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Journal articles on the topic 'Quinolinic acid'

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Published: 4 June 2021

Last updated: 31 January 2023

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

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 (March 1, 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 this study, we examined whether dietary protein level, fatty acid type, namely saturated fatty acid and polyunsaturated fatty acid, and their interaction affect serum quinolinic acid concentration in rats. Male Sprague-Dawley rats (4-weeks old) were fed with 20% casein + 10% stearic acid diet (20C10S), 20% casein + 10% linoleic acid diet (20C10L), 40% casein + 10%stearic acid diet (40C10S), or 40% casein + 10% linoleic acid diet (40C10L) for 8 days, and serum quinolinic acid concentration and ACMSD activity were determined. Serum quinolinic acid concentration was significantly increased in the 40C10L group compared with other three groups. There was also the negative correlation between the sum of liver and kidney ACMSD activities, and serum quinolinic acid concentration per tryptophan intake (r = 0.8209, p < 0.01). Increased serum QA concentrations are probably due to a decreased ACMSD activity.

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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 0,154 mmol/L saline solution likewise. Nitrite levels was decreased in the ipsi- and contralateral striatum and forebrain cortex in the group treated with nitric oxide synthase inhibitors and neurotoxin compared to quinolinic acid-treated animals. In the same structures, activity of glucose-6-phosphate dehydrogenase was also decreased, compared to quinolinic acid-treated animals. These results indicate that application of the nitric oxide synthase inhibitors, supressed nitrite accumulation and glucose-6-phosphate dehydrogenase activity and attenuated quinolinic acid-induced neuronal damage in the striatum and forebrain cortex.

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13

Guillemin, Gilles J. "Quinolinic acid, the inescapable neurotoxin." FEBS Journal 279, no. 8 (March 27, 2012): 1356–65. http://dx.doi.org/10.1111/j.1742-4658.2012.08485.x.

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14

OBRENOVITCH, T. P. "Quinolinic Acid Accumulation During Neuroinflammation." Annals of the New York Academy of Sciences 939, no. 1 (January 25, 2006): 1–10. http://dx.doi.org/10.1111/j.1749-6632.2001.tb03605.x.

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15

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

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16

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

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17

Калиновская, И. В. "Люминесцентные свойства соединений европия(III) с хинолиновой кислотой и фосфорсодержащими нейтральными лигандами." Журнал технической физики 127, no. 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 two stages with endothermic effects and that the complex compounds are stable at temperatures up to 320°С. It is found by IR spectroscopy that quinolinic acid coordinates to the europium(III) ion by two carboxylate ions. The low luminescence intensity of mixed-ligand europium(III) quinolinates is explained by inefficient electronic excitation energy transfer from quinolinic acid and phosphorus-containing neutral ligands to europium ions.

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18

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 (January 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 heights of DMPO/OH radical adducts were measured as 32% ± 1% (baicalin) and 166% ± 27% (quinolinic acid) of that of the control mixture. In order to clarify why baicalin and quinolinic acid exerted opposite effects on the formation of hydroxyl radicals, we measured oxygen consumption in the presence of either compound. Upon the addition of 0.6 mM baicalin (or quinolinic acid) to the control reaction mixture without DMPO and H 2 O 2, the relative oxygen consumption rates were found to be 449% ± 40% (baicalin) and 18% ± 9% (quinolinic acid) of that of the control mixture without DMPO and H 2 O 2, indicating that baicalin facilitated the transfer of electrons from Fe 2+ to dissolved oxygen. Thus, the great majority of Fe 2+ turned into Fe 3+, and the formation of hydroxyl radicals was subsequently inhibited in this reaction.

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19

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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20

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 (March 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]DHROL binding after either quinolinic acid or MPP+ injections did not correlate with changes in striatal blood flow as measured with [14C]iodoantipyrine. These results are consistent with losses of complex I binding sites for radiolabeled rotenoids, produced using cell death (quinolinic acid) or direct competition for the binding site (MPP+). Appropriately radiolabeled rotenoids may be useful for in vivo imaging studies of changes of complex I in neurodegenerative diseases.

