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Academic literature on the topic 'Quinolinic acid'

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Published: 4 June 2021
Last updated: 31 January 2023

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Journal articles on the topic "Quinolinic acid"

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Sundberg, Markku, Rolf Uggla, Reijo Sillanpää, Krzysztof Zborowski, Angel Sánchez-González, Jorma Matikainen, Seppo Kaltia, and Tapio Hase. "Adduct formed by chromium trioxide and zwitterionic quinolinic acid." Open Chemistry 8, no. 3 (June 1, 2010): 486–93. http://dx.doi.org/10.2478/s11532-010-0033-z.

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AbstractChromium trioxide forms an adduct with zwitterionic quinolinic acid. The structure of the product was found to be (quinolinium-3-carboxylato-O)trioxidochromium(VI), determined by single-crystal X-ray diffraction methods. To evaluate the bonding properties of the compound, its structure was optimized at the B3LYP/6-311G* level of theory. The electronic characteristics were investigated by topological methods applied to the total charge density in various model compounds including the title compound, title compound with a HF molecule presenting a hydrogen bonding and anionic moiety. Calculated aromaticity indices indicate that the quinolinic rings tend to conserve their degree of aromaticity against hydrogen bonding. However, when there is hydrogen bonding involving an N-H bond or when the quinolinium zwitterion is deprotonated, there are clear changes in the interaction between chromium trioxide and the quinolinic moiety.
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Heyes, Melvyn P., and Thaddeus S. Nowak. "Delayed Increases in Regional Brain Quinolinic Acid Follow Transient Ischemia in the Gerbil." Journal of Cerebral Blood Flow & Metabolism 10, no. 5 (September 1990): 660–67. http://dx.doi.org/10.1038/jcbfm.1990.119.

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Excessive activity or release of excitatory amino acids has been implicated in the neuronal injury that follows transient cerebral ischemia. To investigate the metabolism of the endogenous excitotoxin, quinolinic acid, and its potential for mediating cell loss following ischemia, the concentrations of quinolinic acid, L-tryptophan, 5-hydroxytryptamine, and 5-hydroxyindoleacetic acid were quantified in gerbil brain regions at different times after 5 or 15 min of ischemia induced by bilateral carotid artery occlusion. Significant elevation of brain tryptophan levels, accompanied by increased 5-hydroxyindoleacetic acid concentrations, occurred during the first several hours of recirculation, but regional brain quinolinic acid concentrations were found either to decrease or remain unchanged during the first 24 h after the ischemic insult. However, significant increases in quinolinic acid concentrations occurred in striatum and hippocampus at 2 days of recirculation after 5 min of ischemia. After a further 4 and 7 days, strikingly large increases in quinolinic acid concentrations were observed in all regions examined, with the highest levels observed in the hippocampus and striatum, regions that also show the most severe ischemic injury. These delayed increases in brain quinolinic acid concentrations are suggested to reflect the presence of activated macrophages, reactive astrocytes, and/or microglia in vulnerable regions during and subsequent to ischemic injury. While the results do not support a role for increased quinolinic acid concentrations in early excitotoxic neuronal damage, the role of the delayed increases in brain quinolinic acid in the progression of postischemic injury and its relevance to postischemic brain function remain to be established.
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Guillemin, Gilles J. "Quinolinic acid: neurotoxicity." FEBS Journal 279, no. 8 (March 27, 2012): 1355. http://dx.doi.org/10.1111/j.1742-4658.2012.08493.x.

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HEYES, Melvyn P., Cristian L. ACHIM, Clayton A. WILEY, Eugene O. MAJOR, Kuniaki SAITO, and Sanford P. MARKEY. "Human microglia convert l-tryptophan into the neurotoxin quinolinic acid." Biochemical Journal 320, no. 2 (December 1, 1996): 595–97. http://dx.doi.org/10.1042/bj3200595.

