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N-acetylserotonin

Also Known As:
N-acetyl-5-hydroxytryptamine; N-acetylhydroxytryptamine
Networked: 49 relevant articles (2 outcomes, 5 trials/studies)

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Bio-Agent Context: Research Results

Experts

1. Anderson, George: 5 articles (10/2019 - 03/2015)
2. Wang, Xin: 3 articles (01/2021 - 08/2013)
3. Ben Shahar, Yoav: 2 articles (04/2019 - 02/2016)
4. Bitterman, Arie: 2 articles (04/2019 - 02/2016)
5. Bitterman, Nir: 2 articles (04/2019 - 02/2016)
6. Coran, Arnold: 2 articles (04/2019 - 02/2016)
7. Pollak, Yulia: 2 articles (04/2019 - 02/2016)
8. Sukhotnik, Igor: 2 articles (04/2019 - 02/2016)
9. Jiang, Jiying: 2 articles (01/2019 - 08/2013)
10. Oxenkrug, Gregory: 2 articles (05/2013 - 08/2012)

Related Diseases

1. Multiple Sclerosis
2. Sleep Initiation and Maintenance Disorders (Insomnia)
3. Reperfusion Injury
4. Inflammation (Inflammations)
11/02/2001 - "The aim of this study was to determine the effect of melatonin and its precursor N-acetylserotonin on the microcirculation during acute inflammation. "
02/01/2020 - "Since plasma concentrations of N-acetylserotonin and melatonin are lower than serotonin, it can be deduced that serotonin plays a key role in modulation of inflammation and the regulatory functions of immune cells, while also protecting cells against oxidative stress."
11/02/2001 - "The effect of melatonin and N-acetylserotonin herein described were observed with concentrations in the range of the nocturnal surge, providing the first evidence for a possible physiological role of these hormones in acute inflammation."
05/01/2013 - "Further research suggested the antidepressant and cognition- enhancing effects of post-serotonin metabolite, N-acetylserotonin (NAS), an agonist to tyrosine kinase B (TrkB) receptor; and link between depression and chronic inflammation-associated disorders (e.g., insulin resistance, hepatitis C virus) via inflammation-induced activation of indoleamine 2,3- dioxygenase, brain located rate-limiting enzyme of TRY - KYN metabolism. "
08/01/2021 - "The metabolites related to heme metabolism (bilirubin, biliverdin), energy metabolism and oxidative stress (2-Octenoylcarnitine, N-Heptanoylglycine, and acetylcysteine), phospholipid metabolism (lysophosphatidic acid, phospholipid acid, and lysophosphatidylethanolamine), and tryptophan metabolism (N-Acetylserotonin, indolepyruvate, and melatonin) were decreased in the range of 2.16%-6.80% for each 10 μg/m3 increase of PM2.5, while thyrotropin-releasing hormone, glutathione, and phosphatidylethanolamine related to energy metabolism and oxidative stress, and phospholipid metabolism were increased in the range of 2.95%-4.90% for each 10 μg/m3 increase of PM2.5. This longitudinal study suggests that higher PM2.5 exposure may induce perturbations in serum metabolic signaling related to oxidative stress and inflammation, and males may be more prone to these metabolic perturbations."
5. Ischemia

Related Drugs and Biologics

1. Melatonin
2. Serotonin (5 Hydroxytryptamine)
3. Tryptophan (L-Tryptophan)
4. 6-hydroxymelatonin
5. N-methyltryptamine
6. nas
7. Enzymes
8. Arylalkylamine N-Acetyltransferase
9. NF-kappa B (NF-kB)
10. Retinaldehyde (Retinal)

Related Therapies and Procedures

1. Therapeutics
2. Injections