A metabolite of tryptophan with a possible role in neurodegenerative disorders. Elevated CSF levels of quinolinic acid are correlated with the severity of neuropsychological deficits in patients who have AIDS.
Quinolinic acid is a physiologically occurring metabolite of the kynurenine pathway, involved in the metabolism of tryptophan, which functions as a neuroexcitatory agent and has been implicated in several neurological disorders, including Huntington's disease and HIV-associated dementia.
Kynurenine is a metabolic product of the amino acid tryptophan, formed via the kynurenine pathway, and serves as an important intermediate in the biosynthesis of nicotinamide adenine dinucleotide (NAD+) and other neuroactive compounds, while also playing a role in immune response regulation and potential involvement in various neurological disorders.
An enzyme that catalyzes the conversion of 3-hydroxyanthranilate to 2-amino-3-carboxymuconate semialdehyde. It was formerly characterized as EC 1.13.1.6.
An oxidation product of tryptophan metabolism. It may be a free radical scavenger and a carcinogen.
Enzymes of the transferase class that catalyze the transfer of a pentose group from one compound to another.
A dioxygenase with specificity for the oxidation of the indoleamine ring of TRYPTOPHAN. It is a LIVER-specific enzyme that is the first and rate limiting enzyme in the kynurenine pathway of TRYPTOPHAN catabolism.
An essential amino acid that is necessary for normal growth in infants and for NITROGEN balance in adults. It is a precursor of INDOLE ALKALOIDS in plants. It is a precursor of SEROTONIN (hence its use as an antidepressant and sleep aid). It can be a precursor to NIACIN, albeit inefficiently, in mammals.
An NADPH-dependent flavin monooxygenase that plays a key role in the catabolism of TRYPTOPHAN by catalyzing the HYDROXYLATION of KYNURENINE to 3-hydroxykynurenine. It was formerly characterized as EC 1.14.1.2 and EC 1.99.1.5.
Toxic substances from microorganisms, plants or animals that interfere with the functions of the nervous system. Most venoms contain neurotoxic substances. Myotoxins are included in this concept.
2-, 3-, or 4-Pyridinecarboxylic acids. Pyridine derivatives substituted with a carboxy group at the 2-, 3-, or 4-position. The 3-carboxy derivative (NIACIN) is active as a vitamin.
Alkaloid isolated from seeds of Peganum harmala L., Zygophyllaceae. It is identical to banisterine, or telepathine, from Banisteria caapi and is one of the active ingredients of hallucinogenic drinks made in the western Amazon region from related plants. It has no therapeutic use, but (as banisterine) was hailed as a cure for postencephalitic Parkinson disease in the 1920's.
A broad-spectrum excitatory amino acid antagonist used as a research tool.
A water-soluble vitamin of the B complex occurring in various animal and plant tissues. It is required by the body for the formation of coenzymes NAD and NADP. It has PELLAGRA-curative, vasodilating, and antilipemic properties.
Striped GRAY MATTER and WHITE MATTER consisting of the NEOSTRIATUM and paleostriatum (GLOBUS PALLIDUS). It is located in front of and lateral to the THALAMUS in each cerebral hemisphere. The gray substance is made up of the CAUDATE NUCLEUS and the lentiform nucleus (the latter consisting of the GLOBUS PALLIDUS and PUTAMEN). The WHITE MATTER is the INTERNAL CAPSULE.
Trioses are monosaccharides, specifically simple sugars, that contain three carbon atoms, and can be glyceraldehydes or dihydroxyacetones, which are important intermediates in metabolic pathways such as glycolysis.
A coenzyme composed of ribosylnicotinamide 5'-diphosphate coupled to adenosine 5'-phosphate by pyrophosphate linkage. It is found widely in nature and is involved in numerous enzymatic reactions in which it serves as an electron carrier by being alternately oxidized (NAD+) and reduced (NADH). (Dorland, 27th ed)
A dioxygenase with specificity for the oxidation of the indoleamine ring of TRYPTOPHAN. It is an extrahepatic enzyme that plays a role in metabolism as the first and rate limiting enzyme in the kynurenine pathway of TRYPTOPHAN catabolism.
A familial disorder inherited as an autosomal dominant trait and characterized by the onset of progressive CHOREA and DEMENTIA in the fourth or fifth decade of life. Common initial manifestations include paranoia; poor impulse control; DEPRESSION; HALLUCINATIONS; and DELUSIONS. Eventually intellectual impairment; loss of fine motor control; ATHETOSIS; and diffuse chorea involving axial and limb musculature develops, leading to a vegetative state within 10-15 years of disease onset. The juvenile variant has a more fulminant course including SEIZURES; ATAXIA; dementia; and chorea. (From Adams et al., Principles of Neurology, 6th ed, pp1060-4)
Picolinic acid is an organic compound that belongs to the class of pyridine derivatives, acting as a chelating agent in mammals, primarily found in the liver and kidneys, and playing a significant role in the metabolism of proteins, vitamins, and minerals.
Substances that act in the brain stem or spinal cord to produce tonic or clonic convulsions, often by removing normal inhibitory tone. They were formerly used to stimulate respiration or as antidotes to barbiturate overdose. They are now most commonly used as experimental tools.
The part of CENTRAL NERVOUS SYSTEM that is contained within the skull (CRANIUM). Arising from the NEURAL TUBE, the embryonic brain is comprised of three major parts including PROSENCEPHALON (the forebrain); MESENCEPHALON (the midbrain); and RHOMBENCEPHALON (the hindbrain). The developed brain consists of CEREBRUM; CEREBELLUM; and other structures in the BRAIN STEM.
The D-enantiomer is a potent and specific antagonist of NMDA glutamate receptors (RECEPTORS, N-METHYL-D-ASPARTATE). The L form is inactive at NMDA receptors but may affect the AP4 (2-amino-4-phosphonobutyrate; APB) excitatory amino acid receptors.

Molecular mode of inhibition of glycogenolysis in rat liver by the dihydropyridine derivative, BAY R3401: inhibition and inactivation of glycogen phosphorylase by an activated metabolite. (1/56)

The racemic prodrug BAY R3401 suppresses hepatic glycogenolysis. BAY W1807, the active metabolite of BAY R3401, inhibits muscle glycogen phosphorylase a and b. We investigated whether BAY R3401 reduces hepatic glycogenolysis by allosteric inhibition or by phosphatase-catalyzed inactivation of phosphorylase. In gel-filtered liver extracts, racemic BAY U6751 (containing active BAY W1807) was tested for inhibition of phosphorylase in the glycogenolytic (in which only phosphorylase a is active) and glycogen-synthetic (for the evaluation of a:b ratios) directions. Phosphorylase inactivation by endogenous phosphatase was also studied. In liver extracts, BAY U6751 (0.9-36 micromol/l) inhibited glycogen synthesis by phosphorylase b (notwithstanding the inclusion of AMP), but not by phosphorylase a. Inhibition of phosphorylase-a-catalyzed glycogenolysis was partially relieved by AMP (500 micromol/l). BAY U6751 facilitated phosphorylase-a dephosphorylation. Isolated hepatocytes and perfused livers were tested for BAY R3401-induced changes in phosphorylase-a:b ratios and glycogenolytic output. Though ineffective in extracts, BAY R3401 (0.25 micromol/l-0.5 mmol/l) promoted phosphorylase-a dephosphorylation in hepatocytes. In perfused livers exposed to dibutyryl cAMP (100 micromol/l) for maximal activation of phosphorylase, BAY R3401 (125 micromol/l) inactivated phosphorylase by 63% but glucose output dropped by 83%. Inhibition of glycogenolysis suppressed glucose-6-phosphate (G6P) levels. Activation of glycogen synthase after phosphorylase inactivation depended on the maintenance of G6P levels by supplementing glucose (50 mmol/l). We conclude that the metabolites of BAY R3401 suppress hepatic glycogenolysis by allosteric inhibition and by the dephosphorylation of phosphorylase a.  (+info)

