:Glutathione Transferase / Q000032:analysis*; D006801:Humans; D007150:Immunohistochemistry; D007515:Islets of Langerhans / Q000201:enzymology*; D007527:Isoenzymes / Q000032:analysis*; D008297:Male; D018384:Oxidative Stress; D010179:Pancreas / Q000201:enzymology; D010190:Pancreatic Neoplasms / Q000201:enzymology; D010195:Pancreatitis / Q000201:enzymology* / Q000209:etiology*
chemical_list: D000911:Antibodies, Monoclonal; D007527:Isoenzymes; D005982:Glutathione Transferase