N-Acetylputrescine

N-Acetylputrescine
Names
IUPAC name
N-(4-aminobutyl)acetamide
Other names
Acetylputrescine; Monoacetylputrescine; NacPut
Identifiers
3D model (JSmol)
ChEBI
ChEMBL
ChemSpider
ECHA InfoCard 100.219.140 Edit this at Wikidata
EC Number
  • 691-457-0
KEGG
UNII
  • InChI=1S/C6H14N2O/c1-6(9)8-5-3-2-4-7/h2-5,7H2,1H3,(H,8,9)
    Key: KLZGKIDSEJWEDW-UHFFFAOYSA-N
  • CC(=O)NCCCCN
Properties
C6H14N2O
Molar mass 130.19 g/mol
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).

N-Acetylputrescine (NacPut), also known as monoacetylputrescine, is an endogenous metabolite of putrescine and a precursor and metabolic intermediate in the biosynthesis of γ-aminobutyric acid (GABA) from putrescine.[1][2][3]

The metabolic pathway is specifically putrescine into N-acetylputrescine by putrescine acetyltransferase (PAT), N-acetylputrescine into N-acetyl-γ-aminobutyraldehyde (N-acetyl-GABAL or N-acetyl-GABA aldehyde) by monoamine oxidase B (MAO-B), N-acetyl-GABAL into N-acetyl-γ-aminobutyric acid (N-acetyl-GABA) by aldehyde dehydrogenase (ALDH), and N-acetyl-GABA into GABA by an unknown deacetylase enzyme.[1][2][3] This pathway is a minor alternative pathway to the major and primary pathway in which GABA is synthesized from glutamate.[1] There is also another alternative pathway in which putrescine is converted into GABA with γ-aminobutyraldehyde (GABAL or GABA aldehyde) as an intermediate instead.[1] It has been estimated that about 2 to 3% of GABA is synthesized from putrescine in the mouse brain, whereas in the case of the rat brain, the amount was negligible.[1]

In 2021, it was discovered that MAO-B does not mediate dopamine catabolism in the rodent striatum but instead participates in striatal GABA synthesis and that synthesized GABA in turn inhibits dopaminergic neurons in this brain area.[4][3] It has been found that MAO-B, via the putrescine pathway, importantly mediates GABA synthesis in astrocytes in various brain areas, including in the hippocampus, cerebellum, striatum, cerebral cortex, and substantia nigra pars compacta (SNpc).[4][3] These findings may warrant a rethinking of the actions of MAO-B inhibitors in the treatment of Parkinson's disease.[4][3]

References

  1. ^ a b c d e Watanabe M, Maemura K, Kanbara K, Tamayama T, Hayasaki H (2002). "GABA and GABA Receptors in the Central Nervous System and Other Organs". A Survey of Cell Biology. International Review of Cytology. Vol. 213. pp. 1–47. doi:10.1016/s0074-7696(02)13011-7. ISBN 978-0-12-364617-0. PMID 11837891.
  2. ^ a b Seiler N (June 2004). "Catabolism of polyamines". Amino Acids. 26 (3): 217–233. doi:10.1007/s00726-004-0070-z. PMID 15221502.
  3. ^ a b c d e Cho HU, Kim S, Sim J, Yang S, An H, Nam MH, Jang DP, Lee CJ (July 2021). "Redefining differential roles of MAO-A in dopamine degradation and MAO-B in tonic GABA synthesis". Exp Mol Med. 53 (7): 1148–1158. doi:10.1038/s12276-021-00646-3. PMC 8333267. PMID 34244591.
  4. ^ a b c Nam MH, Sa M, Ju YH, Park MG, Lee CJ (April 2022). "Revisiting the Role of Astrocytic MAOB in Parkinson's Disease". Int J Mol Sci. 23 (8): 4453. doi:10.3390/ijms23084453. PMC 9028367. PMID 35457272.


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