Increased expression of glutathione s-transferase-π in the islets of patients with primary chronic pancreatitis but not secondary chronic pancreatitis

Alexis B. Ulrich, Bruno M. Schmied, Hosei Matsuzaki, Terence A. Lawson, Helmut Friess, Ke Andren-Sandberg, Markus W. Büchler, Parviz M. Pour

Research output: Contribution to journalArticlepeer-review

17 Scopus citations

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-π (GST-π), 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-π 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-π 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-π 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-π, and lend support to the hypothesis of oxidative stress as the cause of CP.

Original languageEnglish (US)
Pages (from-to)388-394
Number of pages7
JournalPancreas
Volume22
Issue number4
DOIs
StatePublished - 2001

Keywords

  • GST-π
  • Oxidative stress
  • Primary chronic pancreatitis
  • Secondary chronic pancreatitisπ

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism
  • Hepatology
  • Endocrinology

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