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Artykuły w czasopismach na temat „Quinolinic acid”

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Data publikacji: 4 czerwca 2021

Data aktualizacji: 25 lipca 2025

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1

Sundberg, Markku, Rolf Uggla, Reijo Sillanpää, et al. "Adduct formed by chromium trioxide and zwitterionic quinolinic acid." Open Chemistry 8, no. 3 (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. Calc

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2

Sinz, Elizabeth H., Patrick M. Kochanek, Melvyn P. Heyes, et al. "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 (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

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3

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 (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 negati

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4

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 (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 int

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5

Niwa, Toshlmitsu, Hldeo Yoshizumi, Yutaka Emoto, et al. "Accumulation of quinolinic acid in uremic serum and its removal by hemodialysis." Clinical Chemistry 37, no. 2 (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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6

Guillemin, Gilles J. "Quinolinic acid: neurotoxicity." FEBS Journal 279, no. 8 (2012): 1355. http://dx.doi.org/10.1111/j.1742-4658.2012.08493.x.

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7

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 (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-h

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8

Saito, K., C. Y. Chen, M. Masana, J. S. Crowley, S. P. Markey та 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, № 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 mac

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9

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 (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 convu

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10

Egashira, Sato, Saito, and Sanada. "Dietary Protein Level and Dietary Interaction Affect Quinolinic Acid Concentration in Rats." International Journal for Vitamin and Nutrition Research 77, no. 2 (2007): 142–48. http://dx.doi.org/10.1024/0300-9831.77.2.142.

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During tryptophan-niacin conversion, hepatic α-amino-β-carboxymuconate-ε-semialdehyde decarboxylase (ACMSD) [EC4.1.1.45] plays a key role in regulating NAD biosynthesis. ACMSD activity is greatly affected by many factors such as nutritional status and disease. The tryptophan catabolite quinolinic acid has been reported to be associated with the pathogenesis of various disorders and is a potential endogenous toxin. However the effects of dietary protein levels or dietary interaction between protein levels and fatty acid type to this process have not been investigated and are still unknown. In t

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11

HEYES, MELVYN P. "Quinolinic Acid and Inflammation." Annals of the New York Academy of Sciences 679, no. 1 Markers of Ne (1993): 211–16. http://dx.doi.org/10.1111/j.1749-6632.1993.tb18300.x.

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12

Maksimovic, Ivana, Marina Jovanovic, Miodrag Colic, Dejan Micic, Rosa Mihajlovic, and Vesna Selakovic. "Nitric oxide synthase inhibitors prevents quinolinic acid-induced neurotoxicity: the role of nitric oxide and glucose-6-phosphate dehydrogenase in cell death." Jugoslovenska medicinska biohemija 21, no. 3 (2002): 269–74. http://dx.doi.org/10.2298/jmh0203269m.

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In the present study we employed Nw-nitro-L-arginine methyl ester, non-specific potent nitric oxide synthase inhibitor and a selective inhibitor of neuronal nitric oxide synthase, 7-nitroindazole, reportedly to investigate the possible involvement of nitric oxide in quinolinic acid-induced striatal toxicity in the rat. Quinolinic acid was administered unilaterally into striatum of adult Wistar rats in the single dose of 150 nmol/L. The other two group of animals were pretreated with Nw-nitro-L-arginine methyl ester and 7-nitroindazole respectively. Control groups of animals were treated with 0

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13

Калиновская, И. В. "Люминесцентные свойства соединений европия(III) с хинолиновой кислотой и фосфорсодержащими нейтральными лигандами". Журнал технической физики 127, № 8 (2019): 231. http://dx.doi.org/10.21883/os.2019.08.48034.332-18.