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Immune activation leads to accumulations of the neurotoxin and kynurenine pathway metabolite quinolinic acid within the central nervous system of human patients. Whereas macrophages can convert l-tryptophan to quinolinic acid, it is not known whether human brain microglia can synthesize quinolinic acid. Human microglia, peripheral blood macrophages and cultures of human fetal brain cells (astrocytes and neurons) were incubated with [13C6]l-tryptophan in the absence or presence of interferon γ. [13C6]Quinolinic acid was identified and quantified by gas chromatography and electron-capture negative-chemical ionization mass spectrometry. Both l-kynurenine and [13C6]quinolinic acid were produced by unstimulated cultures of microglia and macrophages. Interferon γ, an inducer of indoleamine 2,3-dioxygenase, increased the accumulation of l-kynurenine by all three cell types (to more than 40 µM). Whereas large quantities of [13C6]quinolinic acid were produced by microglia and macrophages (to 438 and 1410 nM respectively), minute quantities of [13C6]quinolinic acid were produced in human fetal brain cultures (not more than 2 nM). Activated microglia and macrophage infiltrates into the brain might be an important source of accelerated conversion of l-tryptophan into quinolinic acid within the central nervous system in inflammatory diseases.
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Sinz, Elizabeth H., Patrick M. Kochanek, Melvyn P. Heyes, Stephen R. Wisniewski, Michael J. Bell, Robert S. B. Clark, Steven T. DeKosky, Andrew R. Blight, and Donald W. Marion. "Quinolinic Acid is Increased in CSF and Associated with Mortality after Traumatic Brain Injury in Humans." Journal of Cerebral Blood Flow & Metabolism 18, no. 6 (June 1998): 610–15. http://dx.doi.org/10.1097/00004647-199806000-00002.

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We tested the hypothesis that quinolinic acid, a tryptophan-derived N-methyl-d-aspartate agonist produced by macrophages and microglia, would be increased in CSF after severe traumatic brain injury (TBI) in humans, and that this increase would be associated with outcome. We also sought to determine whether therapeutic hypothermia reduced CSF quinolinic acid after injury. Samples of CSF ( n = 230) were collected from ventricular catheters in 39 patients (16 to 73 years old) during the first week after TBI, (Glasgow Coma Scale [GCS] < 8). As part of an ongoing study, patients were randomized within 6 hours after injury to either hypothermia (32°C) or normothermia (37°C) treatments for 24 hours. Oth-erwise, patients received standard neurointensive care. Quinolinic acid was measured by mass spectrometry. Univariate and multivariate analyses were used to compare CSF quinolinic acid concentrations with age, gender, GCS, time after injury, mortality, and treatment (hypothermia versus normothermia). Quinolinic acid concentration in CSF increased maximally to 463 ± 128 nmol/L (mean ± SEM) at 72 to 83 hours after TBI. Normal values for quinolinic acid concentration in CSF are less than 50 nmol/L. Quinolinic acid concentration was increased 5-to 50-fold in many patients. There was a powerful association between time after TBI and increased quinolinic acid ( P < 0.00001), and quinolinic acid was higher in patients who died than in survivors ( P = 0.003). Age, gender, GCS, and treatment (32°C versus 37°C) did not correlate with CSF quinolinic acid. These data reveal a large increase in quinolinic acid concentration in CSF after TBI in humans and raise the possibility that this macrophage-derived excitotoxin may contribute to secondary damage.
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Ohashi, Kazuto, Shigeyuki Kawai, and Kousaku Murata. "Secretion of Quinolinic Acid, an Intermediate in the Kynurenine Pathway, for Utilization in NAD + Biosynthesis in the Yeast Saccharomyces cerevisiae." Eukaryotic Cell 12, no. 5 (March 1, 2013): 648–53. http://dx.doi.org/10.1128/ec.00339-12.

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ABSTRACT NAD + is synthesized from tryptophan either via the kynurenine ( de novo ) pathway or via the salvage pathway by reutilizing intermediates such as nicotinic acid or nicotinamide ribose. Quinolinic acid is an intermediate in the kynurenine pathway. We have discovered that the budding yeast Saccharomyces cerevisiae secretes quinolinic acid into the medium and also utilizes extracellular quinolinic acid as a novel NAD + precursor. We provide evidence that extracellular quinolinic acid enters the cell via Tna1, a high-affinity nicotinic acid permease, and thereby helps to increase the intracellular concentration of NAD + . Transcription of genes involved in the kynurenine pathway and Tna1 was increased, responding to a low intracellular NAD + concentration, in cells bearing mutations of these genes; this transcriptional induction was suppressed by supplementation with quinolinic acid or nicotinic acid. Our data thus shed new light on the significance of quinolinic acid, which had previously been recognized only as an intermediate in the kynurenine pathway.
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Niwa, Toshlmitsu, Hldeo Yoshizumi, Yutaka Emoto, Takashl Miyazaki, Naosuml Hashimoto, Naohfto Takeda, Akira Tatematsu, and Kenji Maeda. "Accumulation of quinolinic acid in uremic serum and its removal by hemodialysis." Clinical Chemistry 37, no. 2 (February 1, 1991): 159–61. http://dx.doi.org/10.1093/clinchem/37.2.159.

