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Antioxid Redox Signal. 2011 Nov 15;15(10):2669-81. doi: 10.1089/ars.2011.4065. Epub 2011 Jul 18.

The crucial role of early mitochondrial injury in L-lysine-induced acute pancreatitis.

Author information

1
First Department of Medicine, University of Szeged, Szeged, Hungary.

Abstract

AIMS:

Large doses of intraperitoneally injected basic amino acids, L-arginine, or L-ornithine, induce acute pancreatitis in rodents, although the mechanisms mediating pancreatic toxicity remain unknown. Another basic amino acid, L-lysine, was also shown to cause pancreatic acinar cell injury. The aim of the study was to get insight into the mechanisms through which L-lysine damages the rat exocrine pancreas, in particular to characterize the kinetics of L-lysine-induced mitochondrial injury, as well as the pathologic responses (including alteration of antioxidant systems) characteristic of acute pancreatitis.

RESULTS:

We showed that intraperitoneal administration of 2 g/kg L-lysine induced severe acute necrotizing pancreatitis. L-lysine administration caused early pancreatic mitochondrial damage that preceded the activation of trypsinogen and the proinflammatory transcription factor nuclear factor-κB (NF-κB), which are commonly thought to play an important role in the development of acute pancreatitis. Our data demonstrate that L-lysine impairs adenosine triphosphate synthase activity of isolated pancreatic, but not liver, mitochondria.

INNOVATION AND CONCLUSION:

Taken together, early mitochondrial injury caused by large doses of L-lysine may lead to the development of acute pancreatitis independently of pancreatic trypsinogen and NF-κB activation.

PMID:
21644850
PMCID:
PMC4701124
DOI:
10.1089/ars.2011.4065
[Indexed for MEDLINE]
Free PMC Article

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