Experiments in marine biochemistry. Homarine metabolism in Penaeus duorarum. (2/56)

A fractionation procedure has been developed which permits the isolation of 1 to 2 mg of homarine from a single shrimp. This procedure was used to show that homarine is endogenously synthesized by Penaeus duorarum in the free unbound form, and to study the metabolic precursors involved. Injected DL-[14C]tryptophan was not converted to [14C]homarine. However, [6-14C]quinolinic acid, a known catabolite of tryptophan, is an effective precursor. [2-14C]Acetate and [U-14C]glycerol are effectively converted to [14C]homarine while [14C]bicarbonate is poorly utilized. The injection of L-[U-14C]aspartate resulted in labeled homarine, but the quantity converted was less than expected. Since [14C]glycerol is an effective precursor there is a possibility that quinolinic acid may be formed in P. duorarum by a condensation similar to that of glyceraldehyde 3-phosphate with aspartic acid or a closely related metabolite. It is suggested that decarboxylation of quinolinic acid gives rise to picolinic acid which is methylated to yield homarine. L-[methyl-14C]Methionine efficiently provides the N-methyl carbon presumably via S-adenosylmethionine.  (+info)

NR2B-containing NMDA autoreceptors at synapses on entorhinal cortical neurons. (3/56)

We have previously shown that presynaptic N-methyl-D-aspartate receptors (NMDARs) can facilitate glutamate release onto principal neurons in the entorhinal cortex (EC). In the present study, we have investigated the subunit composition of these presynaptic NMDARs. We recorded miniature alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor-mediated excitatory postsynaptic currents (mEPSCs), from visually identified neurons in layers II and V of the EC in vitro. In both layers, bath application of the NR2A/B subunit-selective agonist, homoquinolinic acid (HQA), resulted in a marked facilitation of mEPSC frequency. Blockade of presynaptic Ca(2+) entry through either NMDARs or voltage-gated Ca(2+) channels with Co(2+) prevented the effects of HQA, confirming that Ca(2+) entry to the terminal was required for facilitation. When the NR2B-selective antagonist, ifenprodil, was applied prior to HQA, the increase in mEPSC frequency was greatly reduced. In addition, we found that an NMDAR antagonist blocked frequency-dependent facilitation of evoked release and reduced mEPSC frequency in layer V. Thus we have demonstrated that NMDA autoreceptors in layer V of the EC bear the NR2B subunit, and that NMDARs are also present at terminals onto superficial neurons.  (+info)

Effect of vitamin B6 on leucine-induced changes in human subjects. (4/56)

Distrubances in the tryptophan-niacin pathway seen in endemic pellagra among sorghum eaters have been ascribed to high dietary intake of leucine. Vitamin B6 plays an important role in several steps of this pathway. Therefore, studies on possible metabolic interrelations between excess dietary leucine and vitamin B6 were undertaken in normal healthy human subjects. The results indicated that vitamin B6 could successfully counteract the effects of leucine on quinolinic acid excretion in urine, and on in vitro nicotinamide nucleotide synthesis by erythrocytes, and also could correct the abnormalities of 5-hydroxytryptamine metabolism induced by excess leucine. These observations suggest that vitamin B6 nutritional status may have a contributory role in the pathogenesis of endemic pellagra.  (+info)

Effects of excess intake of leucine and valine deficiency on tryptophan and niacin metabolites in humans. (5/56)

Nineteen healthy humans (2 men and 17 women) served as experimental subjects in 4 experiments using diets having different levels of leucine and also a valine-deficient diet. The effect of an excess intake of leucine, with and without addition of vitamin B-6, and the effect of a deficiency of valine on urinary excretions of N1-methylnicotinamide, N1-methyl-2-pyridone-5-carboxamide, nicotinic acid, quinolinic acid, and 5-hydroxyindole acetic acid, and on the level of plasma amino acids were investigated. There was no effect of leucine on the excretion of these metabolites, but a marked decrease in the plasma (or serum) valine level was observed. The same decrease was seen when a valine-deficient diet was fed.  (+info)

The effects of inhibition of gluconeogenesis on ketogenesis in starved and diabetic rats. (6/56)

Experiments were performed in which the effects of inhibiting gluconeogenesis on ketone-body formation were examined in vivo in starved and severely streptozotocin-diabetic rats. The infusion of 3-mercaptopicolinate, an inhibitor of gluconeogenesis (DiTullio et al., 1974), caused decreases in blood [glucose] and increases in blood [lactate] and [pyruvate] in both normal and ketoacidotic rats. Patterns of liver gluconeogenic intermediates after 3-mercaptopicolinate infusion suggested inhibition at the level of phosphoenolpyruvate carboxykinase. This was confirmed by measurement of hepatic oxaloacetate concentrations which were increased 5-fold after 3-mercaptopicolinate administration. The infusion of 3-mercaptopicolinate caused a decrease in total ketone-body concentrations of 30% in starved rats and 73% in the diabetic animals. Blood glycerol and hepatic triglyceride concentrations remained unchanged. The decreases in ketone-body concentrations were associated with increases in the calculated hepatic cytosolic and mitochondrial [NADH]/[NAD+] ratios. The decrease in ketogenesis seen after inhibition of gluconeogenesis may have resulted from an inhibition of hepatic fatty acid oxidation by the more reduced mitochondrial redox state. It was concluded that gluconeogenesis may stimulate ketogenesis by as much as 30% in severe diabetic ketoacidosis.  (+info)

Poliovirus induces indoleamine-2,3-dioxygenase and quinolinic acid synthesis in macaque brain. (7/56)