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Abstract Quinolinic acid was first identified in uremic serum by use of gas chromatography/mass spectrometry. Quantification by selected ion monitoring revealed that the serum concentration of quinolinic acid was markedly increased in chronic hemodialysis patients, and that the acid could be removed by conventional hemodialysis. The serum concentration of quinolinic acid was weakly but significantly correlated with the serum uric acid concentration. Accumulation of quinolinic acid in uremic blood may be involved in the pathogenesis of anemia, suppressed immune system, and uremic encephalopathy.
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HEYES, MELVYN P. "Quinolinic Acid and Inflammation." Annals of the New York Academy of Sciences 679, no. 1 Markers of Ne (May 1993): 211–16. http://dx.doi.org/10.1111/j.1749-6632.1993.tb18300.x.

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Saito, K., C. Y. Chen, M. Masana, J. S. Crowley, S. P. Markey, and M. P. Heyes. "4-Chloro-3-hydroxyanthranilate, 6-chlorotryptophan and norharmane attenuate quinolinic acid formation by interferon-γ-stimulated monocytes (THP-1 cells)." Biochemical Journal 291, no. 1 (April 1, 1993): 11–14. http://dx.doi.org/10.1042/bj2910011.

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Accumulation of quinolinic acid and L-kynurenine occurs in the brain and/or blood following immune activation, and may derive from L-tryptophan following induction of indoleamine 2,3-dioxygenase and other kynurenine-pathway enzymes. In the present study a survey of various cell lines derived from either brain or systemic tissues showed that, while all cells examined responded to interferon-gamma by increased conversion of L-[13C6]tryptophan into L-kynurenine (human: B-lymphocytes, neuroblastoma, glioblastoma, lung, liver, kidney; rat brain: microglia, astrocytes and oligodendrocytes), only macrophage-derived cells (peripheral-blood mononuclear cells; THP-1, U-937) and certain liver cells (SKHep1) synthesized [13C6]quinolinic acid. Tumour necrosis factor-alpha enhanced the effects of interferon-gamma in THP-1 cells. Norharmane, 6-chloro-DL-tryptophan and 4-chloro-3-hydroxyanthranilate attenuated quinolinic acid formation by THP-1 cells with IC50 values of 51 microM, 58 microM and 0.11 microM respectively. Norharmane and 6-chloro-DL-tryptophan attenuated L-kynurenine formation with IC50 values of 43 microM and 51 microM respectively, whereas 4-chloro-3-hydroxyanthranilate had no effect on L-kynurenine accumulation. The reductions in L-kynurenine and quinolinic acid formation are consistent with the reports that norharmane is an inhibitor of indoleamine 2,3-dioxygenase, 6-chloro-DL-tryptophan is metabolized through the kynurenine pathway, and 4-chloro-3-hydroxyanthranilate is an inhibitor of 3-hydroxyanthranilate 3,4-dioxygenase. These results suggest that many tissues may contribute to the production of L-kynurenine following indoleamine 2,3-dioxygenase induction and immune activation. Quinolinic acid may be directly synthesized from L-tryptophan in both macrophages and certain types of liver cells, although uptake of quinolinic acid precursors from blood may contribute to quinolinic acid synthesis in cells that cannot convert L-kynurenine into quinolinic acid.
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Heyes, Melvyn P. "Hypothesis: A Role for Quinolinic Acid in the Neuropathology of Glutaric Aciduria Type I." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 14, S3 (August 1987): 441–43. http://dx.doi.org/10.1017/s0317167100037872.

