Common NameL-glutamate
DescriptionGlutamic acid (Glu), also known as L-glutamic acid or as glutamate, the name of its anion, is an alpha-amino acid. These are amino acids in which the amino group is attached to the carbon atom immediately adjacent to the carboxylate group (alpha carbon). Amino acids are organic compounds that contain amino (-NH2) and carboxyl (-COOH) functional groups, along with a side chain (R group) specific to each amino acid. L-glutamic acid is one of 20 proteinogenic amino acids, i.e., the amino acids used in the biosynthesis of proteins. Glutamic acid is found in all organisms ranging from bacteria to plants to animals. It is classified as an acidic, charged (at physiological pH), aliphatic amino acid. In humans it is a non-essential amino acid and can be synthesized via alanine or aspartic acid via alpha-ketoglutarate and the action of various transaminases. Glutamate also plays an important role in the body's disposal of excess or waste nitrogen. Glutamate undergoes deamination, an oxidative reaction catalysed by glutamate dehydrogenase leading to alpha-ketoglutarate. In many respects glutamate is a key molecule in cellular metabolism. Glutamate is the most abundant fast excitatory neurotransmitter in the mammalian nervous system. At chemical synapses, glutamate is stored in vesicles. Nerve impulses trigger release of glutamate from the pre-synaptic cell. In the opposing post-synaptic cell, glutamate receptors, such as the NMDA receptor, bind glutamate and are activated. Because of its role in synaptic plasticity, it is believed that glutamic acid is involved in cognitive functions like learning and memory in the brain. Glutamate transporters are found in neuronal and glial membranes. They rapidly remove glutamate from the extracellular space. In brain injury or disease, they can work in reverse and excess glutamate can accumulate outside cells. This process causes calcium ions to enter cells via NMDA receptor channels, leading to neuronal damage and eventual cell death, and is called excitotoxicity. The mechanisms of cell death include: Damage to mitochondria from excessively high intracellular Ca2+. Glu/Ca2+-mediated promotion of transcription factors for pro-apoptotic genes, or downregulation of transcription factors for anti-apoptotic genes. Excitotoxicity due to glutamate occurs as part of the ischemic cascade and is associated with stroke and diseases like amyotrophic lateral sclerosis, lathyrism, and Alzheimer's disease. Glutamic acid has been implicated in epileptic seizures. Microinjection of glutamic acid into neurons produces spontaneous depolarization around one second apart, and this firing pattern is similar to what is known as paroxysmal depolarizing shift in epileptic attacks. This change in the resting membrane potential at seizure foci could cause spontaneous opening of voltage activated calcium channels, leading to glutamic acid release and further depolarization (http://en.wikipedia.org/wiki/Glutamic_acid). Glutamate was discovered in 1866 when it was extracted from wheat gluten (from where it got its name. Glutamate has an important role as a food additive and food flavoring agent. In 1908, Japanese researcher Kikunae Ikeda identified brown crystals left behind after the evaporation of a large amount of kombu broth (a Japanese soup) as glutamic acid. These crystals, when tasted, reproduced a salty, savory flavor detected in many foods, most especially in seaweed. Professor Ikeda termed this flavor umami. He then patented a method of mass-producing a crystalline salt of glutamic acid, monosodium glutamate.