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21

Fu, Jie, Phillip E. Savage, and Xiuyang Lu. "Hydrothermal Decarboxylation of Pentafluorobenzoic Acid and Quinolinic Acid." Industrial & Engineering Chemistry Research 48, no. 23 (December 2, 2009): 10467–71. http://dx.doi.org/10.1021/ie901182y.

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22

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 (July 18, 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-methyl-D-aspartate receptor agonist, and raised levels in CSF, together with increased levels of inflammatory cytokines, have been reported in mood disorders. Increased quinolinic acid has also been observed in neurodegenerative diseases, including Parkinson’s disease, Alzheimer’s disease, amyotrophic lateral sclerosis, and HIV-related cognitive decline. Oxidative stress in connection with increased indole-dioxygenase (IDO) activity and kynurenine formation may contribute to inflammatory responses and the production of cytokines. Increased formation of quinolinic acid may occur at the expense of kynurenic acid and neuroprotective picolinic acid. While awaiting ongoing research on potential pharmacological interventions on tryptophan metabolism, adequate protein intake with appropriate amounts of tryptophan and antioxidants may offer protection against oxidative stress and provide a balanced set of physiological receptor ligands.

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23

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

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24

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

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25

Yellon, Robert F., Elizabeth Rose, Margaret A. Kenna, William J. Doyle, Margaretha Casselbrant, Warren F. Diven, Theresa L. Whiteside, J. Douglas Swarts, and Melvyn P. Heyes. "Sensorineural Hearing Loss From Quinolinic Acid." Laryngoscope 101, no. 2 (February 1994): 176???181. http://dx.doi.org/10.1288/00005537-199402000-00009.

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26

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

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27

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

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28

Sofic, E., J. Halket, Anna Przyborowska, P. Riederer, H. Beckmann, M. Sandler, and K. Jellinger. "Brain quinolinic acid in Alzheimer's dementia." Journal of Neural Transmission - Parkinson's Disease and Dementia Section 1, no. 1-2 (March 1989): 133. http://dx.doi.org/10.1007/bf02312293.

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29

Sofic, E., J. Halket, A. Przyborowska, P. Riederer, H. Beckmann, M. Sandler, and K. Jellinger. "Brain quinolinic acid in Alzheimer's dementia." European Archives of Psychiatry and Neurological Sciences 239, no. 3 (May 1989): 177–79. http://dx.doi.org/10.1007/bf01739651.

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30

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 (July 17, 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 Paramagnetic Resonance) spectroscopy. Phosphate buffer was used to mimic the physiological pH of cellular systems, while quinolinic acid (pyridine-2,3-dicarboxylic acid) facilitates the experimental procedure by hindering the spontaneous oxidation of Fe(II). The EC50 (the concentration of chemical compounds or plant extracts which halves the intensity of the DMPO–OH adduct) values were determined in all the systems. The results show that, for both the chemical compounds and the plant extracts, there is not a well-defined order for the EC50 values determined in the four hydroxyl radical generating systems. The interactions of phosphate buffer and quinolinic acid with the antioxidants and with potential iron-coordinating ligands present in the plant extracts can justify the observed differences.

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31

Shestopalov, A. V., O. P. Shatova, M. S. Karbyshev, A. M. Gaponov, N. E. Moskaleva, S. A. Appolonova, A. V. Tutelyan, V. V. Makarov, S. M. Yudin, and S. A. Roumiantsev. "“Kynurenine switch” and obesity." Bulletin of Siberian Medicine 20, no. 4 (January 3, 2022): 103–11. http://dx.doi.org/10.20538/1682-0363-2021-4-103-111.

