Component
6-Sulfatoxymelatonin / aMT6s
6-Sulfatoxymelatonin / aMT6s. Species, exposure and limitations are retained in each linked claim.
2 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What acts on it
SULT1A1 had the strongest tested sulfating activity toward 6-hydroxymelatonin.
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 hydroxylated metabolite undergoes another reaction before common urinary measurement.
- 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 630–641
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-sult1a1 SULT1A1 had the strongest tested sulfating activity toward 6-hydroxymelatonin. Condition category: normal nutrient_topic: Melatonin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The hydroxylated metabolite undergoes another reaction before common urinary measurement. 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
Where it participates (unsigned role)
Atenolol treatment was associated with lower urinary aMT6s and a small increase in blood glucose.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/melatonin-research/26946962.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ad9bf60e8f57ef2ec9fe9e4b74b848b9cc0711fe00cf5a9959bf489dd9c8f992", "start_char": 0, "end_char": 1191, "text_sha256": "ad9bf60e8f57ef2ec9fe9e4b74b848b9cc0711fe00cf5a9959bf489dd9c8f992"}
- experimental_model
- Nine-week antihypertensive pharmacogenetic cohort analysis
- exposure
- Atenolol treatment; urinary aMT6s normalized to creatinine
- limitations
- Association study; absence of correlation is not proof of no biological role. It does not support a simple linear explanation of atenolol-related glucose changes by lost melatonin.
- nutrient_topic
- Melatonin research collection; topical membership is not evidence of a direct dietary effect. · Melatonin
- organism
- 232 hypertensive participants reported as Caucasian in PEAR
- plain_language
- Metabolite excretion and glucose changed during the same treatment.
- primary_references
- [melatonin-p26946962] Melatonin Pathway and Atenolol-Related Glucose Dysregulation: Is There a Correlation? (2016). https://pubmed.ncbi.nlm.nih.gov/26946962/ DOI: 10.1111/cts.12389
- tissue_or_cell_type
- Urinary melatonin metabolite and blood glucose
Melatonin: synthesis, receptors, circadian timing and nutrient interactions (2026-09-17) · lines 1241–1252
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Nine-week antihypertensive pharmacogenetic cohort analysis · source_derived_draft · unverified_draft
### melatonin-atenolol-metabolite Atenolol treatment was associated with lower urinary aMT6s and a small increase in blood glucose. Condition category: normal nutrient_topic: Melatonin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Metabolite excretion and glucose changed during the same treatment. organism: 232 hypertensive participants reported as Caucasian in PEAR tissue_or_cell_type: Urinary melatonin metabolite and blood glucose experimental_model: Nine-week antihypertensive pharmacogenetic cohort analysis limitations: Association study; absence of correlation is not proof of no biological role. It does not support a simple linear explanation of atenolol-related glucose changes by lost melatonin. exposure: Atenolol treatment; urinary aMT6s normalized to creatinine evidence_span: {"source_cache": "artifacts/melatonin-research/26946962.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ad9bf60e8f57ef2ec9fe9e4b74b848b9cc0711fe00cf5a9959bf489dd9c8f992", "start_char": 0, "end_char": 1191, "text_sha256": "ad9bf60e8f57ef2ec9fe9e4b74b848b9cc0711fe00cf5a9959bf489dd9c8f992"} [melatonin-p26946962] Melatonin Pathway and Atenolol-Related Glucose Dysregulation: Is There a Correlation? (2016). https://pubmed.ncbi.nlm.nih.gov/26946962/ DOI: 10.1111/cts.12389
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.