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Influence of dietary factors on the pancreatotoxicity of ethionine.

Abstract
Choline deficiency enhances greatly the pancreatotoxicity of DL-ethionine. Mice fed DL-ethionine with a choline-deficient diet develop a fatal acute hemorrhagic pancreatic necrosis with fat necrosis (AHPN) in 5 days. Induction of the AHPN is completely prevented by dietary methionine and drastically reduced by dietary methionine and drastically reduced by dietary choline. The amount of proteins, carbohydrates, and fat in the diet influences its consumption by the animals and thus the severity of the pancreatic pathology. The histogenesis of the process is characterized by widespread alterations of the membranous organelles of the acinar cells, especially the endoplasmic reticulum and the zymogen granules. The onset of the hemorrhagic necrosis of the pancreas is due to an endogenous intraparenchymal activation of the zymogenic proteases, including proelastase. The new experimental model of AHPN appears to mimic very closely the clinical course, the anatomic pathologic lesions, and the postulated pathogenesis of the corresponding human disease.
AuthorsB Lombardi
JournalThe American journal of pathology (Am J Pathol) Vol. 84 Issue 3 Pg. 633-48 (Sep 1976) ISSN: 0002-9440 [Print] United States
PMID786037 (Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S., Review)
Chemical References
  • Enzyme Precursors
  • Phosphatidylcholines
  • Methionine
  • Ethionine
Topics
  • Acute Disease
  • Age Factors
  • Animals
  • Choline Deficiency (complications)
  • Diet
  • Disease Models, Animal
  • Enzyme Precursors (metabolism)
  • Ethionine (adverse effects)
  • Female
  • Hemorrhage (etiology, pathology)
  • Humans
  • Male
  • Methionine (metabolism)
  • Necrosis
  • Pancreas (drug effects, pathology)
  • Pancreatitis (etiology, pathology)
  • Phosphatidylcholines (biosynthesis)
  • Sex Factors

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