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AbstractLuminescent mixed-ligand europium(III) complexes with quinolinic acid and phosphorus-containing neutral ligands with a dimeric structure of the composition Eu_2(QA)_3 · 3Н_2О, Eu_2(QA)_3 · D · 2Н_2О, where QA is quinolinic acid and D is hmpa (hexamethylphosphortriamide), tppo (triphenylphosphinoxide), (hmpa), or Et_6pa (hexaethylphosphortriamide), are synthesized. The thermal and spectral-luminescent properties of the synthesized complex mixed-ligand europium(III) compounds are studied. It is shown that the detachment of water and neutral ligand molecules during thermolysis occurs in t

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14

Nishizaki, Daisuke, and Hideo Iwahashi. "Baicalin Inhibits the Fenton Reaction by Enhancing Electron Transfer from Fe2+ to Dissolved Oxygen." American Journal of Chinese Medicine 43, no. 01 (2015): 87–101. http://dx.doi.org/10.1142/s0192415x15500068.

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Sho-saiko-to is an herbal medicine that is known to have diverse pharmacological activities and has been used for the treatment of various infectious diseases. Here, we examined the effects of baicalin, a compound isolated from Sho-saiko-to, and the effects of the iron chelator quinolinic acid on the Fenton reaction. The control reaction mixture contained 0.1 M 5,5-dimethyl-1-pyrroline N-oxide (DMPO), 0.2 mM H 2 O 2, 0.2 mM FeSO 4( NH 4)2 SO 4, and 40 mM sodium phosphate buffer (pH 7.4). Upon the addition of 0.6 mM baicalin or quinolinic acid to the control reaction mixture, the ESR peak heigh

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15

Kilbourn, Michael R., Avgui Charalambous, Kirk A. Frey, Phillip Sherman, Donald S. Higgins, and J. Timothy Greenamyre. "Intrastriatal Neurotoxin Injections Reduce in Vitro and in Vivo Binding of Radiolabeled Rotenoids to Mitochondrial Complex I." Journal of Cerebral Blood Flow & Metabolism 17, no. 3 (1997): 265–72. http://dx.doi.org/10.1097/00004647-199703000-00003.

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The in vivo and in vitro bindings of radiolabeled rotenoids to mitochondrial complex I of rat striatum were examined after unilateral intrastriatal injections of quinolinic acid or 1-methyl-4-phenylpyridinium salt (MPP+). Quinolinic acid produced significant, similar losses of in vivo binding of [11C]dihydrorotenol ([11C]DHROL: 40%) and in vitro binding of [3H]dihydrorotenone ([3H]DHR: 53%) in the injected striata at 13 days after the injection of neurotoxin. MPP+ reduced in vivo binding of [11C]DHROL (up to −55%) as measured 1.5 to 6 h after its administration. Reductions of in vivo [11C]DHRO

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16

Ningrum, Aji Mustika, Prananda Surya Airlangga, Wiwiek Indriyani Maskoep, and Herdiani Sulistyo Putri. "Relationship of quinolinic acid and serotonin with depression and pain degree in cancer pain patients: a cross-sectional study." Bali Medical Journal 12, no. 3 (2023): 2681–84. http://dx.doi.org/10.15562/bmj.v12i3.4697.

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Link of Video Abstract: https://youtu.be/zg5vubHMcDY Introduction: Chronic pain requires a thorough assessment if it persists in patients with cancer. Depressive disorder is one of the psychosocial problems that can occur in cancer patients. Depressive disorders affect up to 34.4% of patients with cancer in Indonesia, causing increased morbidity and complicating the management of patients. Quinolinic acid (QUIN) and serotonin (5-HT) are chemicals that can affect pain perception and depressive disorders. This study aims to analyze the relationship between quinolinic acid and serotonin levels wi

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17

Guillemin, Gilles J. "Quinolinic acid, the inescapable neurotoxin." FEBS Journal 279, no. 8 (2012): 1356–65. http://dx.doi.org/10.1111/j.1742-4658.2012.08485.x.

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OBRENOVITCH, T. P. "Quinolinic Acid Accumulation During Neuroinflammation." Annals of the New York Academy of Sciences 939, no. 1 (2006): 1–10. http://dx.doi.org/10.1111/j.1749-6632.2001.tb03605.x.

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Holmes, Gregory L. "Quinolinic acid and the kynurenines." Journal of Epilepsy 3, no. 4 (1990): 231. http://dx.doi.org/10.1016/0896-6974(90)90063-5.

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Kilpatrick, I. C. "Quinolinic acid and the kynurenines." Trends in Pharmacological Sciences 10, no. 12 (1989): 513. http://dx.doi.org/10.1016/0165-6147(89)90054-0.

