Showing Metabocard for succinate (BASm0001744)

Common NameSuccinate
DescriptionSuccinic acid (succinate) is a dicarboxylic acid. It is an important component of the citric acid or TCA cycle and is capable of donating electrons to the electron transfer chain. Succinate is found in all living organisms ranging from bacteria to plants to mammals. In eukaryotes, succinate is generated in the mitochondria via the tricarboxylic acid cycle (TCA). Succinate can readily be imported into the mitochondrial matrix by the n-butylmalonate- (or phenylsuccinate-) sensitive dicarboxylate carrier in exchange with inorganic phosphate or another organic acid, e. g. malate (PMID 16143825 ). Succinate can exit the mitochondrial matrix and function in the cytoplasm as well as the extracellular space. Succinate has multiple biological roles including roles as a metabolic intermediate and roles as a cell signalling molecule. Succinate can alter gene expression patterns, thereby modulating the epigenetic landscape or it can exhibit hormone-like signaling functions (PMID: 26971832 ). As such, succinate links cellular metabolism, especially ATP formation, to the regulation of cellular function. Succinate can be broken down or metabolized into fumarate by the enzyme succinate dehydrogenase (SDH), which is part of the electron transport chain involved in making ATP. Dysregulation of succinate synthesis, and therefore ATP synthesis, can happen in a number of genetic mitochondrial diseases, such as Leigh syndrome, and Melas syndrome. Succinate has been found to be associated with D-2-hydroxyglutaric aciduria, which is an inborn error of metabolism. Succinic acid has recently been identified as an oncometabolite or an endogenous, cancer causing metabolite. High levels of this organic acid can be found in tumors or biofluids surrounding tumors. Its oncogenic action appears to due to its ability to inhibit prolyl hydroxylase-containing enzymes. In many tumours, oxygen availability becomes limited (hypoxia) very quickly due to rapid cell proliferation and limited blood vessel growth. The major regulator of the response to hypoxia is the HIF transcription factor (HIF-alpha). Under normal oxygen levels, protein levels of HIF-alpha are very low due to constant degradation, mediated by a series of post-translational modification events catalyzed by the prolyl hydroxylase domain-containing enzymes PHD1, 2 and 3, (also known as EglN2, 1 and 3) that hydroxylate HIF-alpha and lead to its degradation. All three of the PHD enzymes are inhibited by succinate. In humans, urinary succinic acid is produced by Escherichia coli, Pseudomonas aeruginosa, Klebsiella pneumonia, Enterobacter, Acinetobacter, Proteus mirabilis, Citrobacter frundii, Enterococcus faecalis (PMID: 22292465 ). Succinic acid is also found in Actinobacillus, Anaerobiospirillum, Mannheimia, Corynebacterium and Basfia (PMID: 22292465 ; PMID: 18191255 ; PMID: 26360870 ).
Structure
Molecular FormulaC4H6O4
Average Mass118.08800
Monoisotopic Mass118.02661
IUPAC Namebutanedioic acid
Traditional NameSuccinic acid
CAS Registry Number110-15-6
SMILESO=C([O-])CCC(=O)[O-]
InChI IdentifierInChI=1S/C4H6O4/c5-3(6)1-2-4(7)8/h1-2H2,(H,5,6)(H,7,8)
InChI KeyKDYFGRWQOYBRFD-UHFFFAOYSA-N
CHEBI IDCHEBI:30031
HMDB IDHMDB0000254
Pathways
NameSMPDB/PathBank
Oxidative phosphorylation
Arginine and proline metabolism
Valine, leucine and isoleucine degradation
Oxidation of Branched Chain Fatty Acids
Citric Acid Cycle
Ketone Body Metabolism
Glutamate Metabolism
Butyrate Metabolism
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
Beta-Ketothiolase Deficiency
Guanidinoacetate Methyltransferase Deficiency (GAMT Deficiency)
Maple Syrup Urine Disease
Methylmalonic Aciduria
Prolidase Deficiency (PD)
Prolinemia Type II
Propionic Acidemia
3-Methylcrotonyl Coa Carboxylase Deficiency Type I
Isovaleric Aciduria
4-Hydroxybutyric Aciduria/Succinic Semialdehyde Dehydrogenase Deficiency
Hyperinsulinism-Hyperammonemia Syndrome
Hyperprolinemia Type II
Hyperprolinemia Type I
Arginine: Glycine Amidinotransferase Deficiency (AGAT Deficiency)
Ornithine Aminotransferase Deficiency (OAT Deficiency)
Methylmalonate Semialdehyde Dehydrogenase Deficiency
Homocarnosinosis
Phytanic Acid Peroxisomal Oxidation
Refsum Disease
Carnitine Synthesis
Creatine deficiency, guanidinoacetate methyltransferase deficiency
Hyperornithinemia with gyrate atrophy (HOGA)
Hyperornithinemia-hyperammonemia-homocitrullinuria [HHH-syndrome]
L-arginine:glycine amidinotransferase deficiency
3-hydroxyisobutyric acid dehydrogenase deficiency
3-hydroxyisobutyric aciduria
Isobutyryl-coa dehydrogenase deficiency
Isovaleric acidemia
Congenital lactic acidosis
Fumarase deficiency
Mitochondrial complex II deficiency
2-ketoglutarate dehydrogenase complex deficiency
Pyruvate dehydrogenase deficiency (E3)
Pyruvate dehydrogenase deficiency (E2)
Succinic semialdehyde dehydrogenase deficiency
Succinyl CoA: 3-ketoacid CoA transferase deficiency
Warburg Effect
The oncogenic action of 2-hydroxyglutarate
The Oncogenic Action of Succinate
The Oncogenic Action of Fumarate
Glutaminolysis and Cancer
The oncogenic action of L-2-hydroxyglutarate in Hydroxygluaricaciduria
The oncogenic action of D-2-hydroxyglutarate in Hydroxygluaricaciduria
StateSolid
Water Solubility2.11e+02 g/l
logP-0.53
logS0.25
pKa (Strongest Acidic)3.55
pKa (Strongest Basic)Not Available
Hydrogen Acceptor Count4
Hydrogen Donor Count2
Polar Surface Area74.6 Ų
Rotatable Bond Count3
Physiological Charge-2
Formal Charge0
Refractivity23.54 m³·mol⁻¹
Polarizability10.16

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