(HOME) Subject: iron/pancreas

   
   Exp Mol Pathol 1997 Apr;64(2):90-102
   
Iron overload in the rat pancreas following portacaval shunting and dietary
iron supplementation.

    Horne WI, Tandler B, Dubick MA, Niemela O, Brittenham GM, Tsukamoto H
    
   Department of Medicine, Case Western Reserve University, MetroHealth
   Medical Center, Cleveland, Ohio 44109, USA.
   
   Reproduction of pancreatic iron overload in an animal model has been
   difficult to achieve primarily because of the first-pass extraction of
   iron by the liver. We hypothesized that portacaval shunting would
   avoid this hepatic phenomenon and increase pancreatic iron deposition.
   An end-to-side portacaval shunt was surgically created in male
   Sprague-Dawley rats, and they were subsequently fed a carbonyl
   iron-supplemented diet for 17 weeks. This resulted in marked iron
   accumulation in the pancreas (1621 +/- 188 micrograms/g) compared to
   minimal deposition in sham-operated rats fed the same diet (138 +/- 53
   micrograms/g). Iron deposition in the acinar and centroacinar cells
   was confirmed histologically by Gomori staining, as well as by
   ultrastructural examination. Iron overloading was associated with
   enhanced oxidative stress evidenced by a twofold increase in the
   levels of glutathione disulfide and thiobarbituric acid-reactive
   substances. Also, adducts of proteins with malondialdehyde and
   4-hydroxynonenal were demonstrated in acinar and ductal cells. Other
   apparent consequences of iron overload were a 50% reduction in
   pancreatic amylase content and a decrease in pancreatic protein
   concentration. These hypotrophic changes were associated with a
   reduced mass of zymogen granules in the acinar cells noted
   histologically. Our results show that a combination of portacaval
   shunting and carbonyl iron feeding achieve pancreatic iron overload
   and support the role of oxidative stress in the pathogenesis of
   iron-induced damage in the pancreas.
   
   PMID: 9316587, UI: 97462317
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