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Hestad, Knut, Jan Alexander, Helge Rootwelt, and Jan O. Aaseth. "The Role of Tryptophan Dysmetabolism and Quinolinic Acid in Depressive and Neurodegenerative Diseases." Biomolecules 12, no. 7 (2022): 998. http://dx.doi.org/10.3390/biom12070998.

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Emerging evidence suggests that neuroinflammation is involved in both depression and neurodegenerative diseases. The kynurenine pathway, generating metabolites which may play a role in pathogenesis, is one of several competing pathways of tryptophan metabolism. The present article is a narrative review of tryptophan metabolism, neuroinflammation, depression, and neurodegeneration. A disturbed tryptophan metabolism with increased activity of the kynurenine pathway and production of quinolinic acid may result in deficiencies in tryptophan and derived neurotransmitters. Quinolinic acid is an N-me

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Santamaría, Abel, Juan Ordaz‐Moreno, Moisés Rubio‐Osornio, Fausto Solís‐Hernández, and Camilo Ríos. "Neuroprotective Effect of Dapsone against Quinolinate‐ and Kainate‐Induced Striatal Neurotoxicities in Rats." Pharmacology & Toxicology 81, no. 6 (1997): 271–75. http://dx.doi.org/10.1111/j.1600-0773.1997.tb00005.x.

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AbstractWc tested the ability of dapsone, a well‐known antibiotic and antiinflammatory drug, to attenuate both the quinolinic acid (an NMDA agonist of glutamate receptors)‐ and kainic acid (a non‐NMDA agonist of glutamate receptors)‐induced in vivo neurotoxicities in rats. Circling behaviour and striatal γ‐aminobutyric acid (GABA) depiction were considered as behavioural and neurochemical end‐points of brain toxicity. Rotation behaviour, evaluated six days after the intrastriatal injection of quinolinic acid (130±19 ipsilateral turns/hr). was attenuated by doses of 12.5 mg/kg and 25 mg/kg of d

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Sanna, Daniele, and Angela Fadda. "Role of the Hydroxyl Radical-Generating System in the Estimation of the Antioxidant Activity of Plant Extracts by Electron Paramagnetic Resonance (EPR)." Molecules 27, no. 14 (2022): 4560. http://dx.doi.org/10.3390/molecules27144560.

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The scavenging activity of hydroxyl radicals, produced by the Fenton reaction, is commonly used to quantify the antioxidant capacity of plant extracts. In this study, three Fenton systems (Fe/phosphate buffer, Fe/quinolinic acid and Fe/phosphate buffer/quinolinic acid) and the thermal degradation of peroxydisulfate were used to produce hydroxyl radicals; the hydroxyl radical scavenging activity of plant extracts (ginger, blueberry juices and green tea infusion) and chemical compounds (EGCG and GA) was estimated by spin trapping with DMPO (5,5-dimethyl-1-pyrroline N-oxide) and EPR (Electron Par

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Yu, Edward, Christopher Papandreou, Miguel Ruiz-Canela, et al. "Association of Tryptophan Metabolites with Incident Type 2 Diabetes in the PREDIMED Trial: A Case–Cohort Study." Clinical Chemistry 64, no. 8 (2018): 1211–20. http://dx.doi.org/10.1373/clinchem.2018.288720.

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Abstract BACKGROUND Metabolites of the tryptophan–kynurenine pathway (i.e., tryptophan, kynurenine, kynurenic acid, quinolinic acid, 3-hydroxyanthranilic) may be associated with diabetes development. Using a case–cohort design nested in the Prevención con Dieta Mediterránea (PREDIMED) study, we studied the associations of baseline and 1-year changes of these metabolites with incident type 2 diabetes (T2D). METHODS Plasma metabolite concentrations were quantified via LC-MS for n = 641 in a randomly selected subcohort and 251 incident cases diagnosed during 3.8 years of median follow-up. Weighte

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Vasiljevic, Ivana, Marina Jovanovic, Miodrag Colic, et al. "Effects of various nitric oxide synthase inhibitors on quinolinic acid-induced neuronal injury in rats." Jugoslovenska medicinska biohemija 23, no. 1 (2004): 11–18. http://dx.doi.org/10.2298/jmh0401011v.