Accumulation of the neurotoxin quinolinic acid within the brain occurs in a broad spectrum of patients with inflammatory neurologic disease and may be of neuropathologic significance. The production of quinolinic acid was postulated to reflect local induction of indoleamine 2,3-dioxygenase by cytokines in reactive cells and inflammatory cell infiltrates within the central nervous system. To test this hypothesis, macaques received an intraspinal injection of poliovirus as a model of localized inflammatory neurologic disease. Seventeen days later, spinal cord indoleamine 2,3-dioxygenase activity and quinolinic acid concentrations in spinal cord and cerebrospinal fluid were both increased in proportion to the degree of inflammatory responses and neurologic damage in the spinal cord, as well as the severity of motor paralysis. The absolute concentrations of quinolinic acid achieved in spinal cord and cerebrospinal fluid exceeded levels reported to kill spinal cord neurons in vitro. Smaller increases in indoleamine 2,3-dioxygenase activity and quinolinic acid concentrations also occurred in parietal cortex, a poliovirus target area. In frontal cortex, which is not a target for poliovirus, indoleamine 2,3-dioxygenase was not affected. A monoclonal antibody to human indoleamine 2,3-dioxygenase was used to visualize indoleamine 2,3-dioxygenase predominantly in grey matter of poliovirus-infected spinal cord, in conjunction with local inflammatory lesions. Macrophage/monocytes in vitro synthesized [13C6]quinolinic acid from [13C6]L-tryptophan, particularly when stimulated by interferon-gamma. Spinal cord slices from poliovirus-inoculated macaques in vitro also converted [13C6]L-tryptophan to [13C6]quinolinic acid. We conclude that local synthesis of quinolinic acid from L-tryptophan within the central nervous system follows the induction of indoleamine-2,3-dioxygenase, particularly within macrophage/microglia. In view of this link between immune stimulation and the synthesis of neurotoxic amounts of quinolinic acid, we propose that attenuation of local inflammation, strategies to reduce the synthesis of neuroactive kynurenine pathway metabolites, or drugs that interfere with the neurotoxicity of quinolinic acid offer new approaches to therapy in inflammatory neurologic disease.  (+info)

Human macrophages convert L-tryptophan into the neurotoxin quinolinic acid. (8/56)

Substantial increases in the concentrations of the excitotoxin and N-methyl-D-aspartate-receptor agonist quinolinic acid (QUIN) occur in human patients and non-human primates with inflammatory diseases. Such increases were postulated to be secondary to induction of indoleamine 2,3-dioxygenase in inflammatory cells, particularly macrophages, by interferon-gamma. To test this hypothesis, human peripheral-blood macrophages were incubated with L-[13C6]tryptophan in the absence or presence of interferon-gamma. [13C6]QUIN was quantified by gas chromatography and electron-capture negative-chemical-ionization mass spectrometry. [13C6]QUIN was detected in the incubation medium of both unstimulated and stimulated cultures. Exposure to interferon-gamma substantially increased the accumulation of [13C6]QUIN in a dose- and time-dependent manner. The QUIN concentrations achieved exceeded those reported in both cerebrospinal fluid and blood of patients and of non-human primates with inflammatory diseases. Macrophages stimulated with interferon-gamma may be an important source of accelerated L-tryptophan conversion into QUIN in inflammatory diseases.  (+info)

Quinolinic acid is a metabolite found in the human body, produced during the metabolism of tryptophan, an essential amino acid. It is a component of the kynurenine pathway and acts as a neuroexcitatory chemical in the brain. In excessive amounts, quinolinic acid can lead to neurotoxicity, causing damage to neurons and contributing to several neurological disorders such as Huntington's disease, Alzheimer's disease, Parkinson's disease, AIDS-dementia complex, and multiple sclerosis. It also plays a role in the pathogenesis of psychiatric conditions like schizophrenia and major depressive disorder.

Quinolinic acid is a type of organic compound that belongs to the class of heterocyclic compounds known as quinolines, which contain a bicyclic system made up of a benzene ring fused to a piperidine ring. Quinolinic acid is specifically a derivative of quinoline with a carboxylic acid functional group.

In the context of medicine and biology, quinolinic acid is an endogenous excitatory neurotransmitter and a metabolite in the kynurenine pathway of tryptophan metabolism. It is mainly produced in the brain by activated microglia and to some extent by macrophages, neurons, and astrocytes.

Quinolinic acid has been implicated in several neurological disorders, including Huntington's disease, Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis (ALS), HIV-associated dementia, and depression. High levels of quinolinic acid can cause excitotoxicity, which is a process of neurotoxicity induced by excessive stimulation of glutamate receptors leading to neuronal damage or death. It has also been suggested that quinolinic acid may play a role in the pathogenesis of some psychiatric disorders, such as schizophrenia and bipolar disorder.

Kynurenine is an organic compound that is produced in the human body as part of the metabolism of the essential amino acid tryptophan. It is an intermediate in the kynurenine pathway, which leads to the production of several neuroactive compounds and NAD+, a coenzyme involved in redox reactions.

Kynurenine itself does not have any known physiological function, but some of its metabolites have been found to play important roles in various biological processes, including immune response, inflammation, and neurological function. For example, the kynurenine pathway produces several neuroactive metabolites that can act as agonists or antagonists at various receptors in the brain, affecting neuronal excitability, synaptic plasticity, and neurotransmission.

Abnormalities in the kynurenine pathway have been implicated in several neurological disorders, including depression, schizophrenia, Alzheimer's disease, and Huntington's disease. Therefore, understanding the regulation of this pathway and its metabolites has become an important area of research in neuroscience and neuropsychopharmacology.

3-Hydroxyanthranilate 3,4-Dioxygenase is an enzyme that catalyzes the chemical reaction:

3-hydroxyanthranilate + O2 -> 2-amino-3-carboxymuconate semialdehyde

This enzyme is involved in the catabolism of tryptophan, an essential amino acid, through the kynurenine pathway. The reaction catalyzed by this enzyme involves the cleavage of the aromatic ring of 3-hydroxyanthranilate and the formation of 2-amino-3-carboxymuconate semialdehyde, which is further metabolized to produce NAD+ and other products. Defects in this enzyme have been associated with certain neurological disorders.

3-Hydroxyanthranilic acid is an intermediate metabolite in the catabolism (breakdown) of tryptophan, an essential amino acid. It is formed from the oxidation of 3-hydroxykynurenine by the enzyme kynureninase. Further breakdown of 3-hydroxyanthranilic acid can lead to the formation of various other metabolites, including quinolinic acid and picolinic acid, which are involved in the synthesis of nicotinamide adenine dinucleotide (NAD+), a coenzyme that plays a crucial role in cellular metabolism.

Abnormal accumulation or dysregulation of 3-hydroxyanthranilic acid has been implicated in several pathological conditions, including neurodegenerative disorders and certain types of cancer. However, more research is needed to fully understand the role of this metabolite in human health and disease.

Pentosyltransferases are a group of enzymes that catalyze the transfer of a pentose (a sugar containing five carbon atoms) molecule from one compound to another. These enzymes play important roles in various biochemical pathways, including the biosynthesis of nucleotides, glycoproteins, and other complex carbohydrates.

One example of a pentosyltransferase is the enzyme that catalyzes the addition of a ribose sugar to form a glycosidic bond with a purine or pyrimidine base during the biosynthesis of nucleotides, which are the building blocks of DNA and RNA.

Another example is the enzyme that adds xylose residues to proteins during the formation of glycoproteins, which are proteins that contain covalently attached carbohydrate chains. These enzymes are essential for many biological processes and have been implicated in various diseases, including cancer and neurodegenerative disorders.

Tryptophan oxygenase, also known as tryptophan 2,3-dioxygenase (TDO) or tryptophan pyrrolase, is an enzyme that catalyzes the breakdown of the essential amino acid tryptophan. This enzyme requires molecular oxygen and plays a crucial role in regulating tryptophan levels within the body.

The reaction catalyzed by tryptophan oxygenase involves the oxidation of the indole ring of tryptophan, leading to the formation of N-formylkynurenine. This metabolite is further broken down through several enzymatic steps to produce other biologically active compounds, such as kynurenine and niacin (vitamin B3).

