soluble in water, ethanol, benzene, diethyl ether[1]
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
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Chemical compound
Succinic semialdehyde (SSA) is a GABA and GHB metabolite. It is formed from GABA by the action of GABA transaminase (4-aminobutyrate aminotransferase) and further oxidised to become succinic acid, which enters TCA cycle. SSA is oxidized into succinic acid by the enzyme succinic semialdehyde dehydrogenase, which uses NAD+ as a cofactor.[2][3] When the oxidation of succinic semialdehyde to succinic acid is impaired, accumulation of succinic semialdehyde takes place which leads to succinic semialdehyde dehydrogenase deficiency.[3]
In addition to the pathway involving GABA transaminase, gamma-hydroxybutyric acid (GHB) can also be metabolized to SSA via GHB dehydrogenase or by GHB transhydrogenase (D-2-hydroxyglutarate transhydrogenase).[4][5][6][7]
^
Lide, David R. (1998), Handbook of Chemistry and Physics (87 ed.), Boca Raton, Florida: CRC Press, pp. 3–446, ISBN 0-8493-0594-2
^Peng, Qi; Yang, Min; Wang, Wei; Han, Lili; Wang, Guannan; Wang, Pengyue; Zhang, Jie; Song, Fuping (2014-12-20). "Activation of gab cluster transcription in Bacillus thuringiensis by γ-aminobutyric acid or succinic semialdehyde is mediated by the Sigma 54-dependent transcriptional activator GabR". BMC Microbiology. 14 (1): 306. doi:10.1186/s12866-014-0306-3. ISSN 1471-2180. PMC 4279683. PMID 25527261.
^ abStruys, E. A.; Jansen, E. E. W.; Gibson, K. M.; Jakobs, C. (December 2005). "Determination of the GABA analogue succinic semialdehyde in urine and cerebrospinal fluid by dinitrophenylhydrazine derivatization and liquid chromatography–tandem mass spectrometry: Application to SSADH deficiency". Journal of Inherited Metabolic Disease. 28 (6): 913–920. doi:10.1007/s10545-005-0111-0. ISSN 0141-8955. PMID 16435183. S2CID 9956364.
^Busardò FP, Jones AW (January 2015). "GHB pharmacology and toxicology: acute intoxication, concentrations in blood and urine in forensic cases and treatment of the withdrawal syndrome". Current Neuropharmacology. 13 (1): 47–70. doi:10.2174/1570159X13666141210215423. PMC 4462042. PMID 26074743.
^Felmlee MA, Morse BL, Morris ME (January 2021). "γ-Hydroxybutyric Acid: Pharmacokinetics, Pharmacodynamics, and Toxicology". The AAPS Journal. 23 (1): 22. doi:10.1208/s12248-020-00543-z. PMC 8098080. PMID 33417072.
^Taxon ES, Halbers LP, Parsons SM (May 2020). "Kinetics aspects of Gamma-hydroxybutyrate dehydrogenase". Biochimica Et Biophysica Acta. Proteins and Proteomics. 1868 (5): 140376. doi:10.1016/j.bbapap.2020.140376. PMID 31981617.
^Kamal RM, van Noorden MS, Franzek E, Dijkstra BA, Loonen AJ, De Jong CA (March 2016). "The Neurobiological Mechanisms of Gamma-Hydroxybutyrate Dependence and Withdrawal and Their Clinical Relevance: A Review". Neuropsychobiology. 73 (2): 65–80. doi:10.1159/000443173. PMID 27003176.
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(α-ketoglutarate) into succinicsemialdehyde and glutamate. Succinicsemialdehyde is then oxidized into succinic acid by succinicsemialdehyde dehydrogenase and...
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oxobutyric acid, or oxobutanoic acid may refer to: 4-Oxobutanoic acid (succinicsemialdehyde, 4-oxobutyric acid) Dicarbonyl This set index article lists chemical...
healthy volunteers. Vigabatrin is also used to treat seizures in succinicsemialdehyde dehydrogenase deficiency (SSADHD), which is an inborn GABA metabolism...
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(TCA). In this process, 2-oxoglutarate decarboxylase (2OGDC) and succinicsemialdehyde dehydrogenase (SSADH), replace the enzyme 2-oxoglutarate dehydrogenase...
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