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The aetiology of neuronal death in neurodegenerative diseases, including Huntington-s disease, is still unknown. There could be a complex interplay among altered energy metabolism, excitotoxicity and oxidative stress. Our aim was to examine the effects of intrastriatal injection of a selective inhibitor of neuronal nitric oxide synthase, 7-nitroindazole, and a non-specific potent nitric oxide synthase inhibitor, Nw-nitro-L-arginine methyl ester, in order to study the possible involvement of glutathione, an important antioxidant, in quinolinic acid-induced striatal toxicity in the rat. Unilater

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Shibata, Katsumi, and Tsutomu Fukuwatari. "Organ Correlation with Tryptophan Metabolism Obtained by Analyses of TDO-KO and QPRT-KO Mice." International Journal of Tryptophan Research 9 (January 2016): IJTR.S37984. http://dx.doi.org/10.4137/ijtr.s37984.

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The aim of this article is to report the organ-specific correlation with tryptophan (Trp) metabolism obtained by analyses of tryptophan 2,3-dioxygenase knockout (TDO-KO) and quinolinic acid phosphoribosyltransferase knockout (QPRT-KO) mice models. We found that TDO-KO mice could biosynthesize the necessary amount of nicotinamide (Nam) from Trp, resulting in the production of key intermediate, 3-hydroxyanthranilic acid. Upstream metabolites, such as kynurenic acid and xanthurenic acid, in the urine were originated from nonhepatic tissues, and not from the liver. In QPRT-KO mice, the Trp to quin

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Fu, Jie, Phillip E. Savage, and Xiuyang Lu. "Hydrothermal Decarboxylation of Pentafluorobenzoic Acid and Quinolinic Acid." Industrial & Engineering Chemistry Research 48, no. 23 (2009): 10467–71. http://dx.doi.org/10.1021/ie901182y.

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Wiley, Clayton A. "Quinolinic acid and neurodegeneration in AIDS." Journal of Neurovirology 1, no. 5-6 (1995): 328–29. http://dx.doi.org/10.3109/13550289509111021.

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Foster, Alan C., William C. Zinkand, and Robert Schwarcz. "Quinolinic Acid Phosphoribosyltransferase in Rat Brain." Journal of Neurochemistry 44, no. 2 (1985): 446–54. http://dx.doi.org/10.1111/j.1471-4159.1985.tb05435.x.

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Yellon, Robert F., Elizabeth Rose, Margaret A. Kenna, et al. "Sensorineural Hearing Loss From Quinolinic Acid." Laryngoscope 101, no. 2 (1994): 176???181. http://dx.doi.org/10.1288/00005537-199402000-00009.

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Foster, Alan C., Etsuo Okuno, Daniel S. Brougher, and Robert Schwarcz. "A radioenzymatic assay for quinolinic acid." Analytical Biochemistry 158, no. 1 (1986): 98–103. http://dx.doi.org/10.1016/0003-2697(86)90595-6.

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Sofic, E., J. Halket, Anna Przyborowska, et al. "Brain quinolinic acid in Alzheimer's dementia." Journal of Neural Transmission - Parkinson's Disease and Dementia Section 1, no. 1-2 (1989): 133. http://dx.doi.org/10.1007/bf02312293.

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Sofic, E., J. Halket, A. Przyborowska, et al. "Brain quinolinic acid in Alzheimer's dementia." European Archives of Psychiatry and Neurological Sciences 239, no. 3 (1989): 177–79. http://dx.doi.org/10.1007/bf01739651.

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Reynolds, Gavin P., Sally J. Pearson, John Halket, and Merton Sandier. "Brain Quinolinic Acid in Huntington's Disease." Journal of Neurochemistry 50, no. 6 (1988): 1959–68. http://dx.doi.org/10.1111/j.1471-4159.1988.tb02503.x.

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Farup, Per G., Helge Rootwelt, and Knut Hestad. "APOE Polymorphism Is Associated with Changes in the Kynurenine Pathway." Genes 14, no. 10 (2023): 1955. http://dx.doi.org/10.3390/genes14101955.