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ABSTRACT:Glutaric aciduria type I is an autosomal recessive metabolic disorder of children associated with severe dystonic motor disturbances and degeneration in the cerebral cortex, striatum and cerebellum. Biochemical studies demonstrate a deficiency in the enzyme glutaryl-CoA dehydrogenase. This enzyme metabolizes substrate derived from dietary tryptophan that could otherwise be converted to quinolinic acid within the brain. The law of mass action predicts that the production of quinolinic acid should be increased in glutaric aciduria type I. Quinolinic acid is a potent neurotoxin and convulsant when it is injected into the central nervous system of experimental animals. This paper argues that quinolinic acid may accumulate within the brain and cause the neuropathology of glutaric aciduria type I.
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Dissertations / Theses on the topic "Quinolinic acid"

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Allsebrook, Andrew M. "QPRTase : quinolinic acid analogue synthesis and non-enzymic decarboxylation of N-alkylquinolinic acids." Thesis, University of St Andrews, 1998. http://hdl.handle.net/10023/14376.

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Quinolinate phosphoribosyltransferase (QPRTase, E.C. 2.4.2.19) is considered to be a unique enzyme in that it is thought to catalyse two distinct chemical reactions. Both the transfer of a phosphoribosyl group from 5-phosphoribosyl-1- pyrophosphate onto the nitrogen of quinolinic acid and the subsequent decarboxylation of the intermediate to form nicotinic acid mononucleotide are thought to be catalysed by the QPRTase system. Analogues of quinolinic acid were designed as potential inhibitors of QPRTase. These contain acidic groups at the 2- and 3- positions but are unable to decarboxylate. However, such compounds may be able to undergo the phosphoribosyl transfer reaction, potentially increasing their inhibitory potency. These compounds may be useful as "biological tools" allowing the neurological effects of an increase in quinolinic acid levels to be investigated. The compounds may show anti-fungal activity blocking the kynurenine pathway for NAD production. 2-Sulfonicotinic acid was synthesised by the oxidation of 2-mercaptonicotinic acid by either basic potassium permanganate, or iodine, with the structure was confirmed by X-ray crystallography. In biological testing the acid was shown to be neither an agonist nor antagonist of the NMDA receptor, or to be neurotoxic. A number of synthetic routes towards 2-phosphononicotinic acid, an alternative quinolinic acid analogue, were attempted though none were successful. These included orthometallation strategies and palladium coupling reactions to incorporate the phosphonic acid group at the 2- position. Nucleophilic addition routes, methods of building up the pyridine ring and including non-selective phosphonic acid addition were also examined. However, a related derivative, 2-(phosphonomethyl)nicotinic acid, was successfully synthesised. The non-enzymic decarboxylation of N-alkyl quinolinic acids was investigated, for comparison with the decarboxylation reaction catalysed by QPRTase. Both N- methyl and N-ethylquinolinic acid were synthesised, and the pH versus rate profiles measured. The rate maximum for both compounds was at pH 1.5, with the rate decreasing both above and below the maximum. N-Methylquinolinic acid was 10 times faster than quinolinic acid itself, demonstrating the effect of the nitrogen substituent. The N-ethyl derivative decarboxylated a further 1.5 times faster, showing the effect of increasing the size of the substituent. An Arrhenius plot was also carried out, giving an activation energy for the reaction of 153 kJ mol-1. Attempts to prepare the N-propyl derivative were unsuccessful, as decarboxylation occurred very readily to give N- propylnicotinic acid.
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Miranda, Allan F. "Modulation of quinolinic acid-induced excitotoxicity by endogenous kynurenine pathway intermediates." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/nq22484.pdf.

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Urenjak, Jutta A., and Tihomir P. Obrenovitch. "Accumulation of quinolinic acid with euro-inflammation: does it mean excitotoxicity?" Thesis, Kluwer Academic, Plenum Publishers, New York, 2003. http://hdl.handle.net/10454/2833.

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Morgan, Elaine M. "The role of nitric oxide in N-methyl-D-aspartate receptor-mediated neurotoxicity." Thesis, University of Southampton, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.243084.

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Catton, Gemma R. "Mechanistic studies on quinolinate phosphoribosyltransferase /." St Andrews, 2007. http://hdl.handle.net/10023/485.