Tryptophan oxygenase activity is primarily found in the liver and is induced by various factors, including corticosteroids, cytokines, and tryptophan itself. The regulation of this enzyme has implications for several physiological processes, such as immune response, neurotransmitter synthesis, and energy metabolism. Dysregulation of tryptophan oxygenase activity can contribute to the development of various pathological conditions, including neurological disorders and cancer.

Tryptophan is an essential amino acid, meaning it cannot be synthesized by the human body and must be obtained through dietary sources. Its chemical formula is C11H12N2O2. Tryptophan plays a crucial role in various biological processes as it serves as a precursor to several important molecules, including serotonin, melatonin, and niacin (vitamin B3). Serotonin is a neurotransmitter involved in mood regulation, appetite control, and sleep-wake cycles, while melatonin is a hormone that regulates sleep-wake patterns. Niacin is essential for energy production and DNA repair.

Foods rich in tryptophan include turkey, chicken, fish, eggs, cheese, milk, nuts, seeds, and whole grains. In some cases, tryptophan supplementation may be recommended to help manage conditions related to serotonin imbalances, such as depression or insomnia, but this should only be done under the guidance of a healthcare professional due to potential side effects and interactions with other medications.

Kynurenine 3-Monooxygenase (KMO) is an enzyme that is involved in the metabolism of the amino acid tryptophan. Specifically, it is a key enzyme in the kynurenine pathway, which is the primary route of tryptophan breakdown in mammals.

KMO catalyzes the conversion of L-kynurenine to 3-hydroxykynurenine using molecular oxygen and nicotinamide adenine dinucleotide phosphate (NADPH) as cofactors. This reaction is an important step in the production of several neuroactive metabolites, including quinolinic acid and kynurenic acid, which have been implicated in various neurological disorders such as Alzheimer's disease, Parkinson's disease, and depression.

Inhibition of KMO has been suggested as a potential therapeutic strategy for the treatment of these disorders due to its role in regulating the balance between neuroprotective and neurotoxic kynurenine metabolites.

Neurotoxins are substances that are poisonous or destructive to nerve cells (neurons) and the nervous system. They can cause damage by destroying neurons, disrupting communication between neurons, or interfering with the normal functioning of the nervous system. Neurotoxins can be produced naturally by certain organisms, such as bacteria, plants, and animals, or they can be synthetic compounds created in a laboratory. Examples of neurotoxins include botulinum toxin (found in botulism), tetrodotoxin (found in pufferfish), and heavy metals like lead and mercury. Neurotoxic effects can range from mild symptoms such as headaches, muscle weakness, and tremors, to more severe symptoms such as paralysis, seizures, and cognitive impairment. Long-term exposure to neurotoxins can lead to chronic neurological conditions and other health problems.

Niacin, also known as nicotinic acid, is a form of vitamin B3 (B-complex vitamin) that is used by the body to turn food into energy. It is found in various foods including meat, fish, milk, eggs, green vegetables, and cereal grains. Niacin is also available as a dietary supplement and prescription medication.

As a medication, niacin is primarily used to treat high cholesterol levels. It works by reducing the production of LDL (bad) cholesterol in the body and increasing the levels of HDL (good) cholesterol. Niacin can also help lower triglycerides, another type of fat found in the blood.

Niacin is available in immediate-release, sustained-release, and extended-release forms. The immediate-release form can cause flushing of the skin, itching, tingling, and headaches, which can be uncomfortable but are not usually serious. The sustained-release and extended-release forms may have fewer side effects, but they can also increase the risk of liver damage and other serious side effects.

It is important to note that niacin should only be taken under the supervision of a healthcare provider, as it can interact with other medications and have potentially serious side effects.

Harmine is defined medically as an alpha-carboline derivative that is present in various plants including the seeds of Peganum harmala and the bark of Banisteriopsis caapi. It functions as an monoamine oxidase inhibitor (MAOI) and has been used in traditional medicine for its psychoactive properties. It has also been studied for potential anti-cancer, anti-inflammatory, and neuroprotective effects.

Kynurenic acid is a metabolite of the amino acid tryptophan, which is formed through the kynurenine pathway. It functions as an antagonist at glutamate receptors and acts as a neuroprotective agent by blocking excessive stimulation of NMDA receptors in the brain. Additionally, kynurenic acid also has anti-inflammatory properties and is involved in the regulation of the immune response. Abnormal levels of kynurenic acid have been implicated in several neurological disorders such as schizophrenia, epilepsy, and Huntington's disease.

Niacin, also known as vitamin B3 or nicotinic acid, is a water-soluble vitamin that is essential for human health. It is a crucial component of the coenzymes NAD (nicotinamide adenine dinucleotide) and NADP (nicotinamide adenine dinucleotide phosphate), which play key roles in energy production, DNA repair, and cellular signaling.

Niacin can be obtained from various dietary sources, including meat, poultry, fish, legumes, whole grains, and fortified foods. It is also available as a dietary supplement and prescription medication. Niacin deficiency can lead to a condition called pellagra, which is characterized by symptoms such as diarrhea, dermatitis, dementia, and, if left untreated, death.

In addition to its role in energy metabolism and DNA repair, niacin has been shown to have potential benefits for cardiovascular health, including lowering LDL (low-density lipoprotein) cholesterol and triglyceride levels while raising HDL (high-density lipoprotein) cholesterol levels. However, high-dose niacin therapy can also have adverse effects, such as flushing, itching, and liver toxicity, so it should be used under the guidance of a healthcare professional.

The corpus striatum is a part of the brain that plays a crucial role in movement, learning, and cognition. It consists of two structures called the caudate nucleus and the putamen, which are surrounded by the external and internal segments of the globus pallidus. Together, these structures form the basal ganglia, a group of interconnected neurons that help regulate voluntary movement.

The corpus striatum receives input from various parts of the brain, including the cerebral cortex, thalamus, and other brainstem nuclei. It processes this information and sends output to the globus pallidus and substantia nigra, which then project to the thalamus and back to the cerebral cortex. This feedback loop helps coordinate and fine-tune movements, allowing for smooth and coordinated actions.

Damage to the corpus striatum can result in movement disorders such as Parkinson's disease, Huntington's disease, and dystonia. These conditions are characterized by abnormal involuntary movements, muscle stiffness, and difficulty initiating or controlling voluntary movements.

Trioses are simple sugars that contain three carbon atoms and a functional group called a ketone or aldehyde. They are the simplest type of sugar molecule, after monosaccharides such as glyceraldehyde and dihydroxyacetone.

Triose sugars can exist in two structural forms:

* Dihydroxyacetone (DHA), which is a ketotriose with the formula CH2OH-CO-CH2OH, and
* Glyceraldehyde (GA), which is an aldotriose with the formula HO-CHOH-CHO.

Trioses play important roles in various metabolic pathways, including glycolysis, gluconeogenesis, and the Calvin cycle of photosynthesis. In particular, DHA and GA are intermediates in the conversion of glucose to pyruvate during glycolysis, and they are also produced from pyruvate during gluconeogenesis.

Trioses can be synthesized chemically or biochemically through various methods, such as enzymatic reactions or microbial fermentation. They have potential applications in the food, pharmaceutical, and chemical industries, as they can serve as building blocks for more complex carbohydrates or as precursors for other organic compounds.

