Quinolinic acid: a modulator of the heart calcium channel in the rat and a binder of calcium ions

Beskid, M; Finkiewicz-Murawiejska, L; Obmiński, Zbigniew; Wolska, Beata M.

doi:10.1016/s0232-1513(11)80007-1

Cited by 11 publications

(4 citation statements)

References 10 publications

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“…This might aggravate the detrimental effect of free oxygen species reported in AP [18]. Other actions of QUIN include cardiac contractility impairment, probably by modulation of heart calcium channel [25] and the inhibition of erythropoiesis [26].…”

Section: Discussionmentioning

confidence: 99%

Combined perioperative plasma endoglin and VEGF--a assessment in colorectal cancer patients.

Myśliwiec

Pawlak

Kukliński³

et al. 2009

Folia Histochem Cytobiol.

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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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Section: Discussionmentioning

confidence: 99%

Combined perioperative plasma endoglin and VEGF--a assessment in colorectal cancer patients.

Myśliwiec

Pawlak

Kukliński³

et al. 2009

Folia Histochem Cytobiol.

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show abstract

“…However, local accumulation of kynurenine metabolites, in particular, quinolinic acid, following IDO induction may also represent a potentially detrimental event. In fact, quinolinic acid is a potent excitotoxin, and its overproduction has been linked to neuronal damage occurring in brain inflammation (17), initiation of lipid peroxidation (33), and other conditions (3,42). Indeed, quinolinic acid concentration was significantly increased by T. gondii infection (S. Fujigaki and K. Saito, unpublished observation).…”

Section: Discussionmentioning

confidence: 99%

l-Tryptophan-l-Kynurenine Pathway Metabolism Accelerated byToxoplasmagondiiInfection Is Abolished in Gamma Interferon-Gene-Deficient Mice: Cross-Regulation between Inducible Nitric Oxide Synthase and Indoleamine-2,3-Dioxygenase

et al. 2002

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“…In this context, induction of IDO might serve a useful purpose, and further studies on its potentially beneficial roles are warranted. Conversely, accumulated pathophysiologically active kynurenine pathway metabolites following IDO induction may have detrimental consequences for the body, including neurotoxicity, inhibition of gluconeogenesis, reduction of cardiac contractility, and initiation of lipid peroxidation [9,[25][26][27]. A reduction in L-TRP availability might also impair the synthesis of proteins and indoleamines such as serotonin.…”

Section: Discussionmentioning

confidence: 99%

Lipopolysaccharide induction of indoleamine 2,3-dioxygenase is mediated dominantly by an IFN-γ-independent mechanism

et al. 2001

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Quinolinic acid: a modulator of the heart calcium channel in the rat and a binder of calcium ions

Cited by 11 publications

References 10 publications

Combined perioperative plasma endoglin and VEGF--a assessment in colorectal cancer patients.

Combined perioperative plasma endoglin and VEGF--a assessment in colorectal cancer patients.

l-Tryptophan-l-Kynurenine Pathway Metabolism Accelerated byToxoplasmagondiiInfection Is Abolished in Gamma Interferon-Gene-Deficient Mice: Cross-Regulation between Inducible Nitric Oxide Synthase and Indoleamine-2,3-Dioxygenase

Lipopolysaccharide induction of indoleamine 2,3-dioxygenase is mediated dominantly by an IFN-γ-independent mechanism

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