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Kariyawasam, Sandhya Himani. "An investigation into the biochemical changes in Tourette syndrome and associated conditions with a potential for pharmacological manipulation." Thesis, Aston University, 1999. http://publications.aston.ac.uk/10977/.

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Kynurenine (KYN) is the first stable metabolite of the kynurenine pathway, which accounts for over 95% of tryptophan metabolism. Two previous studies by this research group reported elevated plasma KYN in Tourette syndrome (TS) patients when compared with age and sex matched controls and another study showed that KYN potentiated 5-HT2A-mediated head-shakes (HS) in rodents. These movements have been suggested to model tics in TS. This raised the questions how KYN acts in eliciting this response and whether it is an action of its own or of a further metabolite along the kynurenine pathway. In the liver, where most of the kynurenine pathway metabolism takes place under physiological conditions, the first and the rate limiting enzyme is tryptophan-dioxygenase (TDO) which can be induced by cortisol. In extrahepatic tissues the same step of the pathway is catalyzed by indoleamine-dioxygenase (IDO), which is induced by cytokines, predominantly interferon-y (INF-y). Plasma neopterin, which shows parallel increase with KYN following immune stimulation, was also found elevated in one of these studies positively correlating with KYN. In the present work animal studies suggested that KYN potentiates and quinolinic acid (QUINA) dose dependently inhibits the 5-HT2A-mediated HS response in mice. The potentiating effect seen with KYN was suggested to be an effect of KYN itself. Radioligand binding and phosphoinositide (PI) hydrolysis studies were done to explore the mechanisms by which kynurenine pathway metabolites could alter a 5-HT2A-receptor mediated response. None of the kynurenine pathway metabolites tested showed direct binding to 5-HT2A-receptors. PI hydrolysis studies with KYN and QUINA showed that KYN did not have any effect while QUINA inhibited 5-HT2A-mediated PI hydrolysis. Plasma cortisol determination in TS patients with elevated plasma KYN did not show elevated plasma cortisol levels, suggesting that the increase of plasma KYN in these TS patients is unlikely to be due to an increased TDO activity induced by increased cortisol. Attention deficit hyperactivity disorder (ADHD) is commonly associated with TS. Salivary cortisol detected in a group of children primarily affected with ADHD showed significantly lower salivary cortisol levels when compared with age and sex matched controls. Plasma tryptophan, KYN, neopterin, INF-y and KYN/tryptophan ratio and night-time urinary 6-sulphatoxymelatonin (aMT6s) excretion measured in a group of TS patients did not show any difference in their levels when compared with age and sex matched controls, but TS patients failed to show the expected positive correlation seen between plasma INF-y, neopterin and KYN and the negative correlation seen between plasma KYN and night-time urinary aMT6s excretion seen in healthy controls. The relevance of the kynurenine pathway, melatonin secretion and cortisol to Tourette Syndrome and associated conditions and the mechanism by which KYN and QUINA alter the 5-HT2A-receptor mediated HS response are discussed.
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Heron, Paula Michelle. "An investigation of the neuroprotective effects of estrogen in a model of quinolinic acid-induced neurodegeneration." Thesis, Rhodes University, 2002. http://hdl.handle.net/10962/d1003237.