Structure
Molecular FormulaC5H9NO4
Average Mass147.12930
Monoisotopic Mass147.05316
IUPAC Name(2S)-2-aminopentanedioic acid
Traditional NameL-glutamic acid
CAS Registry Number56-86-0
SMILES[NH3+][C@@H](CCC(=O)[O-])C(=O)[O-]
InChI IdentifierInChI=1S/C5H9NO4/c6-3(5(9)10)1-2-4(7)8/h3H,1-2,6H2,(H,7,8)(H,9,10)/t3-/m0/s1
InChI KeyWHUUTDBJXJRKMK-VKHMYHEASA-N
CHEBI IDCHEBI:29985
HMDB IDHMDB0000148
Pathways
NameSMPDB/PathBank
Alanine, aspartate and glutamate metabolism
Nitrogen metabolism
Arginine and proline metabolism
Glutathione metabolism
Glycine, serine and threonine metabolism
One carbon pool by folate
beta-Alanine metabolism
Lysine degradation
Purine metabolism
Tyrosine metabolism
Tryptophan metabolism
Valine, leucine and isoleucine degradation
Nicotinate and nicotinamide metabolism
Propanoate metabolism
Citrullinemia Type I
Carbamoyl Phosphate Synthetase Deficiency
Argininosuccinic Aciduria
Phenylalanine and Tyrosine Metabolism
Cysteine Metabolism
Transcription/Translation
Histidine metabolism
Amino Sugar Metabolism
Urea Cycle
Aspartate Metabolism
Glutamate Metabolism
Arachidonic Acid Metabolism
Piroxicam Action Pathway
Acetylsalicylic Acid Action Pathway
Etodolac Action Pathway
Ketoprofen Action Pathway
Ibuprofen Action Pathway
Rofecoxib Action Pathway
Diclofenac Action Pathway
Sulindac Action Pathway
Celecoxib Action Pathway
Ketorolac Action Pathway
Suprofen Action Pathway
Bromfenac Action Pathway
Indomethacin Action Pathway
Meloxicam Action Pathway
Mefenamic Acid Action Pathway
Oxaprozin Action Pathway
Nabumetone Action Pathway
Valdecoxib Action Pathway
Naproxen Action Pathway
Glucose-Alanine Cycle
Malate-Aspartate Shuttle
2-Hydroxyglutric Aciduria (D And L Form)
2-Methyl-3-Hydroxybutryl CoA Dehydrogenase Deficiency
3-Hydroxy-3-Methylglutaryl-CoA Lyase Deficiency
3-Methylglutaconic Aciduria Type I
3-Methylglutaconic Aciduria Type III
3-Methylglutaconic Aciduria Type IV
5-Oxoprolinuria
Adenosine Deaminase Deficiency
Adenylosuccinate Lyase Deficiency
AICA-Ribosiduria
Alkaptonuria
Beta-Ketothiolase Deficiency
Canavan Disease
Dihydropyrimidine Dehydrogenase Deficiency (DHPD)
Gamma-Glutamyltransferase Deficiency
Glutaric Aciduria Type I
Guanidinoacetate Methyltransferase Deficiency (GAMT Deficiency)
Hawkinsinuria
Histidinemia
Hypoacetylaspartia
Malonic Aciduria
Maple Syrup Urine Disease
Methylmalonic Aciduria
Methylmalonic Aciduria Due to Cobalamin-Related Disorders
Molybdenum Cofactor Deficiency
Ornithine Transcarbamylase Deficiency (OTC Deficiency)
Phenylketonuria
Prolidase Deficiency (PD)
Prolinemia Type II
Purine Nucleoside Phosphorylase Deficiency
Sialuria or French Type Sialuria
Tyrosinemia Type I
Xanthine Dehydrogenase Deficiency (Xanthinuria)
Non Ketotic Hyperglycinemia
Propionic Acidemia
3-Methylcrotonyl Coa Carboxylase Deficiency Type I
Isovaleric Aciduria
Saccharopinuria/Hyperlysinemia II
Salla Disease/Infantile Sialic Acid Storage Disease
Dimethylglycine Dehydrogenase Deficiency
4-Hydroxybutyric Aciduria/Succinic Semialdehyde Dehydrogenase Deficiency
Sarcosinemia
Diflunisal Action Pathway
Lactic Acidemia
Glutathione Synthetase Deficiency
