Component

N-Acetylserotonin

N-Acetylserotonin. Species, exposure and limitations are retained in each linked claim.

7 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What acts on it

  1. Human AANAT transferred an acetyl group from acetyl-CoA to serotonin, producing N-acetylserotonin.

    Human arylalkylamine N-acetyltransferase / AANAT → N-Acetylserotonin source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/melatonin-research/10722724.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7fb8418b17e92c5b3fed5d9c08afdb32f28c922dfe94274d3bb02b7e12b2b8c8", "start_char": 0, "end_char": 1857, "text_sha256": "7fb8418b17e92c5b3fed5d9c08afdb32f28c922dfe94274d3bb02b7e12b2b8c8"}
    experimental_model
    Purified recombinant enzyme substrate-specificity study
    exposure
    Serotonin and radiolabeled acetyl-CoA; product HPLC
    limitations
    Biochemical mechanism, not evidence that dietary B5 or acetyl-CoA availability limits melatonin production in all humans.
    nutrient_topic
    Melatonin research collection; topical membership is not evidence of a direct dietary effect. · Melatonin
    organism
    Human AANAT expressed in bacteria
    plain_language
    Serotonin is modified before it becomes melatonin.
    primary_references
    [melatonin-p10722724] Substrate specificity and inhibition studies of human serotonin N-acetyltransferase. (2000). https://pubmed.ncbi.nlm.nih.gov/10722724/ DOI: 10.1074/jbc.275.12.8794
    tissue_or_cell_type
    Serotonin acetylation

    Melatonin: synthesis, receptors, circadian timing and nutrient interactions (2026-09-17) · lines 175–186

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified recombinant enzyme substrate-specificity study · source_derived_draft · unverified_draft

    ### melatonin-aanat-serotonin Human AANAT transferred an acetyl group from acetyl-CoA to serotonin, producing N-acetylserotonin. Condition category: normal nutrient_topic: Melatonin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Serotonin is modified before it becomes melatonin. organism: Human AANAT expressed in bacteria tissue_or_cell_type: Serotonin acetylation experimental_model: Purified recombinant enzyme substrate-specificity study limitations: Biochemical mechanism, not evidence that dietary B5 or acetyl-CoA availability limits melatonin production in all humans. exposure: Serotonin and radiolabeled acetyl-CoA; product HPLC evidence_span: {"source_cache": "artifacts/melatonin-research/10722724.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7fb8418b17e92c5b3fed5d9c08afdb32f28c922dfe94274d3bb02b7e12b2b8c8", "start_char": 0, "end_char": 1857, "text_sha256": "7fb8418b17e92c5b3fed5d9c08afdb32f28c922dfe94274d3bb02b7e12b2b8c8"} [melatonin-p10722724] Substrate specificity and inhibition studies of human serotonin N-acetyltransferase. (2000). https://pubmed.ncbi.nlm.nih.gov/10722724/ DOI: 10.1074/jbc.275.12.8794
    Complete structured claim and evidence

  2. Human CYP1A2 catalyzed melatonin O-demethylation to a lesser extent than CYP2C19 in the study.

    Human cytochrome P450 1A2 → N-Acetylserotonin source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/melatonin-research/15616152.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "482334074e10503323360f236e00b5b837c5b082a7cda4df000a23d491bff8a2", "start_char": 0, "end_char": 1733, "text_sha256": "482334074e10503323360f236e00b5b837c5b082a7cda4df000a23d491bff8a2"}
    experimental_model
    Recombinant P450 screen and mouse brain comparisons
    exposure
    Eleven P450 isozymes; NADPH-dependent 6-hydroxylation/O-demethylation
    limitations
    Catalytic capacity in an enzyme assay is not whole-body contribution. CYP1B1 is an extrahepatic route; human proteins are not substituted for mouse knockout identity.
    nutrient_topic
    Melatonin research collection; topical membership is not evidence of a direct dietary effect. · Melatonin
    organism
    Human recombinant enzymes; separate mouse knockout experiment
    plain_language
    Removing the methyl group returns a molecule with the identity of a synthetic precursor.
    primary_references
    [melatonin-p15616152] Metabolism of melatonin by human cytochromes p450. (2005). https://pubmed.ncbi.nlm.nih.gov/15616152/ DOI: 10.1124/dmd.104.002410
    tissue_or_cell_type
    Oxidative melatonin metabolism

    Melatonin: synthesis, receptors, circadian timing and nutrient interactions (2026-09-17) · lines 617–628

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant P450 screen and mouse brain comparisons · source_derived_draft · unverified_draft