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The hippocampus, located in the medial temporal lobe, is an important region of the brain responsible for the formation of memory. Thus, any agent that induces stress in this area has detrimental effects and could lead to various types of dementia. Such agents include the neurotoxin, Quinolinic acid. Quinolinic acid (QUIN) is a neurotoxic metabolite of the tryptophan-kynurenine pathway and is an endogenous glutamate agonist that selectively injures and kills vulnerable neurons via the activation of the NMDA class of excitatory amino acid receptors. Estrogen is a female hormone that is responsible for reproduction. However, in the last decade estrogen has been shown to exhibit a wide range of actions on the brain, including neuroprotection. Estrogen has been shown to exhibit intrinsic antioxidant activity and protects cultured neurons against oxidative cell death. This is achieved by estrogen’s ability to scavenge free radicals, which is dependent on the presence of the hydroxyl group at the C3 position on the A ring of the steroid molecule. Numerous studies have shown that estrogen protects neurons against various toxic substances and may play a role in delaying the onset of neurodegenerative diseases, such as Alzheimer’s disease. Neuronal damage due to oxidative stress has been implicated in several neurodegenerative disorders. The detection and measurement of lipid peroxidation is the evidence most frequently cited to support the involvement of free radical reactions in toxicology and in human disease. The study aims to elucidate and further characterise the mechanism behind estrogen’s neuroprotection, using QUIN as a model of neurotoxicity. Initial studies confirm estrogen’s ability to scavenge potent free radicals. In addition, the results show that estrogen forms an interaction with iron (II) and also acts at the NMDA receptor as an agonist. Both mechanisms reduce the ability of QUIN to cause damage to neurons, since QUIN-induced toxicity is dependent on the activation of the NMDA receptor and the formation of a complex with iron (II) to induce lipid peroxidation. Heat shock proteins, especially Hsp 70 play a role in cytoprotection by capturing denatured proteins and facilitating the refolding of these proteins once the stress has been relieved. Estrogen has been shown to increase the level of expression of Hsp70, both inducible and cognate forms of the protein. This suggests that estrogen helps to protect against cellular protein damage induced by any form of stress the cell may encounter. The discovery of neuroprotective agents, such as estrogen, is becoming important as accumulating evidence indicates a protective role in vivo. Thus further research may favour the use of these agents in the treatment of several neurodegenerative disorders. Considering how devastating diseases, such as Alzheimer’s disease, are to a patient and the patient’s families, the discovery of new protective agents are a matter of urgency.
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Thian, Stefanie. "The quinolinic acid lesion of the neostriatum examined in the context of neuronal transplantation." Thesis, University of Cambridge, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624769.

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Ting, Ka Ka Clinical School St Vincent's Hospital Faculty of Medicine UNSW. "Quinolinic acid and its effect on the astrocyte with relevance to the pathogenesis of Alzheimer??s disease." Publisher:University of New South Wales. Clinical School - St Vincent's Hospital, 2008. http://handle.unsw.edu.au/1959.4/41288.

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There is evidence that the excitotoxin quinolinic acid (QUIN) synthesized through the kynurenine pathway (KP) by activated microglia may play a role in the pathogenesis of several major neuroinflammatory diseases and more particularly in Alzheimer??s disease (AD). The hypothesis of this project is QUIN affects the function and morphology of astrocytes. In this study I used human foetal astrocytes stimulated with AD associated cytokines including IFN-gamma, TNF-alpha, TGF-alpha and different concentrations of QUIN ranging from low physiological to high excitotoxic concentrations. I found that QUIN induces IL-1beta expression in human astrocytes and subsequently, contribute to the inflammatory cascade that is present in AD pathology. Glial fibrillary acid protein (GFAP) and vimentin protein expression were complementary in expression to each other after 24 hr stimulation with different QUIN doses. However, there were marked increases in GFAP levels and reduction in vimentin levels compared to controls with QUIN treatment indicating that QUIN can trigger astrogliosis in human astrocytes. Glutamine synthetase (GS) activity was used as a functional metabolic test for astrocytes and I found a dose-dependent inhibition of GS activity by QUIN. This inhibition was inversely correlated with iNOS expression whereby reduced GS activity is accompanied with an increase expression of iNOS in human astrocytes. These results suggest that reduction in GS activity can lead to accumulation of extracellular glutamate then leading to exacerbated excitotoxicity via NMDA receptor over-activation and ultimately neuronal death. PCR array results showed that at least four different pathways were activated with pathological concentration of QUIN including p38 MAPK that is associated with pro-inflammatory cytokine production, ERK/MAPK growth and differentiation that can modulate structural proteins, mitochondrial-induced apoptotic cascade and cell cycle control pathway. QUIN-induced astrogliosis and excitotoxicity could lead to glial scar formation and prevention of axonal growth thus exacerbation of neurodegeneration via synaptosomal NMDA receptor over-activation. All together, this study showed that, in the context of AD, QUIN is an important factor for astroglial activation, dysregulation and death, which can be mediated by the previously mentioned pathways.
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Chen, Yiquan Medical Sciences Faculty of Medicine UNSW. "The involvement of the Kynurenine pathway in amyotrophic lateral sclerosis." Publisher:University of New South Wales. Medical Sciences, 2009. http://handle.unsw.edu.au/1959.4/43774.