NAD (Nicotinamide Adenine Dinucleotide) is a coenzyme found in all living cells. It plays an essential role in cellular metabolism, particularly in redox reactions, where it acts as an electron carrier. NAD exists in two forms: NAD+, which accepts electrons and becomes reduced to NADH. This pairing of NAD+/NADH is involved in many fundamental biological processes such as generating energy in the form of ATP during cellular respiration, and serving as a critical cofactor for various enzymes that regulate cellular functions like DNA repair, gene expression, and cell death.

Maintaining optimal levels of NAD+/NADH is crucial for overall health and longevity, as it declines with age and in certain disease states. Therefore, strategies to boost NAD+ levels are being actively researched for their potential therapeutic benefits in various conditions such as aging, neurodegenerative disorders, and metabolic diseases.

Indoleamine-2,3-dioxygenase (IDO) is an enzyme that catalyzes the oxidation of L-tryptophan to N-formylkynurenine, which is the first and rate-limiting step in the kynurenine pathway. This enzymatic reaction plays a crucial role in regulating tryptophan metabolism and immune responses. IDO is expressed in various tissues, including the brain, liver, and placenta, as well as in some immune cells such as dendritic cells and macrophages. It can be upregulated by inflammatory stimuli, and its expression has been associated with immune tolerance and suppression of T-cell responses. IDO is also being investigated as a potential therapeutic target for various diseases, including cancer, autoimmune disorders, and neuropsychiatric conditions.

Huntington Disease (HD) is a genetic neurodegenerative disorder that affects both cognitive and motor functions. It is characterized by the progressive loss of neurons in various areas of the brain, particularly in the striatum and cortex. The disease is caused by an autosomal dominant mutation in the HTT gene, which codes for the huntingtin protein. The most common mutation is a CAG repeat expansion in this gene, leading to the production of an abnormal form of the huntingtin protein that is toxic to nerve cells.

The symptoms of HD typically appear between the ages of 30 and 50, but they can start earlier or later in life. The early signs of HD may include subtle changes in mood, cognition, and coordination. As the disease progresses, individuals with HD experience uncontrolled movements (chorea), emotional disturbances, cognitive decline, and difficulties with communication and swallowing. Eventually, they become dependent on others for their daily needs and lose their ability to walk, talk, and care for themselves.

There is currently no cure for HD, but medications and therapies can help manage the symptoms of the disease and improve quality of life. Genetic testing is available to confirm the diagnosis and provide information about the risk of passing the disease on to future generations.

Picolinic acid is not specifically classified as a medical term, but it is a type of organic compound that belongs to the class of molecules known as pyridinecarboxylic acids. These are carboxylic acids derived from pyridine by the substitution of a hydrogen atom with a carboxyl group.

Picolinic acid, specifically, is a pyridine derivative with a carboxyl group at the 2-position of the ring. It is naturally produced in the body and can be found in various tissues and fluids, including the brain, where it plays a role in the metabolism of amino acids, particularly tryptophan.

In addition to its physiological functions, picolinic acid has been studied for its potential therapeutic applications. For example, it has been shown to have antibacterial and antifungal properties, and may also play a role in heavy metal chelation and neuroprotection. However, more research is needed to fully understand the medical significance of this compound.

Convulsants are substances or agents that can cause seizures or convulsions. These can be medications, toxins, or illnesses that lower the seizure threshold and lead to abnormal electrical activity in the brain, resulting in uncontrolled muscle contractions and relaxation. Examples of convulsants include bromides, strychnine, organophosphate pesticides, certain antibiotics (such as penicillin or cephalosporins), and alcohol withdrawal. It is important to note that some medications used to treat seizures can also have convulsant properties at higher doses or in overdose situations.

The brain is the central organ of the nervous system, responsible for receiving and processing sensory information, regulating vital functions, and controlling behavior, movement, and cognition. It is divided into several distinct regions, each with specific functions:

1. Cerebrum: The largest part of the brain, responsible for higher cognitive functions such as thinking, learning, memory, language, and perception. It is divided into two hemispheres, each controlling the opposite side of the body.
2. Cerebellum: Located at the back of the brain, it is responsible for coordinating muscle movements, maintaining balance, and fine-tuning motor skills.
3. Brainstem: Connects the cerebrum and cerebellum to the spinal cord, controlling vital functions such as breathing, heart rate, and blood pressure. It also serves as a relay center for sensory information and motor commands between the brain and the rest of the body.
4. Diencephalon: A region that includes the thalamus (a major sensory relay station) and hypothalamus (regulates hormones, temperature, hunger, thirst, and sleep).
5. Limbic system: A group of structures involved in emotional processing, memory formation, and motivation, including the hippocampus, amygdala, and cingulate gyrus.

The brain is composed of billions of interconnected neurons that communicate through electrical and chemical signals. It is protected by the skull and surrounded by three layers of membranes called meninges, as well as cerebrospinal fluid that provides cushioning and nutrients.

2-Amino-5-phosphonovalerate (APV) is a neurotransmitter receptor antagonist that is used in research to study the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors. These receptors are involved in various physiological processes, including learning and memory, and are also implicated in a number of neurological disorders. APV works by binding to the NMDA receptor and blocking its activity, which allows researchers to study the role of these receptors in different biological processes. It is not used as a therapeutic drug in humans.

