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5-Hydroxyindoleacetaldehyde

5-Hydroxyindoleacetaldehyde (5-HIAL), also known as 5-hydroxytryptaldehyde or as serotonin aldehyde, is an inactive metabolite and metabolic intermediate of the monoamine neurotransmitter serotonin (5-hydroxytryptamine; 5-HT).


Column 1Column 2
IUPAC name
2-(5-hydroxy-1H-indol-3-yl)acetaldehyde
Other names
5-Hydroxyindole-acetaldehyde; 5-HIAL; 5-HIAAL; 5-Hydroxytryptaldehyde; 5-Hydroxyindole-3-acetaldehyde; Serotonin aldehyde
CAS Number.mw-parser-output .plainlist ol,.mw-parser-output .plainlist ul{line-height:inherit;list-style:none;margin:0;padding:0}.mw-parser-output .plainlist ol li,.mw-parser-output .plainlist ul li{margin-bottom:0}1892-21-3 Y
3D model (JSmol)Interactive image
ChEBICHEBI:50157
ChemSpider67261
IUPHAR/BPS6634
KEGGC05634
PubChem CID74688
UNIIDAE26MT2UK
CompTox Dashboard (EPA)DTXSID60172318
InChI
InChI=1S/C10H9NO2/c12-4-3-7-6-11-10-2-1-8(13)5-9(7)10/h1-2,4-6,11,13H,3H2Key: OBFAPCIUSYHFIE-UHFFFAOYSA-N
SMILES
C1=CC2=C(C=C1O)C(=CN2)CC=O
Chemical formulaC10H9NO2
Molar mass175.18 g/mol
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).

Infobox references | |

5-Hydroxyindoleacetaldehyde (5-HIAL), also known as 5-hydroxytryptaldehyde or as serotonin aldehyde, is an inactive metabolite and metabolic intermediate of the monoamine neurotransmitter serotonin (5-hydroxytryptamine; 5-HT).

5-HIAL is formed from serotonin by oxidative deamination via monoamine oxidase (MAO). MAO-mediated deamination is the primary metabolic pathway of serotonin inactivation. Monoamine oxidase A (MAO-A) has about 120-fold higher affinity for serotonin than monoamine oxidase B (MAO-B). In relation to this, MAO-A is the main isozyme of MAO involved in serotonin degradation.

Following its formation, 5-HIAL is metabolized by aldehyde dehydrogenase (ALDH) to form 5-hydroxyindoleacetic acid (5-HIAA). 5-HIAL can also be converted into small amounts of 5-hydroxytryptophol (5-HTOL; also known as 5-hydroxyindolethanol or 5-HIET) by either aldehyde reductase (ALR/ALDR) or alcohol dehydrogenase (ADH). However, brain concentrations of 5-HTOL are only 1 to 5% of those of 5-HIAA.

Use of ethanol (alcohol) can dramatically increase 5-HTOL formation by inhibiting ALDH and enhancing ADH activity. As a result, the ratio of 5-HTOL to 5-HIAA is a sensitive and reliable marker of recent ethanol ingestion and has been suggested for use in clinical and forensic contexts.

Besides oxidative deamination by MAO into 5-HIAL, serotonin can also be conjugated by glucuronidation via glucuronyltransferases, conjugated by sulfation via sulfotransferases, acetylated and then methylated into melatonin (N-acetyl-5-methoxytryptamine) (which occurs mainly in the pineal gland), and converted into certain other metabolites like 5-hydroxyindole thiazoladine carboxylic acid (5-HITCA). However, these secondary metabolic pathways appear to play only a minor role in serotonin metabolism.

5-HIAL has been implicated in producing neurotoxicity and in the development and progression of neurodegenerative diseases.

  • Indoleacetaldehyde (IAL)
  • 3,4-Dihydroxyphenylacetaldehyde (DOPAL)
  • 3,4-Dihydroxyphenylglycolaldehyde (DOPEGAL)
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