open access

Vol 47, No 2 (2009)
Original paper
Submitted: 2011-12-19
Published online: 2009-12-10
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Tryptophan metabolism in experimental necrotizing acute pancreatitis

Piotr Myśliwiec1, Hanna Myśliwiec2, Dariusz Pawlak34, Krystyna Pawlak35, Włodzimierz Buczko6, Marek Baltaziak7, Jacek Dadan1
DOI: 10.2478/v10042-009-0074-3
·
Folia Histochem Cytobiol 2009;47(2):231-236.
Affiliations
  1. I Department of General and Endocrinological Surgery University of Warmia and Mazury, Olsztyn, Poland
  2. Department of Dermatology and Venereology University of Warmia and Mazury, Olsztyn, Poland
  3. Department of Monitored Pharmacotherapy University of Warmia and Mazury, Olsztyn, Poland
  4. Department of Medical Science University of Warmia and Mazury, Olsztyn, Poland
  5. Department of Nephrology and Transplantology University of Warmia and Mazury, Olsztyn, Poland
  6. Department of Pharmacodynamics University of Warmia and Mazury, Olsztyn, Poland
  7. Department of Clinical Pathology, Medical University of Bialystok University of Warmia and Mazury, Olsztyn, Poland

open access

Vol 47, No 2 (2009)
ORIGINAL PAPERS
Submitted: 2011-12-19
Published online: 2009-12-10

Abstract

Pancreatic encephalopathy is a serious, often lethal complication of acute pancreatitis (AP). Its pathomechanism remains obscure. We have previously described increased blood levels of quinolinic acid (QUIN) – an endogeneous neurotoxine – during edematous experimental acute pancreatitis. Several other metabolites of tryptophan (TRP) are also known to be neuroactive. The aim of the present study was to assess tryptophan and its main metabolites: kynurenine (KYN), 3-hydroxykynurenine, quinolinic acid (QUIN), kynurenic acid (KYNA), serotonin (5HT) during experimental acute necrotizing acute pancreatitis. Experimental necrotizing acute pancreatitis was induced in rats by intraductal injection of 5% sodium taurocholate. Control groups consisted of sham-operated and not operated rats. The animals were sacrificed 5 and 24 hours after the operation. We evaluated -amylase, pancreas weight and histology as parameters of pancreatitis. A simplified neurological scoring system was applied. To assess TRP and its metabolites in plasma, we used high performance liquid chromatography. Five hours after the onset of AP we found significant increase in TRP metabolites: QUIN, KYNA, KYN, and 3HKYN in the plasma of animals with AP, as compared to the control group. When assessed 24 hours after induction of AP, those changes were no longer observed in blood. Instead, a decrease in TRP level appeared. Increase in plasma QUIN was associated with neurologic disturbances. In the present study we demonstrated transient activation of kynurenine pathway during early stages of experimental necrotizing AP, with increased blood levels of QUIN, KYNA, KYN, and 3HKYN and subsequent depletion of TRP. As some kynurenine derivatives, e.g. quinolinic acid, are endogenous toxins, they might contribute to neurologic and other organs disturbances during AP.

Abstract

Pancreatic encephalopathy is a serious, often lethal complication of acute pancreatitis (AP). Its pathomechanism remains obscure. We have previously described increased blood levels of quinolinic acid (QUIN) – an endogeneous neurotoxine – during edematous experimental acute pancreatitis. Several other metabolites of tryptophan (TRP) are also known to be neuroactive. The aim of the present study was to assess tryptophan and its main metabolites: kynurenine (KYN), 3-hydroxykynurenine, quinolinic acid (QUIN), kynurenic acid (KYNA), serotonin (5HT) during experimental acute necrotizing acute pancreatitis. Experimental necrotizing acute pancreatitis was induced in rats by intraductal injection of 5% sodium taurocholate. Control groups consisted of sham-operated and not operated rats. The animals were sacrificed 5 and 24 hours after the operation. We evaluated -amylase, pancreas weight and histology as parameters of pancreatitis. A simplified neurological scoring system was applied. To assess TRP and its metabolites in plasma, we used high performance liquid chromatography. Five hours after the onset of AP we found significant increase in TRP metabolites: QUIN, KYNA, KYN, and 3HKYN in the plasma of animals with AP, as compared to the control group. When assessed 24 hours after induction of AP, those changes were no longer observed in blood. Instead, a decrease in TRP level appeared. Increase in plasma QUIN was associated with neurologic disturbances. In the present study we demonstrated transient activation of kynurenine pathway during early stages of experimental necrotizing AP, with increased blood levels of QUIN, KYNA, KYN, and 3HKYN and subsequent depletion of TRP. As some kynurenine derivatives, e.g. quinolinic acid, are endogenous toxins, they might contribute to neurologic and other organs disturbances during AP.

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Keywords

acute pancreatitis; tryptophan; kynurenine; 3-hydroxykynurenine; kynurenic acid; quinolinic acid; serotonin

About this article
Title

Tryptophan metabolism in experimental necrotizing acute pancreatitis

Journal

Folia Histochemica et Cytobiologica

Issue

Vol 47, No 2 (2009)

Article type

Original paper

Pages

231-236

Published online

2009-12-10

DOI

10.2478/v10042-009-0074-3

Bibliographic record

Folia Histochem Cytobiol 2009;47(2):231-236.

Keywords

acute pancreatitis
tryptophan
kynurenine
3-hydroxykynurenine
kynurenic acid
quinolinic acid
serotonin

Authors

Piotr Myśliwiec
Hanna Myśliwiec
Dariusz Pawlak
Krystyna Pawlak
Włodzimierz Buczko
Marek Baltaziak
Jacek Dadan

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