... and other amino acids. Lesions in the pallidum can suppress effects of quinolinic acid in monkeys injected with quinolinic acid ... Quinolinic acid has also been found in HAND patients brains. In fact, the amount of quinolinic acid found in the brain of HAND ... Quinolinic acid (abbreviated QUIN or QA), also known as pyridine-2,3-dicarboxylic acid, is a dicarboxylic acid with a pyridine ... Quinolinic acid levels are too high at these sites to be controlled by KYNA, causing neurotoxicity to occur. Quinolinic acid ...
The kynurenine pathway of tryptophan metabolism includes quinolinic acid (QA) which is both a selective agonist at N-methyl-D- ... Quinolinic acid induces neuritogenesis in SH-SY5Y neuroblastoma cells independently of NMDA receptor activation Eur J Neurosci ... The kynurenine pathway of tryptophan metabolism includes quinolinic acid (QA) which is both a selective agonist at N-methyl-D- ... Retinoic acid (RA, 10 μm) induced differentiation of SH-SY5Y cells into a neuronal phenotype showing neurite growth. QA (50-150 ...
138946-42-6Biological Activity:Quinolinic acid-d3 is the deuterium labeled Quinolinic acid. Quinolinic acid is an endogenous N- ... We do not sell to patients.Quinolinic acid-d3CAS No. : ... Quinolinic acid-d3 is the deuterium labeled Quinolinic acid. ... Quinolinic acid is an endogenous N-methyl-D-aspartate (NMDA) receptor agonist synthesized from L-tryptophan via the kynurenine ... Related Small Molecules:D-α-Hydroxyglutaric acid disodium;Nicotinamide N-oxide;3-Hydroxyglutaric acid-d5;DPPC-d62;SDMA-d6;2- ...
Quinolinic acid is intended for Pharmaceuticals applications. All information about [13C4,15N]-Quinolinic acid is provided in ...
Kynurenic acid (KYNA) is an endogenous tryptophan (Trp) metabolite known to possess neuroprotective property. KYNA plays ... shift in the balance of the Trp-KYN metabolic system toward the relative excess of neurotoxic molecules such as quinolinic acid ... the α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor, and the kainic acid receptor [7,8,9,10]. Furthermore ... Rozsa, E.; Robotka, H.; Vecsei, L.; Toldi, J. The Janus-face kynurenic acid. J. Neural Transm. 2008, 115, 1087-1091. [Google ...
4-Chloro-3-hydroxyanthranilate attenuate quinolinic acid accumulation in brain following transient cerebral ischemia in the ... 4-Chloro-3-hydroxyanthranilate attenuate quinolinic acid accumulation in brain following transient cerebral ischemia in the ... 4-Chloro-3-hydroxyanthranilate attenuate quinolinic acid accumulation in brain following transient cerebral ischemia in the ... T1 - 4-Chloro-3-hydroxyanthranilate attenuate quinolinic acid accumulation in brain following transient cerebral ischemia in ...
Relationship of quinolinic acid and serotonin with depression and pain degree in cancer pain patients: a cross-sectional study ... Conclusion: Quinolinic acid and serotonin levels are related to depression and pain degree in cancer pain patients (p,0.05), ... Quinolinic acid (QUIN) and serotonin (5-HT) are chemicals that can affect pain perception and depressive disorders. This study ... The patients quinolinic acid and serotonin plasma were collected through blood samples and assessed using enzyme-linked ...
The regulation of quinolinic acid in human immunodeficiency virus-infected monocytes.﻽. Nottet HS, Flanagan EM, Flanagan CR, ... Valproic acid adjunctive therapy for HIV-associated cognitive impairment: a first report.﻽. Schifitto G, Peterson DR, Zhong J, ... Effects of valproic acid coadministration on plasma efavirenz and lopinavir concentrations in human immunodeficiency virus- ... A randomized, double-blind, placebo-controlled trial of deprenyl and thioctic acid in human immunodeficiency virus-associated ...
14 Stone T W. Neuropharmacology of quinolinic and kynurenic acids. Pharmacol Rev. 1993; 45 309-379 ... Regional brain amino acid and neurotransmitter derangements during abdominal sepsis and septic encephalopathy in the rat. The ... Effect of branched chain amino acid enrichment of total parenteral nutrition on nitrogen sparing and clinical outcome of sepsis ...
Encapsulated cell-based biodelivery of meteorin is neuroprotective in the quinolinic acid rat model of neurodegenerative ... 1-octanesulfonic acid (OSA) sodium salt, triethylamine (TEA), 70% perchloric acid (PCA), 85% phosphoric acid and sodium ... Mice were injected with 1.5 μl 6-OHDA (2 μg/μl in 0.02% ascorbic acid in saline) or 1 μl 6-OHDA (3 μg/μl in 0.02% ascorbic acid ... 10G, H). By definition, the desaturation of saturated fatty acid (SFA) to mono-unsaturated fatty acid (MUFA) could not be ruled ...
IDK® Quinolinic acid (QinA) ELISA. Article number: K 7736. Test-Category. ELISA ...
Formic acid, acetic acid, oxalic acid, acrylic acid, etc., are cited as the organic carboxylic acid and acetic anhydride, etc ... are used as the organic carboxylic acid anhydride. The organic carboxylic acid, etc., are added in an amount of 0.01-5.0 pts.wt ... The acrylonitrile is preferably used in an amount of ≥4.0 mol based on 1 mol sulfuric acid. COPYRIGHT: (C)1992,JPO&Japio ... CONSTITUTION: Acrylonitrile is reacted with sulfuric acid at ≥95% concentration and isobutylene in the presence of an organic ...
Transgenic mice expressing a Huntingtons disease mutation are resistant to quinolinic acid-induced striatal excitotoxicity. ... The IT15 gene is composed of 67 exons and encodes a protein of 3,144 amino acids, called huntingtin (2). Exon 1 contains a CAG ... trinucleotide repeat that encodes the amino acid glutamine, followed by another repeat that encodes proline. In unaffected ...
... anthranilic acid,quinolinic acid) with diverse neurophysiological functions(Stone, 1993; Moroni, 1999). In plants,tryptophan is ... The free amino acid L-tryptophan is the natural chemoattractant for sperm of the red abalone Haliotis rufescens. This ... Amino acids react with OPA (o-phthalaldehyde) to yield fluorescent derivatives that can be separated and quantified by ... As a control for increasing the concentration of an amino acid in the sea water medium, sperm were also imaged around eggs in a ...
1999b), and after excitotoxic lesioning with quinolinic acid of the striatum (Roitberg et al. 2002). The effect of PDE-Is in ... Palfi S, Ferrante RJ, Brouillet E, Beal MF, Dolan R, Guyot MC, Peschanski M, Hantraye P (1996) Chronic 3-nitropropionic acid ...
Noakes R, Spelman L, Williamson R. Is the L-tryptophan metabolite quinolinic acid responsible for eosinophilic fasciitis?. Clin ... An investigator injected himself with quinolinic acid, an L-tryptophan metabolite, and developed peripheral eosinophilia and ...
Epithelial Cells Niacinamide Nad Zinc Quinolinic Acid Metabolic Caenorhabditis Elegans Acoustics Purine Nucleoside ... Uridine monophosphate synthetase enables eukaryotic de novo NAD,sup,+,/sup, biosynthesis from quinolinic acid. Melanie ... Uridine monophosphate synthetase enables eukaryotic de novo NAD,sup,+,/sup, biosynthesis from quinolinic acid. Melanie ...
Involved in the catabolism of quinolinic acid (QA). Gene Name:. QPRT. Uniprot ID:. Q15274 Molecular weight:. 30815.28. ... McCormick GT, Sanchez RM: Pyridine extractability of acid-fastness from Mycobacterium leprae. Int J Lepr Other Mycobact Dis. ...
The neurotoxin was 0.09 m quinolinic acid (Sigma, Poole, UK) dissolved in a phosphate buffer, pH 7.0-7.2. ... animals received two bilateral injections of 0.4 μl of quinolinic acid at the following coordinates: AP, +3.0 mm from bregma; L ...
Papaverine, a Phosphodiesterase 10A Inhibitor, Ameliorates Quinolinic Acid-Induced Synaptotoxicity in Human Cortical Neurons. ... towards quinolinic acid (QUIN)-induced excitotoxicity utilizing human major cortical neurons. Cytotoxicity potential of PAP was ...