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Amyotrophic lateral sclerosis (ALS) is a progressive and fatal motor neuron disease of unclear aetiology, although the general consensus is of a multifactorial disease. The kynurenine pathway (KP), activated during neuroinflammation, is emerging as a possible contributory factor in ALS. The KP is the major route for tryptophan (TRP) catabolism. The intermediates generated can be either neurotoxic, such as quinolinic acid (QUIN), or neuroprotective, such as picolinic acid (PIC), an important endogenous metal chelator. The first and inducible enzyme is indoleamine 2,3-dioxygenase (IDO). As the extent of the involvement of the KP in ALS is unknown, the main aim of this thesis was to attempt to answer that question. The techniques used in this work include HPLC, GC/MS, RT-PCR, immunohistochemistry and immunocyctochemsitry. The main findings of this project are: (1) the complete KP is present in the mouse motor neuron cell line, NSC-34; (2) QUIN toxicity on NSC-34 cells may be ameliorated through the administration of NMDA antagonists, neuroprotective kynurenines, kynurenine inhibitor and QUIN monoclonal antibody; (3) in ALS patients, QUIN CSF and serum levels are significantly elevated, while PIC serum levels are significantly reduced; (4) ALS brain and spinal cord tissue show extensive microglia activation and positive immunoreactivity IDO and QUIN in spinal motor neurons and Betz cells in the motor cortex; and (5) kynurenine pathway inhibitor and analogue, R061-8048 and tranilast, are able to prolong the survival in the G93A SOD1 ALS transgenic mouse model. In conclusion, this study provide the first strong evidence for the involvement of the KP in ALS, and these data point to an inflammation-driven excitotoxic-chelation defective mechanism in ALS, which is amenable to KP analogue and inhibitor in ALS transgenic mice.
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Books on the topic "Quinolinic acid"

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Armstrong, Sally Fiona. Concentrations of quinolinic and kynuretic acid in patients with Alzheimer's disease and controls and their relationship to restlessness and mood states. London: University of Surrey Roehampton, 2000.

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W, Stone T., ed. Quinolinic acid and the kynurenines. Boca Raton, Fla: CRC Press, 1989.

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Erickson, W. Randal. Studies on advanced intermediates in the biosynthesis of streptonigrin. 1987.

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Book chapters on the topic "Quinolinic acid"

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Goda, K., R. Kishimoto, S. Shimizu, Y. Hamane, and M. Ueda. "Quinolinic Acid and Active Oxygens." In Advances in Experimental Medicine and Biology, 247–54. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0381-7_38.

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Schwarcz, R., E. Okuno, and C. Köhler. "Endogenous Excitotoxins: Focus on Quinolinic Acid." In Excitatory Amino Acids, 381–96. London: Palgrave Macmillan UK, 1986. http://dx.doi.org/10.1007/978-1-349-08479-1_25.

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Schwarcz, R., and F. Du. "Quinolinic Acid and Kynurenic Acid in the Mammalian Brain." In Advances in Experimental Medicine and Biology, 185–99. Boston, MA: Springer New York, 1991. http://dx.doi.org/10.1007/978-1-4684-5952-4_17.

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Schwarcz, R., C. Speciale, E. Okuno, E. D. French, and C. Köhler. "Quinolinic Acid: A Pathogen in Seizure Disorders?" In Advances in Experimental Medicine and Biology, 697–707. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-7971-3_53.

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Vezzani, A., J. B. P. Gramsbergen, C. Speciale, and R. Schwarcz. "Production of Quinolinic Acid and Kynurenic Acid by Human Glioma." In Advances in Experimental Medicine and Biology, 691–95. Boston, MA: Springer New York, 1991. http://dx.doi.org/10.1007/978-1-4684-5952-4_95.

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Stone, T. W., J. H. Connick, J. I. Addae, D. A. S. Smith, and P. A. Brooks. "The Neuropharmacology of Quinolinic Acid and the Kynurenines." In Excitatory Amino Acids, 367–80. London: Palgrave Macmillan UK, 1986. http://dx.doi.org/10.1007/978-1-349-08479-1_24.