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Background: APOE polymorphism and the Kynurenine pathway (KP) are associated with many disorders, but little is known about associations between APOE polymorphism and the KP. This study explored the associations between the KP and APOE polymorphism in disorders associated with APOE polymorphism and changes in the KP. Methods: Subjects with morbid obesity before and after bariatric surgery (numbers 139 and 95, respectively), depression (number 49), and unspecified neurological symptoms (number 39) were included. The following grouping of the APOE genotypes was used: E2 = ɛ2ɛ2 + ɛ2ɛ3, E3 = ɛ3ɛ3

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Fathi, Anwar Abdulghani, Yassir Shakeeb Al Jawaheri, and Shaimaa Samir Ismaee. "Synthesis of some new substituted imines from aldehydes and ketones derived from quinolinic acid." Ecletica Quimica 48, no. 2 (2023): 49–65. http://dx.doi.org/10.26850/1678-4618eqj.v48.2.2023.p49-65.

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In this paper, some substituted imines compounds have been prepared from quinolinic acid as a starting material. Firstly, the quinolinic acid was treated with acetic anhydride and acetic acid to form furo[3,4-b]pyridine-5,7-dione (1); the resulting compound was heated with urea to form 5H-pyrrolo[3,4-b]pyridine-5,7(6H)-dione (2). After that, it was treated with potassium hydroxide to give potassium 5,7-dioxo-5,7-dihydropyrrolo[3,4-b]pyridin-6-dione, which was directly and easily converted to 6-(2-([1,1'-biphenyl]-4-yl)-2-oxoethyl)-5H-pyrrolo[3,4-b]pyridine-5,7(6H)-dione (3) by the reaction wit

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Zhang, Chi, Juan Huang, Wei Wei, and Zhengbo Chen. "Colorimetric identification of lanthanide ions based on two carboxylic acids as an artificial tongue." Analyst 145, no. 9 (2020): 3359–63. http://dx.doi.org/10.1039/d0an00357c.

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Kozhevnikova, M. V., A. V. Krivova, E. O. Korobkova, et al. "Comparative analysis of tryptophan and downstream metabolites of the kynurenine and serotonin pathways in patients with arterial hypertension and coronary artery disease." Kardiologiia 62, no. 11 (2022): 40–48. http://dx.doi.org/10.18087/cardio.2022.11.n2283.

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Aim To compare serum concentrations of tryptophane (Trp) and its metabolites in subjects with no cardiovascular disease (CVD) and patients with СVD, including arterial hypertension (AH) and ischemic heart disease (IHD).Material and methods This study included 131 participants; 58 participants (11 of them with documented peripheral atherosclerosis) were included into the AH group, 46 participants were included into the IHD group, and 27 participants with no signs of CVD were included into the control group. Plasma concentrations of Trp and its metabolites were measured by high-performance liqui

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Kubicova, Lenka, Franz Hadacek, and Vladimir Chobot. "Quinolinic Acid: Neurotoxin or Oxidative Stress Modulator?" International Journal of Molecular Sciences 14, no. 11 (2013): 21328–38. http://dx.doi.org/10.3390/ijms141121328.

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Cammer, Wendy. "Oligodendrocyte killing by quinolinic acid in vitro." Brain Research 896, no. 1-2 (2001): 157–60. http://dx.doi.org/10.1016/s0006-8993(01)02017-0.

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Bruyn, R. P. M., and J. C. Stoof. "The quinolinic acid hypothesis in Huntington's chorea." Journal of the Neurological Sciences 95, no. 1 (1990): 29–38. http://dx.doi.org/10.1016/0022-510x(90)90114-3.

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Kozlovskii, V. L., I. V. Prakh'e, and N. V. Geinisman. "Neurodegenerative and convulsant action of quinolinic acid." Neurophysiology 22, no. 3 (1991): 267–70. http://dx.doi.org/10.1007/bf01052636.

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Keilhoff, Gerburg, and Gerald Wolf. "Memantine prevents quinolinic acid-induced hippocampal damage." European Journal of Pharmacology 219, no. 3-4 (1992): 451–54. http://dx.doi.org/10.1016/0014-2999(92)90487-o.

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Batshaw, Mark L., Michael B. Robinson, Keith Hyland, Sina Djali, and Melvyn P. Heyes. "Quinolinic acid in children with congenital hyperammonemia." Annals of Neurology 34, no. 5 (1993): 676–81. http://dx.doi.org/10.1002/ana.410340509.

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Blesl, C., A. Tmava, A. Baranyi, et al. "The Kynurenine pathway in pancreatic carcinoma." European Psychiatry 41, S1 (2017): S480. http://dx.doi.org/10.1016/j.eurpsy.2017.01.564.

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IntroductionPancreatic carcinoma (PC) belongs to the most aggressive tumours worldwide, with a five year survival of 7%. Mostly, diagnosis is made in late stages, as by now no early detection method is available. Symptoms of depression occur frequently before diagnosis of PC. PC and depression are both known to go along with changes in the kynurenine-pathway.ObjectivesThis study aimed to examine the kynurenine pathway (Figure 1) and evaluate a possible depression in newly diagnosed PC patients in comparison to healthy controls (HC).Methods26 PC patients and 26 age and sex matched HC participat

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Wang, Yifan, Kathy Fange Liu, Yu Yang, Ian Davis, and Aimin Liu. "Observing 3-hydroxyanthranilate-3,4-dioxygenase in action through a crystalline lens." Proceedings of the National Academy of Sciences 117, no. 33 (2020): 19720–30. http://dx.doi.org/10.1073/pnas.2005327117.

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The synthesis of quinolinic acid from tryptophan is a critical step in the de novo biosynthesis of nicotinamide adenine dinucleotide (NAD+) in mammals. Herein, the nonheme iron-based 3-hydroxyanthranilate-3,4-dioxygenase responsible for quinolinic acid production was studied by performing time-resolvedin crystalloreactions monitored by UV-vis microspectroscopy, electron paramagnetic resonance (EPR) spectroscopy, and X-ray crystallography. Seven catalytic intermediates were kinetically and structurally resolved in the crystalline state, and each accompanies protein conformational changes at the

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Smith, Karen E., Perry A. Gerakines, and Michael P. Callahan. "Metabolic precursors in astrophysical ice analogs: implications for meteorites and comets." Chemical Communications 51, no. 59 (2015): 11787–90. http://dx.doi.org/10.1039/c5cc03272e.

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Park, Hyunjin, Myong Yong Choi, Cheol Joo Moon, and Tae Ho Kim. "Crystal structure ofN-[2-(cyclohexylsulfanyl)ethyl]quinolinic acid imide." Acta Crystallographica Section E Crystallographic Communications 73, no. 9 (2017): 1372–74. http://dx.doi.org/10.1107/s2056989017012142.

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The title compound, C15H18N2O2S {systematic name: 6-[2-(cyclohexylsulfanyl)ethyl]-5H-pyrrolo[3,4-b]pyridine-5,7(6H)-dione}, was obtained from the reaction of pyridine-2,3-dicarboxylic anhydride (synonym: quinolinic anhydride) with 2-(cyclohexylsulfanyl)ethylamine. The dihedral angle between the mean plane of the cyclohexyl ring and the quinolinic acid imide ring is 25.43 (11)°. In the crystal, each molecule forms two C—H...O hydrogen bonds and one weak C—O...π [O...ring centroid = 3.255 (2) Å] interaction with neighbouring molecules to generate a ladder structure along theb-axis direction. The

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Heyes, Melvyn P. "Metabolism and neuropathologic significance of quinolinic acid and kynurenic acid." Biochemical Society Transactions 21, no. 1 (1993): 83–89. http://dx.doi.org/10.1042/bst0210083.

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Kohler, C., LG Eriksson, PR Flood, JA Hardie, E. Okuno, and R. Schwarcz. "Quinolinic acid metabolism in the rat brain. Immunohistochemical identification of 3-hydroxyanthranilic acid oxygenase and quinolinic acid phosphoribosyltransferase in the hippocampal region." Journal of Neuroscience 8, no. 3 (1988): 975–87. http://dx.doi.org/10.1523/jneurosci.08-03-00975.1988.

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