    ### melatonin-cyp-1a2-demethylation Human CYP1A2 catalyzed melatonin O-demethylation to a lesser extent than CYP2C19 in the study. Condition category: normal nutrient_topic: Melatonin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing the methyl group returns a molecule with the identity of a synthetic precursor. organism: Human recombinant enzymes; separate mouse knockout experiment tissue_or_cell_type: Oxidative melatonin metabolism experimental_model: Recombinant P450 screen and mouse brain comparisons limitations: Catalytic capacity in an enzyme assay is not whole-body contribution. CYP1B1 is an extrahepatic route; human proteins are not substituted for mouse knockout identity. exposure: Eleven P450 isozymes; NADPH-dependent 6-hydroxylation/O-demethylation evidence_span: {"source_cache": "artifacts/melatonin-research/15616152.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "482334074e10503323360f236e00b5b837c5b082a7cda4df000a23d491bff8a2", "start_char": 0, "end_char": 1733, "text_sha256": "482334074e10503323360f236e00b5b837c5b082a7cda4df000a23d491bff8a2"} [melatonin-p15616152] Metabolism of melatonin by human cytochromes p450. (2005). https://pubmed.ncbi.nlm.nih.gov/15616152/ DOI: 10.1124/dmd.104.002410
    Complete structured claim and evidence

  3. Human CYP2C19 catalyzed melatonin O-demethylation.

    Human cytochrome P450 2C19 → N-Acetylserotonin source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/melatonin-research/15616152.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "482334074e10503323360f236e00b5b837c5b082a7cda4df000a23d491bff8a2", "start_char": 0, "end_char": 1733, "text_sha256": "482334074e10503323360f236e00b5b837c5b082a7cda4df000a23d491bff8a2"}
    experimental_model
    Recombinant P450 screen and mouse brain comparisons
    exposure
    Eleven P450 isozymes; NADPH-dependent 6-hydroxylation/O-demethylation
    limitations
    Catalytic capacity in an enzyme assay is not whole-body contribution. CYP1B1 is an extrahepatic route; human proteins are not substituted for mouse knockout identity.
    nutrient_topic
    Melatonin research collection; topical membership is not evidence of a direct dietary effect. · Melatonin
    organism
    Human recombinant enzymes; separate mouse knockout experiment
    plain_language
    Removing the methyl group returns a molecule with the identity of a synthetic precursor.
    primary_references
    [melatonin-p15616152] Metabolism of melatonin by human cytochromes p450. (2005). https://pubmed.ncbi.nlm.nih.gov/15616152/ DOI: 10.1124/dmd.104.002410
    tissue_or_cell_type
    Oxidative melatonin metabolism

    Melatonin: synthesis, receptors, circadian timing and nutrient interactions (2026-09-17) · lines 604–615

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant P450 screen and mouse brain comparisons · source_derived_draft · unverified_draft

    ### melatonin-cyp-2c19-demethylation Human CYP2C19 catalyzed melatonin O-demethylation. Condition category: normal nutrient_topic: Melatonin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing the methyl group returns a molecule with the identity of a synthetic precursor. organism: Human recombinant enzymes; separate mouse knockout experiment tissue_or_cell_type: Oxidative melatonin metabolism experimental_model: Recombinant P450 screen and mouse brain comparisons limitations: Catalytic capacity in an enzyme assay is not whole-body contribution. CYP1B1 is an extrahepatic route; human proteins are not substituted for mouse knockout identity. exposure: Eleven P450 isozymes; NADPH-dependent 6-hydroxylation/O-demethylation evidence_span: {"source_cache": "artifacts/melatonin-research/15616152.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "482334074e10503323360f236e00b5b837c5b082a7cda4df000a23d491bff8a2", "start_char": 0, "end_char": 1733, "text_sha256": "482334074e10503323360f236e00b5b837c5b082a7cda4df000a23d491bff8a2"} [melatonin-p15616152] Metabolism of melatonin by human cytochromes p450. (2005). https://pubmed.ncbi.nlm.nih.gov/15616152/ DOI: 10.1124/dmd.104.002410
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. The human AANAT assay used acetyl-CoA as the acetyl donor in N-acetylserotonin formation.

    Acetyl-CoA → Human arylalkylamine N-acetyltransferase / AANAT source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/melatonin-research/10722724.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7fb8418b17e92c5b3fed5d9c08afdb32f28c922dfe94274d3bb02b7e12b2b8c8", "start_char": 0, "end_char": 1857, "text_sha256": "7fb8418b17e92c5b3fed5d9c08afdb32f28c922dfe94274d3bb02b7e12b2b8c8"}
    experimental_model
    Purified recombinant enzyme substrate-specificity study
    exposure
    Serotonin and radiolabeled acetyl-CoA; product HPLC
    limitations
    Biochemical mechanism, not evidence that dietary B5 or acetyl-CoA availability limits melatonin production in all humans.
    nutrient_topic
    Melatonin research collection; topical membership is not evidence of a direct dietary effect. · Melatonin
    organism
    Human AANAT expressed in bacteria
    plain_language
    This connects melatonin synthesis to the B5-derived coenzyme-A system.
    primary_references
    [melatonin-p10722724] Substrate specificity and inhibition studies of human serotonin N-acetyltransferase. (2000). https://pubmed.ncbi.nlm.nih.gov/10722724/ DOI: 10.1074/jbc.275.12.8794
    tissue_or_cell_type
    Serotonin acetylation