4B). Specifically within the DIET group, a decrease in quinolinic acid, L-tryptophan, and L-phenylalanine, was observed, while ... including polyunsaturated fatty acids (t(40) = −2.05, p = 0.047), omega-3 fatty acids (Z = −3.4, p = 0.001) as well as some ... quinolinic acid, which is a NMDA agonist and can exert neurotoxic effects which can disrupt neurotransmission in high ... Szalardy L, Zadori D, Toldi J, Fulop F, Klivenyi P, Vecsei L. Manipulating kynurenic acid levels in the brain-on the edge ...
Quinolinic Acid and Chronic Cancer Pain Fikri Bariz, Christrijogo Sumartono Waloejo, Prananda Surya Airlangga, Prihatma ...
Additionally, 3-hydroxyanthranillic acid further transforms to quinolinic acid (QUIN) by 3-hydroxyanthranillic acid 3,4- ... Reduction of kynurenic acid to quinolinic acid ratio in both the depressed and remitted phases of major depressive disorder. ... kynurenic acid; QUIN: quinolinic acid; THC: ∆9-tetrahydrocannabinol; TNFα: tumor necrosis factor α; Trp: tryptophan; SRT: ... kynurenic acid; QUIN: quinolinic acid; THC: ∆9-tetrahydrocannabinol; TNFα: tumor necrosis factor α; Trp: tryptophan; SRT: ...
Sources of the neurotoxin quinolinic acid in the brain of HIV-1-infected patients and retrovirus-infected macaques. Faseb ... Human microglia convert l-tryptophan into the neurotoxin quinolinic acid. The Biochemical Journal. 320: 595-7. PMID 8973572 DOI ... Quantitation of human immunodeficiency virus, immune activation factors, and quinolinic acid in AIDS brains. The Journal of ...
They found that suicide attempters had more than twice as much quinolinic acid in their spinal fluid as the healthy people, ... The results also showed decreased quinolinic acid levels among a subset of patients who came back six months later, when their ... The body produces quinolinic acid as part of the immune response that creates inflammation. ... Brundin and colleagues examined glutamate activity by measuring quinolinic acid -- which flips a chemical switch that makes ...
Quinolinic acid protects rat cerebellar granule cells from glutamate-induced apoptosis.. The effects of quinolinic acid (QUIN) ... Quinolinic acid protects rat cerebellar granule cells from glutamate-induced apoptosis. Sei, Y., Fossom, L., Goping, G., ...
New Evidence on Hypoglycemic Effect of Quinolinic Acid in Diabetic Rats. M.R. Dayer, I. Safari and M.S. Dayer ... Organic Acids Production and Phosphate Solubilization by Phosphate Solubilizing Microorganisms (PSM) Under in vitro Conditions ...
Now, a team of scientists in Australia is using that finding to develop a blood test to measure levels of quinolinic acid in ... Last year, researchers in Sweden published a study linking suicide attempts to higher-than-usual levels of quinolinic acid, a ... and to further investigate the role of quinolinic acid in brain diseases like Alzheimers disease, autism and schizophrenia. ...
keywords = "Encephalopathy, Influenza, Kynurenine, Metabolome, Quinolinic acid",. author = "Yuka Torii and Yoshihiko Kawano and ... During the acute phase of disease, three metabolites (succinic acid, undecanoic acid, and kynurenine) were significantly higher ... During the acute phase of disease, three metabolites (succinic acid, undecanoic acid, and kynurenine) were significantly higher ... During the acute phase of disease, three metabolites (succinic acid, undecanoic acid, and kynurenine) were significantly higher ...
Striatal progenitors derived from human ES cells mature into DARPP32 neurons in vitro and in quinolinic acid-lesioned rats. ... Transplantation of the LGE-patterned progenitors in quinolinic acid-lesioned rats (a model for Huntington disease) has ... GABA (γ-aminobutyric acid)-ergic. interneurons and projection neurons, as well as cholinergic. interneurons and projection ... Retinoic acid signalling specifies intermediate character in the developing telencephalon. Development. 131:4323-4332.. ...
  • This pathway is important for its production of the coenzyme nicotinamide adenine dinucleotide (NAD+) and produces several neuroactive intermediates including quinolinic acid, kynurenine (KYN), kynurenic acid (KYNA), 3-hydroxykynurenine (3-HK), and 3-hydroxyanthranilic acid (3-HANA). (wikipedia.org)
  • While quinolinic acid cannot pass the BBB, kynurenic acid, tryptophan and 3-hydroxykynurenine do and subsequently act as precursors to the production of quinolinic acid in the brain. (wikipedia.org)
  • Kynurenic acid (KYNA) is an endogenous tryptophan (Trp) metabolite known to possess neuroprotective property. (mdpi.com)
  • L-tryptophan is an amino acid that is converted to form many important neurochemicals including serotonin, kynurenine, kynurenic acid, and quinolinic acid. (technologynetworks.com)
  • Type I and II interferons (IFNs) stimulate the KYN/TRP pathway, producing elevated QA/kynurenic acid (KA), a potential neurotoxic imbalance that may contribute to SLE-mediated cognitive dysfunction. (bmj.com)
  • Quinolinic acid (abbreviated QUIN or QA), also known as pyridine-2,3-dicarboxylic acid, is a dicarboxylic acid with a pyridine backbone. (wikipedia.org)
  • Quinolinic acid (QUIN) and serotonin (5-HT) are chemicals that can affect pain perception and depressive disorders. (balimedicaljournal.org)
  • The current examine was undertaken to find out the potential neuroprotective results and the related mechanism of papaverine (PAP), a PDE10A isoenzyme inhibitor, towards quinolinic acid (QUIN)-induced excitotoxicity utilizing human major cortical neurons. (aabioetica.org)
  • Quinolinic acid is a downstream product of the kynurenine pathway, which metabolizes the amino acid tryptophan. (wikipedia.org)
  • Quinolinic acid is a byproduct of the kynurenine pathway, which is responsible for catabolism of tryptophan in mammals. (wikipedia.org)
  • Quinolinic acid is an endogenous N-methyl-D-aspartate (NMDA) receptor agonist synthesized from L-tryptophan via the kynurenine pathway and thereby has the potential of mediating N-methyl-D-aspartate neuronal damage and dysfunction [2] . (epigenetics-modulation-frontier.com)
  • An investigator injected himself with quinolinic acid, an L-tryptophan metabolite, and developed peripheral eosinophilia and subcutaneous inflammatory lesions resembling eosinophilic fasciitis. (medscape.com)
  • Objective Quinolinic acid (QA), a kynurenine (KYN)/tryptophan (TRP) pathway metabolite, is an N-methyl-D-aspartate receptor agonist that can produce excitotoxic neuron damage. (bmj.com)
  • A very small proportion of tryptophan is also transformed into indol derivatives, such as indoxyl acetic acid. (wikipathways.org)
  • In an unusual experiment, an investigator injected himself subcutaneously with quinolinic acid, an L-tryptophan metabolite, resulting in peripheral blood eosinophilia and dermal and subcutaneous inflammatory lesions resembling those of eosinophilic fasciitis and increased transforming growth factor beta-1 (TGFB1) deposition. (medscape.com)
  • Quinolinic acid affects neurons located mainly in the hippocampus, striatum, and neocortex, due to the selectivity toward quinolinic acid by the specific NMDA receptors residing in those regions. (wikipedia.org)
  • At cellular level, the telencephalon is populated by a large diversity of neurons, including glutamatergic projection neurons, GABA (γ-aminobutyric acid)-ergic interneurons and projection neurons, as well as cholinergic interneurons and projection neurons. (intechopen.com)
  • PA28γ also improved cell viability in mutant huntingtin-expressing striatal neurons exposed to pathological stressors, such as the excitotoxin quinolinic acid and the reversible proteasome inhibitor MG132. (science20.com)
  • Regional brain amino acid and neurotransmitter derangements during abdominal sepsis and septic encephalopathy in the rat. (thieme-connect.de)