Hyperinsulinism-Hyperammonemia Syndrome
Pyruvate Carboxylase Deficiency
GABA-Transaminase Deficiency
Primary Hyperoxaluria Type I
Leukotriene C4 Synthesis Deficiency
Argininemia
Hyperprolinemia Type II
Hyperprolinemia Type I
Arginine: Glycine Amidinotransferase Deficiency (AGAT Deficiency)
Ornithine Aminotransferase Deficiency (OAT Deficiency)
Lesch-Nyhan Syndrome (LNS)
Gout or Kelley-Seegmiller Syndrome
Tyrosinemia Type 2 (or Richner-Hanhart syndrome)
Tyrosinemia Type 3 (TYRO3)
Methylmalonate Semialdehyde Dehydrogenase Deficiency
Homocarnosinosis
Tay-Sachs Disease
Azathioprine Action Pathway
Mercaptopurine Action Pathway
Disulfiram Action Pathway
Thioguanine Action Pathway
Methotrexate Action Pathway
Dimethylglycine Dehydrogenase Deficiency
Hyperglycinemia, non-ketotic
Ureidopropionase Deficiency
Carnosinuria, carnosinemia
Tyrosinemia, transient, of the newborn
Dopamine beta-hydroxylase deficiency
Beta-mercaptolactate-cysteine disulfiduria
5-oxoprolinase deficiency
Gamma-glutamyl-transpeptidase deficiency
Malonyl-coa decarboxylase deficiency
Creatine deficiency, guanidinoacetate methyltransferase deficiency
Hyperornithinemia with gyrate atrophy (HOGA)
Hyperornithinemia-hyperammonemia-homocitrullinuria [HHH-syndrome]
L-arginine:glycine amidinotransferase deficiency
Xanthinuria type I
Xanthinuria type II
3-hydroxyisobutyric acid dehydrogenase deficiency
3-hydroxyisobutyric aciduria
Isobutyryl-coa dehydrogenase deficiency
Isovaleric acidemia
Hyperlysinemia I, Familial
Hyperlysinemia II or Saccharopinuria
Monoamine oxidase-a deficiency (MAO-A)
G(M2)-Gangliosidosis: Variant B, Tay-sachs disease
Adenine phosphoribosyltransferase deficiency (APRT)
Mitochondrial DNA depletion syndrome
Myoadenylate deaminase deficiency
Methylenetetrahydrofolate Reductase Deficiency (MTHFRD)
Succinic semialdehyde dehydrogenase deficiency
Pyridoxine dependency with seizures
Warburg Effect
Antipyrine Action Pathway
Antrafenine Action Pathway
Carprofen Action Pathway
Etoricoxib Action Pathway
Fenoprofen Action Pathway
Flurbiprofen Action Pathway
Magnesium salicylate Action Pathway
Lumiracoxib Action Pathway
Lornoxicam Action Pathway
Phenylbutazone Action Pathway
Nepafenac Action Pathway
Trisalicylate-choline Action Pathway
Tolmetin Action Pathway
Tiaprofenic Acid Action Pathway
Tenoxicam Action Pathway
Salsalate Action Pathway
Salicylate-sodium Action Pathway
Salicylic Acid Action Pathway
Acetaminophen Action Pathway
2-aminoadipic 2-oxoadipic aciduria
3-Phosphoglycerate dehydrogenase deficiency
Cystinosis, ocular nonnephropathic
Folate malabsorption, hereditary
The oncogenic action of 2-hydroxyglutarate
Glutaminolysis and Cancer
The oncogenic action of L-2-hydroxyglutarate in Hydroxygluaricaciduria
The oncogenic action of D-2-hydroxyglutarate in Hydroxygluaricaciduria
StateSolid
Water Solubility8.06e+01 g/l
logP-3.54
logS-0.26
pKa (Strongest Acidic)1.88
pKa (Strongest Basic)9.54
Hydrogen Acceptor Count5
Hydrogen Donor Count3
Polar Surface Area100.62 Ų
Rotatable Bond Count4
Physiological Charge-1
Formal Charge0
Refractivity31.29 m³·mol⁻¹
Polarizability13.49

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