Quinolinic acid

製品コードS3624 バッチS362401

印刷

化学情報

Chemical Structure Synonyms pyridine-2,3-dicarboxylic acid, QUIN Storage
(From the date of receipt)		 3 years -20°C powder
1 years -80°C in solvent
化学式

C7H5NO4
分子量 167.12 CAS No. 89-00-9
Solubility (25°C)* 体外 DMSO 25 mg/mL (149.59 mM)
Water 3 mg/mL (17.95 mM)
Ethanol Insoluble
* <1 mg/ml means slightly soluble or insoluble.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

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生物活性

製品説明 Quinolinic Acid (pyridine-2,3-dicarboxylic acid, QUIN), a neuroactive metabolite of the kynurenine pathway, is an agonist of N-methyl-D-aspartate (NMDA) receptor.
in vitro QUIN is an agonist of N-methyl-D-aspartate (NMDA) receptor, and it has a high in vivo potency as an excitotoxin. Although QUIN has an uptake system, its neuronal degradation enzyme is rapidly saturated, and the rest of extracellular QUIN can continue stimulating the NMDA receptor. QUIN (10 μM) prevents of glutamate-induced excitotoxicity in primary cultures of rat cerebellar granule neurons, nevertheless mature organotypic cultures of rat corticostriatal system or caudate nucleus chronically exposed to 100 nM QUIN for up to 7 weeks show focal degeneration characterized by the presence of vacuoles in neuropil, swollen dendrites, occasional swollen post-synaptic elements, and degenerated neurons. In vitro QUIN treatment of human primary foetal neurons leads to a substantial increase of tau phosphorylation at multiple positions. The increase in QUIN-induced phosphorylation of tau is attributed to a decrease in the expression and activity of the major tau phosphatases. QUIN can inhibit B monoamine oxidase (MAO-B) in human brain synaptosomal mitochondria and also can be a potent inhibitor of phosphoenolpyruvate carboxykinase (EC 4.1.1.32) from rat liver cytoplasm, an important enzyme in the gluconeogenesis pathway that converts oxaloacetate to phosphoenolpyruvate. QUIN can increase free radical production by inducing NOS activity in astrocytes and neurons, leading to oxidative stress, increasing both poly(ADP-ribose) polymerase (PARP) activity and extracellular lactate dehydrogenase (LDH) activity[1].
in vivo Quinolinic acid (QUIN), a neuroactive metabolite of the kynurenine pathway, is normally presented in nanomolar concentrations in human brain and cerebrospinal fluid (CSF) and is often implicated in the pathogenesis of a variety of human neurological diseases. The concentration of QUIN varies among different brain regions, with the cerebral cortex containing approximately 1.8 nmol/g wet weight; almost 2-fold than that found in the hippocampus (1 nmol/g wet weight). Intraarterial administration of either micromolar or millimolar concentrations of QUIN results in only negligible accumulations of this metabolite in the brain, suggesting that the central nervous system (CNS) appears to be well protected by the blood brain barrier (BBB) from peripheral QUIN. QUIN can also increase glutamate release and inhibit its reuptake by astrocytes, thus increasing its concentration in the microenvironments, causing neurotoxicity and also limiting glutamate to glutamine recycling in astrocytes by decreasing glutamine synthetase activity. Intrastriatal injection of QUIN provokes a decrease of cellular respiration and ATP levels[1].

プロトコル(参考用のみ)

動物実験 動物モデル C57Bl/6J mice
投薬量 30 nmol
投与方法 Intracerebral injection

長期の保管のために-20°Cの下で製品を保ってください。

人間や獣医の診断であるか治療的な使用のためにでない。

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