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| glutaric acid |
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| CHEBI:17859 |
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| An α,ω-dicarboxylic acid that is a linear five-carbon dicarboxylic acid. |
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This entity has been manually annotated by the ChEBI Team.
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CHEBI:43097, CHEBI:5434, CHEBI:24330
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| No supplier information found for this compound. |
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Molfile
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SDF
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more structures >>
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| Glutaric acid is the organic compound with the formula C3H6(COOH)2. Although the related "linear" dicarboxylic acids adipic and succinic acids are water-soluble only to a few percent at room temperature, the water-solubility of glutaric acid is over 50% (w/w). |
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Read full article at Wikipedia
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| InChI=1S/C5H8O4/c6-4(7)2-1-3-5(8)9/h1-3H2,(H,6,7)(H,8,9) |
| JFCQEDHGNNZCLN-UHFFFAOYSA-N |
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Daphnia magna
(NCBI:txid35525)
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See:
Mixtures of similarly acting compounds in Daphnia magna: From gene to metabolite and beyondTine Vandenbrouck, Oliver A.H. Jones, Nathalie Dom, Julian L. Griffin, Wim De CoenEnvironment International 36 (2010) 254-268
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Homo sapiens
(NCBI:txid9606)
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See:
PubMed
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Bronsted acid
A molecular entity capable of donating a hydron to an acceptor (Bronsted base).
(via oxoacid )
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human metabolite
Any mammalian metabolite produced during a metabolic reaction in humans (Homo sapiens).
Daphnia magna metabolite
A Daphnia metabolite produced by the species Daphnia magna.
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View more via ChEBI Ontology
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1,3-Propanedicarboxylic acid
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KEGG COMPOUND
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1,5-pentanedioic acid
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NIST Chemistry WebBook
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Glutaric acid
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KEGG COMPOUND
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GLUTARIC ACID
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PDBeChem
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Glutarsäure
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ChEBI
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Pentanedioic acid
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KEGG COMPOUND
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110-94-1
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CAS Registry Number
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KEGG COMPOUND
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110-94-1
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CAS Registry Number
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NIST Chemistry WebBook
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110-94-1
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CAS Registry Number
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ChemIDplus
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1209725
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Reaxys Registry Number
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Reaxys
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26809
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Gmelin Registry Number
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Gmelin
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Tian F, Fu X, Gao J, Ying Y, Hou L, Liang Y, Ning Q, Luo X (2014)
Glutaric acid-mediated apoptosis in primary striatal neurons.
BioMed research international 2014, 484731 [PubMed:24900967]
[show Abstract]
Glutaric acid (GA) has been implicated in the mechanism of neurodegeneration in glutaric aciduria type I. In the present study, the potential cytotoxic effects of GA (0.1~50 mM for 24~96 h) were examined in cultured primary rat striatal neurons. Results showed increase in the number of cells labeled by annexin-V or with apoptotic features shown by Hoechst/PI staining and transmission electron microscopy (TEM) and upregulation of the expression of mRNA as well as the active protein fragments caspase 3, suggesting involvement of the caspase 3-dependent apoptotic pathway in GA-induced striatal neuronal death. This effect was in part suppressed by the N-methyl-D-aspartate (NMDA) receptor antagonist MK-801 but not the α -amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) antagonist 6-cyano-7-nitroquinoxalone-2,3-dione (CNQX). Thus, GA may trigger neuronal damage partially through apoptotic pathway and via activation of NMDA receptors in cultured primary striatal neurons. | Pusti S, Das N, Nayek K, Biswas S (2014)
A treatable neurometabolic disorder: glutaric aciduria type 1.
Case reports in pediatrics 2014, 256356 [PubMed:24587932]
[show Abstract]
Glutaric aciduria type 1 (GA-1) is an autosomal recessive disorder of lysine, hydroxylysine, and tryptophan metabolism caused by deficiency of glutaryl-CoA dehydrogenase. It results in the accumulation of 3-hydroxyglutaric and glutaric acid. Affected patients can present with brain atrophy and macrocephaly and with acute dystonia secondary to striatal degeneration in most cases triggered by an intercurrent childhood infection with fever between 6 and 18 months of age. We report two such cases with macrocephaly, typical MRI pictures, and tandem mass spectrometry suggestive of glutaric aciduria type 1. | Olivera-Bravo S, Isasi E, Fernández A, Rosillo JC, Jiménez M, Casanova G, Sarlabós MN, Barbeito L (2014)
White matter injury induced by perinatal exposure to glutaric acid.
Neurotoxicity research 25, 381-391 [PubMed:24297153]
[show Abstract]
Glutaric acid (GA) is a neurotoxic metabolite that accumulates in the CNS of patients with glutaric acidemia-I (GA-I), a neurometabolic disease caused by deficient activity of glutaryl-CoA dehydrogenase. Most GA-I patients display characteristic CNS lesions, mainly in the gray and white matter of basal ganglia and cerebral cortex. Neurons and astrocytes are believed to be vulnerable to millimolar concentrations of GA. However, little is known about the effects of GA on oligodendrocytes (OL) and the myelination process in the postnatal brain. Here, we show that a single intracerebroventricular administration of GA to rat neonatal pups induced a selective and long-lasting myelination failure in the striatum but no deleterious effect in the myelination of the corpus callosum. At 45 days post-GA injection, the myelinated area of striatal axonal bundles was decreased by 35 %, and the expression of myelin basic protein and myelin-associated glycoprotein (MAG) reduced by 25 and 60 %, respectively. This was accompanied by long lasting cytopathology features in MAG and CC-1-expressing OLs, which was confirmed by transmission electron microscopy. Remarkably, GA did not induce acute loss of pre-OLs in the striatum as assessed by NG2 or PDGFRα immunohistochemistry, suggesting an indirect and progressive mechanism for OL damage. In accordance, GA-induced white matter injury was restricted to the striatum and associated to GA-induced astrocytosis and neuronal loss. In conclusion, the current evidence indicates a pathogenic mechanism by which GA can permanently affect myelin status. |
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