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Aim. To assess the concentrations of bacterial and eukaryotic metabolites mainly involved in indole, kynurenine, and serotonin pathways of tryptophan metabolism in a cohort of patients with obesity. Materials and methods. Using high-performance liquid chromatography with mass spectrometric detection, the concentrations of several serum metabolites, such as kynurenine, kynurenic acid, anthranilic acid, xanthurenic acid, quinolinic acid, 5-hydroxyindole-3-acetate, tryptamine, serotonin, indole-3-lactate, indole-3-acetate, indole-3- butyrate, indole-3-carboxaldehyde, indole-3-acrylate, and indole-3-propionate, were analyzed in a cohort of obese patients compared with healthy volunteers.Results. It was found that serum levels of tryptophan metabolites of microbial and eukaryotic origin were significantly increased in obese patients. Therefore, the concentration of kynurenine in the blood serum in obese patients was 2,413 ± 855 nmol / l, while in healthy volunteers of the same age group, the level of kynurenine in the blood serum was 2,122 ± 863 nmol / l. In obese patients, two acids formed due to kynurenine metabolism; the concentrations of kynurenic and quinolinic acids were increased in the blood serum. The concentration of kynurenic acid in the blood serum in obese patients was 21.1 ± 9.26 nmol / l, and in healthy patients, it was 16.8 ± 8.37 nmol / l. At the same time, the level of quinolinic acid in the blood serum in obese patients was 73.1 ± 54.4 nmol / l and in healthy volunteers – 56.8 ± 34.1 nmol / l. Normally, the level of quinolinic acid is 3.4 times higher than the concentration of kynurenic acid, and in case of obesity, there is a comparable increase in these acids in the blood serum.From indole derivatives, mainly of microbial origin, the concentrations of indole-3-lactate, indole-3-butyrate, and indole-3-acetate were significantly increased in the blood serum of obese patients. In obese patients, the serum concentration of 5-hydroxyindole-3-acetate was elevated to 74.6 ± 75.8 nmol / l (in healthy volunteers – 59.4 ± 36.6 nmol / l); indole-3-lactate – to 523 ± 251 nmol / l (in healthy volunteers – 433 ± 208 nmol / l); indole-3-acetate – to 1,633 ± 1,166 nmol / l (in healthy volunteers – 1,186 ± 826 nmol / l); and indole-3-butyrate – to 4.61 ± 3.31 nmol / l (in healthy volunteers – 3.85 ± 2.51 nmol / l).Conclusion. In case of obesity, the utilization of tryptophan was intensified by both the microbiota population and the macroorganism. It was found that obese patients had higher concentrations of kynurenine, quinolinic and kynurenic acids, indole-3-acetate, indole-3-lactate, indole-3-butyrate, and 5-hydroxyindole-3-acetate. Apparently, against the background of increased production of proinflammatory cytokines by adipocytes in obese patients, the “kynurenine switch” was activated which contributed to subsequent overproduction of tryptophan metabolites involved in the immune function of the macroorganism.

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Vasiljevic, Ivana, Marina Jovanovic, Miodrag Colic, Rosa Mihajlovic, Mirjana Djukic, Milica Ninkovic, and Zivorad Malicevic. "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. Unilateral administration of quinolinic acid to rat striatum in a single dose of 150 nmol/L was used as a model of Huntington-s disease. The other group of animals were pretreated with 7- nitroindazole and Nw-nitro-L-arginine methyl ester, respectively. Control groups were treated with saline solution and olive oil, respectively. Content of total glutathione, was increased in the ipsi- and contralateral striatum, forebrain cortex, basal forebrain and hippocampus in the groups treated with nitric oxid synthase inhibitors and quinolinic acid compared to the quinolinic acid-treated animals. These results support the hypothesis that oxygen free radicals contribute to excitotoxic neuronal injury, and also that nitric oxide synthase inhibitors could be potential neuroprotective agents in Huntington-s disease.

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Yu, Edward, Christopher Papandreou, Miguel Ruiz-Canela, Marta Guasch-Ferre, Clary B. Clish, Courtney Dennis, Liming Liang, et al. "Association of Tryptophan Metabolites with Incident Type 2 Diabetes in the PREDIMED Trial: A Case–Cohort Study." Clinical Chemistry 64, no. 8 (August 1, 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. Weighted Cox models adjusted for age, sex, body mass index, and other T2D risk factors were used. RESULTS Baseline tryptophan was associated with higher risk of incident T2D (hazard ratio = 1.29; 95% CI, 1.04–1.61 per SD). Positive changes in quinolinic acid from baseline to 1 year were associated with a higher risk of T2D (hazard ratio = 1.39; 95% CI, 1.09–1.77 per SD). Baseline tryptophan and kynurenic acid were directly associated with changes in homeostatic model assessment for insulin resistance (HOMA-IR) from baseline to 1 year. Concurrent changes in kynurenine, quinolinic acid, 3-hydroxyanthranilic acid, and kynurenine/tryptophan ratio were associated with baseline-to-1-year changes in HOMA-IR. CONCLUSIONS Baseline tryptophan and 1-year increases in quinolinic acid were positively associated with incident T2D. Baseline and 1-year changes in tryptophan metabolites predicted changes in HOMA-IR. Tryptophan levels may initially increase and then deplete as diabetes progresses in severity.