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Guillemin, Gilles J., Kieran R. Williams, Danielle G. Smith, George A. Smythe, Juliana Croitoru-Lamoury, and Bruce J. Brew. "QUINOLINIC ACID IN THE PATHOGENESIS OF ALZHEIMER’S DISEASE." In Advances in Experimental Medicine and Biology, 167–76. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0135-0_19.

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Heyes, Melvyn P., Eugene O. Major, Kuniaki Sato, and Sanford M. Markey. "Quantification of Quinolinic Acid Metabolism by Macrophages and Astrocytes." In Technical Advances in AIDS Research in the Human Nervous System, 317–25. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1949-2_23.

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Mawatari, K., K. Oshida, F. Iinuma, and M. Watanabe. "Determination of Quinolinic Acid by Liquid Chromatography with Fluorimetric Detection." In Advances in Experimental Medicine and Biology, 697–701. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0381-7_112.

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Bergqvist, P. B. F., M. P. Heyes, and F. Bengtsson. "Is Quinolinic Acid Involed in the Pathogenesis of Hepatic Encephalopathy?" In Advances in Experimental Medicine and Biology, 397–405. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0381-7_61.

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Conference papers on the topic "Quinolinic acid"

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Pattanayak, Subrat Kumar. "Quantum chemical study on the NLO and NBO properties of 4-hydroxy quinoline-2-carboxylic acid." In 2ND INTERNATIONAL CONFERENCE ON CONDENSED MATTER AND APPLIED PHYSICS (ICC 2017). Author(s), 2018. http://dx.doi.org/10.1063/1.5032823.

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Luo, Ya-Nan, Zhi-Chen Liu, Hui-Ying Jiang, Li-Ying Yu, and Xiao-Yang Yu. "A NEW NICKEL COORDINATION POLYMER CONSTRUCTED FROM 4-[(8-HYDROX -Y 5-QUINOLINYL) AZO]-BENZENESULFONIC ACID: SYNTHESIS, STRUCTURE AND PROPERTY." In International Conference on New Materials and Intelligent Manufacturing (ICNMIM). Volkson Press, 2018. http://dx.doi.org/10.26480/icnmim.01.2018.323.325.

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Manabe, S., H. Yanagisawa, S. Ishikawa, Y. Kitagawa, K. Tohyama, S. Abe, and O. Wada. "TRYPTOPHAN PYROLYSIS PRODUCTS FOUND IN COOKED FOODS INHIBIT HUMAN PLATELET AGGREGATION BY INHIBITING CYCLOOXYGENASE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643402.

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Abstract:
Humans are exposed to numerous toxic compounds in foods. During the past decade, several carcinogenic heterocyclic amines have been reported to be present in the cooked foods. Recently, we reported that some of the carcinogenic heterocyclic amines isolated from foods were present in human plasma. In order to know the effects of the carcinogens isolated from foods on the cell function, we investigated the effects of the carcinogenic heterocyclic amines including Trp-P-1(3-amino-l,4-dimethyl-5H-pyrido❘4,3-b❘indole) and Trp-P-2(3-amino-1-methyl-5H-pyrido❘4,3-b❘indole) on human platelet aggregation and polymorphonuclear leukocyte aggregation. Only tryptophan pyrolysis products, Trp-P-1 and Trp-P-2, had potent inhibitory effects on human platelet aggregation when platelets were preincubated with the carcinogens for 15 min. Other carcinogenic heterocyclic amines such as glutamic acid pyrolysates (Glu-P-1 and Glu-P-2) and 3H-imidazo ❘4,5-f❘quinoline-2-amines(IQ and MelQ) did show no effect on platelet aggregation even at 100 μM.The autoradiogram demonstrated that Tryptophan pyrolysis products, Trp-P-1 and Trp-P-2, dose-dependently inhibited the formation of HHT,PGD2,PGE2 and TXB2 induced by sodium arachidonate in human platelets labeled with ❘ 14c❘ arachidonic acid. Moreover, Trp-P-1 and Trp-P-2 did not show significant effects on leukocyte aggregation induced by sodium arachidonate (0.75mM) even at lOOnM. It is concluded that Trp-P-1 and Trp-P-2 isolated from cooked foodstuffs have potent inhibitory effects on the cyclo-oxygenase pathway of the platelet. Therefore, human platelet function might be affected with daily foods containing tryptophan pyrolysis products in vivo.
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