  • Last year, researchers in Sweden published a study linking suicide attempts to higher-than-usual levels of quinolinic acid, a neurotransmitter associated with inflammation. (popsci.com)
  • Excitatory synaptic transmission in the brain is predominantly mediated by the neurotransmitter glutamate, while inhibitory transmission is mediated mainly by the neurotransmitter gamma-amino butyric acid (GABA). (frontiersin.org)
  • It is a building block of proteins, participates in the citric acid and urea cycles, and is a neurotransmitter. (unboundmedicine.com)
  • The effect of amino acid infusions. (thieme-connect.de)
  • Exon 1 contains a CAG trinucleotide repeat that encodes the amino acid glutamine, followed by another repeat that encodes proline. (jci.org)
  • C 4 H 7 NO 4 , a nonessential amino acid. (unboundmedicine.com)
  • Quinolinic acid may undergo further decarboxylation to nicotinic acid (niacin): Oxidation of aspartate by the enzyme aspartate oxidase gives iminosuccinate, containing the two carboxylic acid groups that are found in quinolinic acid. (wikipedia.org)
  • The main route of the kynurenine pathway leads to the formation of N -formyl kynurenine, L -kynurenine, 3-hydroxykynurenine, 3-hydroxyanthra- nilic acid, quinolinic acid, nicotinic acid, and in fine nicotinamine adenine dinucleotides. (wikipathways.org)
  • NaMN is then adenylylated to form nicotinic acid adenine dinucleotide (NaAD+), which is converted to NAD+. (wikipathways.org)
  • JAK2 inhibition is neuroprotective and reduces astrogliosis after quinolinic acid striatal lesion in adult mice. (mbfbioscience.com)
  • Condensation of iminosuccinate with glyceraldehyde-3-phosphate, mediated by quinolinate synthase, affords quinolinic acid. (wikipedia.org)
  • When inflammation occurs, quinolinic acid is produced in excessive levels through the kynurenine pathway. (wikipedia.org)
  • Additional lateral branches of the kynurenine pathway lead to the formation of other terminal kynurenines, such as KA, xanthurenic acid, and anthranilic acid. (wikipathways.org)
  • In this study, the antinociceptive activity of (-)-linalool was examined in two different pain models in mice: the acetic acid-induced writhing response, a model of inflammatory pain, and the hot plate test, a model of supraspinal analgesia. (researchgate.net)
  • Glacial (highly purified) acetic acid contains at least 99.5% acetic acid by weight. (unboundmedicine.com)
  • The period of BBB opening was exploited to focally deliver to the brain parenchyma a systemically administered neurotoxin (quinolinic acid) that is well tolerated peripherally and otherwise impermeable to the BBB. (thejns.org)
  • This study aims to analyze the relationship between quinolinic acid and serotonin levels with depression and pain degree in cancer pain patients. (balimedicaljournal.org)
  • The patient's quinolinic acid and serotonin plasma were collected through blood samples and assessed using enzyme-linked immunosorbent assay (ELISA) method. (balimedicaljournal.org)
  • Spearman's comparison test determined the correlation between quinolinic acid and serotonin levels with depression and pain degree. (balimedicaljournal.org)
  • Spearman's comparison test was conducted on quinolinic acid and serotonin levels against depression degree and pain degree, resulting in a weak correlation. (balimedicaljournal.org)
  • Quinolinic acid produces its toxic effect through several mechanisms, primarily as its function as an NMDA receptor agonist, which triggers a chain of deleterious effects, but also through lipid peroxidation, and cytoskeletal destabilization. (wikipedia.org)
  • While astrocytes do not produce quinolinic acid directly, they do produce KYNA, which when released from the astrocytes can be taken in by migroglia that can in turn increase quinolinic acid production. (wikipedia.org)
  • Quinolinic acid's neuroactive and excitatory properties are a result of NMDA receptor agonism in the brain. (wikipedia.org)
  • The quinolinic acid produced in microglia is then released and stimulates NMDA receptors, resulting in excitatory neurotoxicity. (wikipedia.org)
  • Under inflammatory conditions and conditions of T cell activation, leukocytes are retained in the brain by cytokine and chemokine production, which can lead to the breakdown of the BBB, thus increasing the quinolinic acid that enters the brain. (wikipedia.org)
  • The gliotoxic effects of quinolinic acid further amplify the inflammatory response. (wikipedia.org)
  • Lapin followed up this research by demonstrating that quinolinic acid could induce convulsions when injected into mice brain ventricles. (wikipedia.org)
  • C 3 H 4 O 2 , a colorless corrosive acid used in making acrylic polymers and resins. (unboundmedicine.com)
  • Creatine reduces 3-nitropropionic-acid-induced cognitive and motor abnormalities in rats. (neurotree.org)
  • Studies have demonstrated that quinolinic acid may be involved in many psychiatric disorders, neurodegenerative processes in the brain, as well as other disorders. (wikipedia.org)
  • Within the brain, quinolinic acid is only produced by activated microglia and macrophages. (wikipedia.org)
  • Furthermore, quinolinic acid has been shown to play a role in destabilization of the cytoskeleton within astrocytes and brain endothelial cells, contributing to the degradation of the BBB, which results in higher concentrations of quinolinic acid in the brain. (wikipedia.org)
  • Arguably, the test will be more useful as a research tool than a diagnostic one-scientists could use it to probe the relationship between the body's immune system and depression , and to further investigate the role of quinolinic acid in brain diseases like Alzheimer's disease, autism and schizophrenia. (popsci.com)
  • Quinolinic acid released from polymeric brain implants causes behavioral and neuroanatomical alterations in a rodent model of Huntington's disease. (neurotree.org)
  • H 3 BO 3 , a white crystalline acid that in water forms a very weak acid solution poisonous to plants and animals. (unboundmedicine.com)
  • in diabetic ketoacidosis, when the conversion of fatty acids to ketones increases. (unboundmedicine.com)
  • After this, Schwarcz demonstrated that elevated quinolinic acid levels could lead to axonal neurodegeneration. (wikipedia.org)
  • High levels of quinolinic acid can lead to hindered neuronal function or even apoptotic death. (wikipedia.org)
  • Now, a team of scientists in Australia is using that finding to develop a blood test to measure levels of quinolinic acid in the blood. (popsci.com)
  • Microglia and macrophages produce the vast majority of quinolinic acid present in the body. (wikipedia.org)
  • C 4 H 8 O 3 , any of the acids present in the urine, esp. (unboundmedicine.com)
  • The NHIRD can be found at http://nhird.nhri.org.tw/en/index.htm and is provided to scientists for research purposes. (psychiatrist.com)
  • One of the earliest reported syntheses of this quinolinic acid was by Zdenko Hans Skraup, who found that methyl-substituted quinolines could be oxidized to quinolinic acid by potassium permanganate. (wikipedia.org)
  • The acid is found in many foods. (unboundmedicine.com)
  • An acid reacts with a metal to form a salt, neutralizes bases, and turns litmus paper red. (unboundmedicine.com)
  • Quinolinic acid is intended for Pharmaceuticals applications. (alsachim.com)
  • ABBR: AHA Any of a class of water-soluble acids derived from fruit or milk, having a hydroxyl moiety in the first position in the molecule. (unboundmedicine.com)
  • Na and Nam are also converted to nicotinuric acid and N-methylnicotinamide elimination products. (wikipathways.org)
  • Corticosteroids inhibit formation of arachidonic acid from phospholipids when cell membranes are damaged. (unboundmedicine.com)

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