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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 quinolinic acid conversion ratio was 6%; this value was higher than expected. Furthermore, we found that QPRT activity in hetero mice was half of that in wild-type (WT) mice. Urine quinolinic acid levels remain unchanged in both hetero and WT mice, and the conversion ratio of Trp to Nam was also unaffected. Collectively, these findings show that QPRT was not the rate-limiting enzyme in the conversion. In conclusion, the limiting factors in the conversion of Trp to Nam are the substrate amounts of 3-hydroxyanthranilic acid and activity of 3-hydroxyanthranilic acid 3,4-dioxygenase in the liver.

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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 (October 25, 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 (March 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 (January 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 (September 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 (November 1993): 676–81. http://dx.doi.org/10.1002/ana.410340509.

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Rudzite, Vera, Edite Jurika, Janis Jirgensons, Inga Herpfer, Günter Weiss, Helmut Wachter, and Dietmar Fuchs. "The Influence of Kynurenine and Its Metabolites on Lipid Metabolism." Pteridines 8, no. 3 (September 1997): 201–5. http://dx.doi.org/10.1515/pteridines.1997.8.3.201.

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Summary Incorporation of fatty acids into phospholipids has been investigated using samples of rat liver tissue homogenate, Krebs-Ringer-phosphate buffer (pH=7.4) containing 0.3% albumin, fatty acid mixture and glycerol. The addition of L-kynurenine (4 nmoljg wet weight) to incubation medium induced an increase of palmitic, oleic and linolenic acid and decrease of linoleic and arachidonic acid incorporation into phospholipids. These changes of fatty acid incorporation into phospholipids were followed by increase of cholesterol and decrease of phospholipids content in samples. The addition of 3-hydroxykynurenine (1.8 and 4 nmoljg wet weight), 3-hydroxyanthranilic acid (2.2 and 4 nmoljg wet weight) ,1n..:l quinolinic acid (2.4 and 4 nmoljg wet weight) to incubation medium for phospholipid biosynthesis ill vitro induced a decrease of stearic, palrnitic and linoleic acid and an increase of oleic and especially arachidonic acid incorporation into phospholipids. These changes were accompanied by a decrease of cholesterol content in samples. The influence of kynurenine on fatty acid incorporation into phospholipids was similar to that of neopterin observed earlier. The other tryptophan degradation products behaved similar to the reduced pteridine derivatives. Our results allow to suggest that L-kynurenine decreases, while 3-hydroxykynurenine, 3-hydroxyanthranilic acid and quinolinic acid increase membrane fluidity in the studied concentrations.

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

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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 (August 25, 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 ladders are linked by weak C—O...π [O...ring centroid = 3.330 (2) Å] interactions, resulting in sheets extending parallel to theabplane. The molecular structure is broadly consistent with theoretical calculations performed by density functional theory (DFT).

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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 (March 1, 1988): 975–87. http://dx.doi.org/10.1523/jneurosci.08-03-00975.1988.

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45

Kozhevnikova, M. V., A. V. Krivova, E. O. Korobkova, A. A. Ageev, K. M. Shestakova, N. E. Moskaleva, S. A. Appolonova, E. V. Privalova, and Yu N. Belenkov. "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 (November 30, 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 liquid chromatography in combination with a triple quadrupole analyzer.Results Comparison of the three study groups revealed significant differences in concentrations of Trp (р=0.029), kynurenine (p<0.001), kynurenine/Trp ratio (p<0.001), quinolinic acid (р=0.007), kynurenic acid (р=0.003), serotonin (p<0.001), and 5‑hydroxyindoleacetic acid (5‑HIAA) (р=0.011). When the AH group was subdivided into subgroups without and with documented peripheral atherosclerosis, the intergroup differences remained for concentrations of kynurenine, kynurenine/Trp ratio, quinolinic acid, kynurenic acid, serotonin, and 5‑HIAA. Also, correlations were found between concentrations of Trp metabolites and laboratory and instrumental data, primarily inflammatory markers. Conclusion Analysis of serum concentrations of Trp and its metabolites in CVD patients showed increases in kynurenine, kynurenine/Trp ratio, quinolinic acid, kynurenic acid, and 5‑HIAA along with decreases in concentrations of Trp and serotonin in the groups of AH, AH with documented peripheral atherosclerosis, and IHD.