    Melatonin: synthesis, receptors, circadian timing and nutrient interactions (2026-09-17) · lines 188–199

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified recombinant enzyme substrate-specificity study · source_derived_draft · unverified_draft

    ### melatonin-aanat-acetyl-coa The human AANAT assay used acetyl-CoA as the acetyl donor in N-acetylserotonin formation. Condition category: normal nutrient_topic: Melatonin research collection; topical membership is not evidence of a direct dietary effect. plain_language: This connects melatonin synthesis to the B5-derived coenzyme-A system. organism: Human AANAT expressed in bacteria tissue_or_cell_type: Serotonin acetylation experimental_model: Purified recombinant enzyme substrate-specificity study limitations: Biochemical mechanism, not evidence that dietary B5 or acetyl-CoA availability limits melatonin production in all humans. exposure: Serotonin and radiolabeled acetyl-CoA; product HPLC evidence_span: {"source_cache": "artifacts/melatonin-research/10722724.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7fb8418b17e92c5b3fed5d9c08afdb32f28c922dfe94274d3bb02b7e12b2b8c8", "start_char": 0, "end_char": 1857, "text_sha256": "7fb8418b17e92c5b3fed5d9c08afdb32f28c922dfe94274d3bb02b7e12b2b8c8"} [melatonin-p10722724] Substrate specificity and inhibition studies of human serotonin N-acetyltransferase. (2000). https://pubmed.ncbi.nlm.nih.gov/10722724/ DOI: 10.1074/jbc.275.12.8794
    Complete structured claim and evidence

  2. Human ASMT catalyzes the terminal methylation step converting N-acetylserotonin to melatonin using SAM.

    Human acetylserotonin O-methyltransferase / ASMT → Melatonin source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/melatonin-research/22775292.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6896e0a7e08f764e1ff8c370601b0477c594e4e1c945df52d0f564e9049a9349", "start_char": 0, "end_char": 1205, "text_sha256": "6896e0a7e08f764e1ff8c370601b0477c594e4e1c945df52d0f564e9049a9349"}
    experimental_model
    X-ray structure and radioenzymatic variant characterization
    exposure
    SAM-dependent methyltransferase structure and enzyme activity assays
    limitations
    Reduced recombinant enzyme activity does not quantify pineal secretion or diagnose a sleep problem in an individual. Variant effects differ; no single universal melatonin-deficiency syndrome.
    nutrient_topic
    Melatonin research collection; topical membership is not evidence of a direct dietary effect. · Melatonin
    organism
    Human ASMT and 20 nonsynonymous variants
    plain_language
    A methyl group completes the molecule.
    primary_references
    [melatonin-p22775292] Crystal structure and functional mapping of human ASMT, the last enzyme of the melatonin synthesis pathway. (2013). https://pubmed.ncbi.nlm.nih.gov/22775292/ DOI: 10.1111/j.1600-079x.2012.01020.x
    tissue_or_cell_type
    Final melatonin synthesis step

    Melatonin: synthesis, receptors, circadian timing and nutrient interactions (2026-09-17) · lines 201–212

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · X-ray structure and radioenzymatic variant characterization · source_derived_draft · unverified_draft

    ### melatonin-asmt-methylation Human ASMT catalyzes the terminal methylation step converting N-acetylserotonin to melatonin using SAM. Condition category: normal nutrient_topic: Melatonin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A methyl group completes the molecule. organism: Human ASMT and 20 nonsynonymous variants tissue_or_cell_type: Final melatonin synthesis step experimental_model: X-ray structure and radioenzymatic variant characterization limitations: Reduced recombinant enzyme activity does not quantify pineal secretion or diagnose a sleep problem in an individual. Variant effects differ; no single universal melatonin-deficiency syndrome. exposure: SAM-dependent methyltransferase structure and enzyme activity assays evidence_span: {"source_cache": "artifacts/melatonin-research/22775292.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6896e0a7e08f764e1ff8c370601b0477c594e4e1c945df52d0f564e9049a9349", "start_char": 0, "end_char": 1205, "text_sha256": "6896e0a7e08f764e1ff8c370601b0477c594e4e1c945df52d0f564e9049a9349"} [melatonin-p22775292] Crystal structure and functional mapping of human ASMT, the last enzyme of the melatonin synthesis pathway. (2013). https://pubmed.ncbi.nlm.nih.gov/22775292/ DOI: 10.1111/j.1600-079x.2012.01020.x
    Complete structured claim and evidence