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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 (July 30, 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 active site. Among them, a monooxygenated, seven-membered lactone intermediate as a monodentate ligand of the iron center at 1.59-Å resolution was captured, which presumably corresponds to a substrate-based radical species observed by EPR using a slurry of small-sized single crystals. Other structural snapshots determined at around 2.0-Å resolution include monodentate and subsequently bidentate coordinated substrate, superoxo, alkylperoxo, and two metal-bound enol tautomers of the unstable dioxygenase product. These results reveal a detailed stepwise O-atom transfer dioxygenase mechanism along with potential isomerization activity that fine-tunes product profiling and affects the production of quinolinic acid at a junction of the metabolic pathway.

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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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Blesl, C., A. Tmava, A. Baranyi, A. Meinitzer, A. Painold, A. Holl, V. Stadlbauer-Köllner, H. P. Kapfhammer, and S. Mörkl. "The Kynurenine pathway in pancreatic carcinoma." European Psychiatry 41, S1 (April 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 participated in this study. We investigated serum-levels of kynurenine, kynurenic-acid, quinolinic-acid and tryptophan. To diagnose features of depression SKID-II and BDI were used.ResultsNone of the participants fulfilled criteria of a depressive episode. Regarding BDI-scores, 2 PC-patients showed features of mild depression. PC patients showed significantly lower tryptophan-levels (P = 0.05) and significantly increased quinolinic-acid levels (P = 0.01) compared to HC. Quinolinic-acid levels were correlated with BDI (r = 0.23, P = 0.02).ConclusionsOur study results imply IDO-activation and kynurenine-pathway activation by showing decreased tryptophan and high quinolonic-acid levels in our PC patients compared to HC. Larger studies are needed to gather further insight in the kynurenine pathway in PC.Disclosure of interestThe authors have not supplied their declaration of competing interest.Figure 1

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Ko¨hler, C., L. G. Eriksson, E. Okuno, and R. Schwarcz. "Localization of quinolinic acid metabolizing enzymes in the rat brain. immunohistochemical studies using antibodies to 3-hydroxyanthranilic acid oxygenase and quinolinic acid phosphoribosyltransferase." Neuroscience 27, no. 1 (October 1988): 49–76. http://dx.doi.org/10.1016/0306-4522(88)90219-9.

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Garavaglia, Silvia, Alessandro Galizzi, and Menico Rizzi. "Allosteric Regulation of Bacillus subtilis NAD Kinase by Quinolinic Acid." Journal of Bacteriology 185, no. 16 (August 15, 2003): 4844–50. http://dx.doi.org/10.1128/jb.185.16.4844-4850.2003.

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ABSTRACT NADP is essential for biosynthetic pathways, energy, and signal transduction. In living organisms, NADP biosynthesis proceeds through the phosphorylation of NAD with a reaction catalyzed by NAD kinase. We expressed, purified, and characterized Bacillus subtilis NAD kinase. This enzyme represents a new member of the inorganic polyphosphate [poly(P)]/ATP NAD kinase subfamily, as it can use poly(P), ATP, or other nucleoside triphosphates as phosphoryl donors. NAD kinase showed marked positive cooperativity for the substrates ATP and poly(P) and was inhibited by its product, NADP, suggesting that the enzyme plays a major regulatory role in NADP biosynthesis. We discovered that quinolinic acid, a central metabolite in NAD(P) biosynthesis, behaved like a strong allosteric activator for the enzyme. Therefore, we propose that NAD kinase is a key enzyme for both NADP metabolism and quinolinic acid metabolism.

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