  3. SULT1C4 had the strongest tested sulfating activity toward N-acetylserotonin.

    Human sulfotransferase 1C4 / SULT1C4 → N-Acetylserotonin sulfate source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/melatonin-research/26577053.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ab887dc7012d5f393de52ecf842b67282d51b61bac705b9ab187c1a3e24331d5", "start_char": 0, "end_char": 1378, "text_sha256": "ab887dc7012d5f393de52ecf842b67282d51b61bac705b9ab187c1a3e24331d5"}
    experimental_model
    Thirteen human SULT enzymes, labeled cells and tissue cytosols
    exposure
    6-hydroxymelatonin and N-acetylserotonin substrates; sulfate metabolic labeling
    limitations
    Enzyme ranking applies to tested conditions. Sulfation is a separate step from P450 hydroxylation; no dietary sulfur threshold was established.
    nutrient_topic
    Melatonin research collection; topical membership is not evidence of a direct dietary effect. · Melatonin
    organism
    Human recombinant enzymes, HepG2 and Caco-2 cells
    plain_language
    The precursor has its own conjugation route, separate from melatonin methylation.
    primary_references
    [melatonin-p26577053] Sulfation of 6-hydroxymelatonin, N-acetylserotonin and 4-hydroxyramelteon by the human cytosolic sulfotransferases (SULTs). (2016). https://pubmed.ncbi.nlm.nih.gov/26577053/ DOI: 10.3109/00498254.2015.1107656
    tissue_or_cell_type
    Sulfate conjugation

    Melatonin: synthesis, receptors, circadian timing and nutrient interactions (2026-09-17) · lines 643–654

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Thirteen human SULT enzymes, labeled cells and tissue cytosols · source_derived_draft · unverified_draft

    ### melatonin-sult1c4 SULT1C4 had the strongest tested sulfating activity toward N-acetylserotonin. Condition category: normal nutrient_topic: Melatonin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The precursor has its own conjugation route, separate from melatonin methylation. organism: Human recombinant enzymes, HepG2 and Caco-2 cells tissue_or_cell_type: Sulfate conjugation experimental_model: Thirteen human SULT enzymes, labeled cells and tissue cytosols limitations: Enzyme ranking applies to tested conditions. Sulfation is a separate step from P450 hydroxylation; no dietary sulfur threshold was established. exposure: 6-hydroxymelatonin and N-acetylserotonin substrates; sulfate metabolic labeling evidence_span: {"source_cache": "artifacts/melatonin-research/26577053.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ab887dc7012d5f393de52ecf842b67282d51b61bac705b9ab187c1a3e24331d5", "start_char": 0, "end_char": 1378, "text_sha256": "ab887dc7012d5f393de52ecf842b67282d51b61bac705b9ab187c1a3e24331d5"} [melatonin-p26577053] Sulfation of 6-hydroxymelatonin, N-acetylserotonin and 4-hydroxyramelteon by the human cytosolic sulfotransferases (SULTs). (2016). https://pubmed.ncbi.nlm.nih.gov/26577053/ DOI: 10.3109/00498254.2015.1107656
    Complete structured claim and evidence

  4. Myricetin inhibited serotonin N-acetyltransferase activity in the reported enzyme assay.

    Myricetin → AANAT preparation in myricetin study; species unresolved in accessed abstract source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    AANAT activity screen; substrate-site interaction proposed from docking.
    limitations
    Binding site and species are not independently established by the accessed abstract.
    nutrient_topic
    Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
    plain_language
    A step on the serotonin-to-melatonin route can be inhibited.
    primary_references
    The flavonoid myricetin reduces nocturnal melatonin levels in the blood through the inhibition of serotonin N-acetyltransferase. · 2013 · https://pubmed.ncbi.nlm.nih.gov/24076393/ · DOI 10.1016/j.bbrc.2013.09.076

    Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 564–570

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · AANAT activity screen; substrate-site interaction proposed from docking. · source_derived_draft · unverified_draft

    ## myricetin-aanat A step on the serotonin-to-melatonin route can be inhibited. Myricetin inhibited serotonin N-acetyltransferase activity in the reported enzyme assay. Model: AANAT activity screen; substrate-site interaction proposed from docking. Limitations: Binding site and species are not independently established by the accessed abstract. Evidence access: Primary abstract The flavonoid myricetin reduces nocturnal melatonin levels in the blood through the inhibition of serotonin N-acetyltransferase. · 2013 · https://pubmed.ncbi.nlm.nih.gov/24076393/ · DOI 10.1016/j.bbrc.2013.09.076
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards