Nutrient chapter

Myricetin

Myricetin is a plant flavonol, distinct from myricitrin and dihydromyricetin. Explore its sulfate and microbial metabolites, selenium-dependent thioredoxin machinery, glutathione, copper, vitamin E, calcium, purine oxidation and melatonin links. Enzyme, cell and animal experiments retain their limits. The APE1 disagreement has its own discussion page. No human myricetin-deficiency syndrome is established.

96 recorded mechanisms · 6 availability situations · 8 preserved sources. Draft and verified records are labeled separately.

Read recorded mechanisms Open recursive mind map

The mechanisms

What the sources say this nutrient does, one relationship at a time. Plain wording comes first; the technical statement follows.

Following 50 or 100 mg/kg oral myricetin in rats, reported absolute bioavailability was 9.62% or 9.74%; plasma samples underwent beta-glucuronidase/sulfatase hydrolysis before quantification.
Myricetin → Rat plasma total hydrolysable myricetin exposure source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Rat oral/intravenous UPLC-MS/MS comparison.
limitations
Do not use these percentages as human absorption or unconjugated target exposure.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
The measurement includes releasable conjugates, not just free parent.
primary_references
Quantitative determination of myricetin in rat plasma by ultra performance liquid chromatography tandem mass spectrometry and its absolute bioavailability. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24357136/ · DOI 10.1055/s-0033-1363220
trigger_kind
biomarker_context Imported condition classification; unverified.
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 12–18
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat oral/intravenous UPLC-MS/MS comparison. · source_derived_draft · unverified_draft
## myricetin-total-exposure The measurement includes releasable conjugates, not just free parent. Following 50 or 100 mg/kg oral myricetin in rats, reported absolute bioavailability was 9.62% or 9.74%; plasma samples underwent beta-glucuronidase/sulfatase hydrolysis before quantification. Model: Rat oral/intravenous UPLC-MS/MS comparison. Limitations: Do not use these percentages as human absorption or unconjugated target exposure. Evidence access: Primary abstract Quantitative determination of myricetin in rat plasma by ultra performance liquid chromatography tandem mass spectrometry and its absolute bioavailability. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24357136/ · DOI 10.1055/s-0033-1363220
Complete structured claim and evidence
Human-donor intestinal bacterial cultures yielded Myricetin through the reported deglycosylation route.
Myricitrin / myricetin 3-O-rhamnoside → Myricetin source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Four active isolates selected from about 100 colonies from one healthy female donor; most identified as Escherichia.
limitations
Mass-spectrometric pathway assignment; no specific enzyme or population-wide conversion rate established.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
Gut processing produces a chemically different molecule.
primary_references
Identification of the metabolites of myricitrin produced by human intestinal bacteria in vitro using ultra-performance liquid chromatography/quadrupole time-of-flight mass spectrometry. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24882500/ · DOI 10.1517/17425255.2014.918954
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 20–26
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Four active isolates selected from about 100 colonies from one healthy female donor; most identified as Escherichia. · source_derived_draft · unverified_draft
## myricetin-microbial-deglycosylation Gut processing produces a chemically different molecule. Human-donor intestinal bacterial cultures yielded Myricetin through the reported deglycosylation route. Model: Four active isolates selected from about 100 colonies from one healthy female donor; most identified as Escherichia. Limitations: Mass-spectrometric pathway assignment; no specific enzyme or population-wide conversion rate established. Evidence access: Primary abstract Identification of the metabolites of myricitrin produced by human intestinal bacteria in vitro using ultra-performance liquid chromatography/quadrupole time-of-flight mass spectrometry. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24882500/ · DOI 10.1517/17425255.2014.918954
Complete structured claim and evidence
Human-donor intestinal bacterial cultures yielded Quercitrin / quercetin 3-O-rhamnoside through the reported dehydroxylation route.
Myricitrin / myricetin 3-O-rhamnoside → Quercitrin / quercetin 3-O-rhamnoside source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Four active isolates selected from about 100 colonies from one healthy female donor; most identified as Escherichia.
limitations
Mass-spectrometric pathway assignment; no specific enzyme or population-wide conversion rate established.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
Gut processing produces a chemically different molecule.
primary_references
Identification of the metabolites of myricitrin produced by human intestinal bacteria in vitro using ultra-performance liquid chromatography/quadrupole time-of-flight mass spectrometry. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24882500/ · DOI 10.1517/17425255.2014.918954
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 28–34
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Four active isolates selected from about 100 colonies from one healthy female donor; most identified as Escherichia. · source_derived_draft · unverified_draft
## myricetin-microbial-dehydroxylation Gut processing produces a chemically different molecule. Human-donor intestinal bacterial cultures yielded Quercitrin / quercetin 3-O-rhamnoside through the reported dehydroxylation route. Model: Four active isolates selected from about 100 colonies from one healthy female donor; most identified as Escherichia. Limitations: Mass-spectrometric pathway assignment; no specific enzyme or population-wide conversion rate established. Evidence access: Primary abstract Identification of the metabolites of myricitrin produced by human intestinal bacteria in vitro using ultra-performance liquid chromatography/quadrupole time-of-flight mass spectrometry. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24882500/ · DOI 10.1517/17425255.2014.918954
Complete structured claim and evidence
Human-donor intestinal bacterial cultures yielded Quercetin through the reported subsequent deglycosylation route.
Quercitrin / quercetin 3-O-rhamnoside → Quercetin source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Four active isolates selected from about 100 colonies from one healthy female donor; most identified as Escherichia.
limitations
Mass-spectrometric pathway assignment; no specific enzyme or population-wide conversion rate established.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
Gut processing produces a chemically different molecule.
primary_references
Identification of the metabolites of myricitrin produced by human intestinal bacteria in vitro using ultra-performance liquid chromatography/quadrupole time-of-flight mass spectrometry. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24882500/ · DOI 10.1517/17425255.2014.918954
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 36–42
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Four active isolates selected from about 100 colonies from one healthy female donor; most identified as Escherichia. · source_derived_draft · unverified_draft
## myricetin-microbial-quercetin Gut processing produces a chemically different molecule. Human-donor intestinal bacterial cultures yielded Quercetin through the reported subsequent deglycosylation route. Model: Four active isolates selected from about 100 colonies from one healthy female donor; most identified as Escherichia. Limitations: Mass-spectrometric pathway assignment; no specific enzyme or population-wide conversion rate established. Evidence access: Primary abstract Identification of the metabolites of myricitrin produced by human intestinal bacteria in vitro using ultra-performance liquid chromatography/quadrupole time-of-flight mass spectrometry. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24882500/ · DOI 10.1517/17425255.2014.918954
Complete structured claim and evidence
Oxidized myricetin reacted chemically with ammonia to form 4′-NH2-myricetin, structurally confirmed by NMR and LC-MS.
Myricetin quinone, oxidation intermediate → 4′-NH2-myricetin source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Cell-free chemistry.
limitations
Not an established ammonia-detoxification therapy or enzyme-catalyzed pathway.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
Reactive nitrogen can become part of a new metabolite.
primary_references
Biotransformation of Myricetin: A Novel Metabolic Pathway to Produce Aminated Products in Mice. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31087612/ · DOI 10.1002/mnfr.201900203
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 44–50
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Cell-free chemistry. · source_derived_draft · unverified_draft
## myricetin-amination-chemistry Reactive nitrogen can become part of a new metabolite. Oxidized myricetin reacted chemically with ammonia to form 4′-NH2-myricetin, structurally confirmed by NMR and LC-MS. Model: Cell-free chemistry. Limitations: Not an established ammonia-detoxification therapy or enzyme-catalyzed pathway. Evidence access: Primary abstract Biotransformation of Myricetin: A Novel Metabolic Pathway to Produce Aminated Products in Mice. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31087612/ · DOI 10.1002/mnfr.201900203
Complete structured claim and evidence
Myricetin oxidation to a quinone intermediate enabled the reported cell-free amination reaction.
Myricetin → Myricetin quinone, oxidation intermediate source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Chemical biotransformation experiments.
limitations
An intermediate in this reaction is not a measured human circulating concentration.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
Oxidation creates a more reactive form.
primary_references
Biotransformation of Myricetin: A Novel Metabolic Pathway to Produce Aminated Products in Mice. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31087612/ · DOI 10.1002/mnfr.201900203
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 52–58
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Chemical biotransformation experiments. · source_derived_draft · unverified_draft
## myricetin-quinone-formation Oxidation creates a more reactive form. Myricetin oxidation to a quinone intermediate enabled the reported cell-free amination reaction. Model: Chemical biotransformation experiments. Limitations: An intermediate in this reaction is not a measured human circulating concentration. Evidence access: Primary abstract Biotransformation of Myricetin: A Novel Metabolic Pathway to Produce Aminated Products in Mice. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31087612/ · DOI 10.1002/mnfr.201900203
Complete structured claim and evidence
Mono-methylated myricetin was recorded among metabolites in the mouse biotransformation study.
Myricetin → Mono-O-methylated myricetin; positional isomer unresolved source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Mouse metabolite analysis.
limitations
Methylation position and responsible enzyme are not established by the accessed abstract; no claim of SAM depletion.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
Methylation adds another distinct molecular form.
primary_references
Biotransformation of Myricetin: A Novel Metabolic Pathway to Produce Aminated Products in Mice. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31087612/ · DOI 10.1002/mnfr.201900203
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 60–66
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse metabolite analysis. · source_derived_draft · unverified_draft
## myricetin-methyl-metabolite Methylation adds another distinct molecular form. Mono-methylated myricetin was recorded among metabolites in the mouse biotransformation study. Model: Mouse metabolite analysis. Limitations: Methylation position and responsible enzyme are not established by the accessed abstract; no claim of SAM depletion. Evidence access: Primary abstract Biotransformation of Myricetin: A Novel Metabolic Pathway to Produce Aminated Products in Mice. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31087612/ · DOI 10.1002/mnfr.201900203
Complete structured claim and evidence
The study identified 3,4,5-trihydroxyphenylacetic acid as a microbial-derived myricetin metabolite investigated for further amination.
Myricetin → 3,4,5-Trihydroxyphenylacetic acid source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Mouse biotransformation study.
limitations
No specific strain, enzyme or human conversion fraction established by this record.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
Microbial breakdown produces a smaller chemical scaffold.
primary_references
Biotransformation of Myricetin: A Novel Metabolic Pathway to Produce Aminated Products in Mice. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31087612/ · DOI 10.1002/mnfr.201900203
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 68–74
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse biotransformation study. · source_derived_draft · unverified_draft
## myricetin-ring-cleavage-product Microbial breakdown produces a smaller chemical scaffold. The study identified 3,4,5-trihydroxyphenylacetic acid as a microbial-derived myricetin metabolite investigated for further amination. Model: Mouse biotransformation study. Limitations: No specific strain, enzyme or human conversion fraction established by this record. Evidence access: Primary abstract Biotransformation of Myricetin: A Novel Metabolic Pathway to Produce Aminated Products in Mice. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31087612/ · DOI 10.1002/mnfr.201900203
Complete structured claim and evidence
4′-NH2-myricetin was identified against a synthetic standard in feces of myricetin-treated mice.
Myricetin → 4′-NH2-myricetin source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Mouse oral-gavage metabolism study.
limitations
Detection does not identify the forming compartment or establish human production.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
The new molecule was also detected after dosing an animal.
primary_references
Biotransformation of Myricetin: A Novel Metabolic Pathway to Produce Aminated Products in Mice. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31087612/ · DOI 10.1002/mnfr.201900203
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 76–82
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse oral-gavage metabolism study. · source_derived_draft · unverified_draft
## myricetin-amination-mice The new molecule was also detected after dosing an animal. 4′-NH2-myricetin was identified against a synthetic standard in feces of myricetin-treated mice. Model: Mouse oral-gavage metabolism study. Limitations: Detection does not identify the forming compartment or establish human production. Evidence access: Primary abstract Biotransformation of Myricetin: A Novel Metabolic Pathway to Produce Aminated Products in Mice. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31087612/ · DOI 10.1002/mnfr.201900203
Complete structured claim and evidence
LC-MS analysis supported amination of Mono-O-methylated myricetin; positional isomer unresolved in myricetin-treated mice.
Mono-O-methylated myricetin; positional isomer unresolved → Aminated mono-O-methylated myricetin; positional isomer unresolved source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Mouse fecal/plasma metabolite analysis after oral dosing.
limitations
Structural certainty differs from the NMR-confirmed parent amination product; no human flux measured.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
Downstream products can undergo further chemistry.
primary_references
Biotransformation of Myricetin: A Novel Metabolic Pathway to Produce Aminated Products in Mice. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31087612/ · DOI 10.1002/mnfr.201900203
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 84–90
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse fecal/plasma metabolite analysis after oral dosing. · source_derived_draft · unverified_draft
## myricetin-methyl-amination Downstream products can undergo further chemistry. LC-MS analysis supported amination of Mono-O-methylated myricetin; positional isomer unresolved in myricetin-treated mice. Model: Mouse fecal/plasma metabolite analysis after oral dosing. Limitations: Structural certainty differs from the NMR-confirmed parent amination product; no human flux measured. Evidence access: Primary abstract Biotransformation of Myricetin: A Novel Metabolic Pathway to Produce Aminated Products in Mice. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31087612/ · DOI 10.1002/mnfr.201900203
Complete structured claim and evidence
LC-MS analysis supported amination of 3,4,5-Trihydroxyphenylacetic acid in myricetin-treated mice.
3,4,5-Trihydroxyphenylacetic acid → Aminated 3,4,5-trihydroxyphenylacetic acid; positional assignment unresolved source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Mouse fecal/plasma metabolite analysis after oral dosing.
limitations
Structural certainty differs from the NMR-confirmed parent amination product; no human flux measured.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
Downstream products can undergo further chemistry.
primary_references
Biotransformation of Myricetin: A Novel Metabolic Pathway to Produce Aminated Products in Mice. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31087612/ · DOI 10.1002/mnfr.201900203
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 92–98
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse fecal/plasma metabolite analysis after oral dosing. · source_derived_draft · unverified_draft
## myricetin-acid-amination Downstream products can undergo further chemistry. LC-MS analysis supported amination of 3,4,5-Trihydroxyphenylacetic acid in myricetin-treated mice. Model: Mouse fecal/plasma metabolite analysis after oral dosing. Limitations: Structural certainty differs from the NMR-confirmed parent amination product; no human flux measured. Evidence access: Primary abstract Biotransformation of Myricetin: A Novel Metabolic Pathway to Produce Aminated Products in Mice. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31087612/ · DOI 10.1002/mnfr.201900203
Complete structured claim and evidence
Plasma aminated trihydroxyphenylacetic acid was higher after 200 mg/kg myricetin than after 100 or 400 mg/kg.
Myricetin → Aminated 3,4,5-trihydroxyphenylacetic acid; positional assignment unresolved source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Mouse oral-gavage comparison.
limitations
High experimental doses; no human optimal dose follows.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
More administered parent did not always mean more of a metabolite.
primary_references
Biotransformation of Myricetin: A Novel Metabolic Pathway to Produce Aminated Products in Mice. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31087612/ · DOI 10.1002/mnfr.201900203
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 100–106
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse oral-gavage comparison. · source_derived_draft · unverified_draft
## myricetin-acid-dose-nonlinearity More administered parent did not always mean more of a metabolite. Plasma aminated trihydroxyphenylacetic acid was higher after 200 mg/kg myricetin than after 100 or 400 mg/kg. Model: Mouse oral-gavage comparison. Limitations: High experimental doses; no human optimal dose follows. Evidence access: Primary abstract Biotransformation of Myricetin: A Novel Metabolic Pathway to Produce Aminated Products in Mice. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31087612/ · DOI 10.1002/mnfr.201900203
Complete structured claim and evidence
The parent inhibited human SLCO1B1 transport in vitro, IC50 6.4 micromolar.
Myricetin → Human OATP1B1 / SLCO1B1 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Human transporter-overexpressing cells.
limitations
Probe-substrate potency is not a measured clinical drug interaction.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
Transport competition can depend on the metabolite.
primary_references
Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 108–114
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human transporter-overexpressing cells. · source_derived_draft · unverified_draft
## myricetin-parent-slco1b1 Transport competition can depend on the metabolite. The parent inhibited human SLCO1B1 transport in vitro, IC50 6.4 micromolar. Model: Human transporter-overexpressing cells. Limitations: Probe-substrate potency is not a measured clinical drug interaction. Evidence access: Primary full text Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021
Complete structured claim and evidence
The parent inhibited human SLCO2B1 transport in vitro, IC50 0.4 micromolar.
Myricetin → Human organic anion transporting polypeptide 2B1 / SLCO2B1 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Human transporter-overexpressing cells.
limitations
Probe-substrate potency is not a measured clinical drug interaction.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
Transport competition can depend on the metabolite.
primary_references
Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 116–122
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human transporter-overexpressing cells. · source_derived_draft · unverified_draft
## myricetin-parent-slco2b1 Transport competition can depend on the metabolite. The parent inhibited human SLCO2B1 transport in vitro, IC50 0.4 micromolar. Model: Human transporter-overexpressing cells. Limitations: Probe-substrate potency is not a measured clinical drug interaction. Evidence access: Primary full text Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021
Complete structured claim and evidence
The parent bound human serum albumin with high affinity and moderately displaced the Site I marker warfarin in vitro.
Myricetin → Human serum albumin source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Albumin fluorescence and ultrafiltration assays.
limitations
Not demonstrated displacement toxicity or a change in patient anticoagulation.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
Carrier binding changes the freely available fraction.
primary_references
Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 124–130
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Albumin fluorescence and ultrafiltration assays. · source_derived_draft · unverified_draft
## myricetin-parent-albumin Carrier binding changes the freely available fraction. The parent bound human serum albumin with high affinity and moderately displaced the Site I marker warfarin in vitro. Model: Albumin fluorescence and ultrafiltration assays. Limitations: Not demonstrated displacement toxicity or a change in patient anticoagulation. Evidence access: Primary full text Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021
Complete structured claim and evidence
At 20 micromolar, the parent did not inhibit diclofenac hydroxylation in the human CYP2C9 assay.
Myricetin → Human cytochrome P450 2C9 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Recombinant human enzymes; 5 micromolar substrate.
limitations
Restricted substrate, concentration and preparation; earlier CYP2C9 assays gave different potency.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
A transporter interaction does not imply strong CYP inhibition.
primary_references
Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 132–138
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Recombinant human enzymes; 5 micromolar substrate. · source_derived_draft · unverified_draft
## myricetin-parent-cyp2c9 A transporter interaction does not imply strong CYP inhibition. At 20 micromolar, the parent did not inhibit diclofenac hydroxylation in the human CYP2C9 assay. Model: Recombinant human enzymes; 5 micromolar substrate. Limitations: Restricted substrate, concentration and preparation; earlier CYP2C9 assays gave different potency. Evidence access: Primary full text Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021
Complete structured claim and evidence
At 20 micromolar, the parent did not significantly inhibit mephenytoin hydroxylation in the human CYP2C19 assay.
Myricetin → Human cytochrome P450 2C19 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Recombinant human enzymes; 5 micromolar substrate.
limitations
Restricted substrate, concentration and preparation; earlier CYP2C9 assays gave different potency.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
A transporter interaction does not imply strong CYP inhibition.
primary_references
Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 140–146
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Recombinant human enzymes; 5 micromolar substrate. · source_derived_draft · unverified_draft
## myricetin-parent-cyp2c19 A transporter interaction does not imply strong CYP inhibition. At 20 micromolar, the parent did not significantly inhibit mephenytoin hydroxylation in the human CYP2C19 assay. Model: Recombinant human enzymes; 5 micromolar substrate. Limitations: Restricted substrate, concentration and preparation; earlier CYP2C9 assays gave different potency. Evidence access: Primary full text Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021
Complete structured claim and evidence
At 20 micromolar, the parent reduced testosterone hydroxylation by less than 10% in the human CYP3A4 assay.
Myricetin → Human cytochrome P450 3A4 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Recombinant human enzymes; 5 micromolar substrate.
limitations
Restricted substrate, concentration and preparation; earlier CYP2C9 assays gave different potency.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
A transporter interaction does not imply strong CYP inhibition.
primary_references
Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 148–154
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Recombinant human enzymes; 5 micromolar substrate. · source_derived_draft · unverified_draft
## myricetin-parent-cyp3a4 A transporter interaction does not imply strong CYP inhibition. At 20 micromolar, the parent reduced testosterone hydroxylation by less than 10% in the human CYP3A4 assay. Model: Recombinant human enzymes; 5 micromolar substrate. Limitations: Restricted substrate, concentration and preparation; earlier CYP2C9 assays gave different potency. Evidence access: Primary full text Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021
Complete structured claim and evidence
The sulfate inhibited human SLCO1B1 transport in vitro, IC50 1.7 micromolar.
Myricetin 3′-O-sulfate → Human OATP1B1 / SLCO1B1 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Human transporter-overexpressing cells.
limitations
Probe-substrate potency is not a measured clinical drug interaction.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
Transport competition can depend on the metabolite.
primary_references
Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 156–162
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human transporter-overexpressing cells. · source_derived_draft · unverified_draft
## myricetin-sulfate-slco1b1 Transport competition can depend on the metabolite. The sulfate inhibited human SLCO1B1 transport in vitro, IC50 1.7 micromolar. Model: Human transporter-overexpressing cells. Limitations: Probe-substrate potency is not a measured clinical drug interaction. Evidence access: Primary full text Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021
Complete structured claim and evidence
The sulfate inhibited human SLCO2B1 transport in vitro, IC50 0.3 micromolar.
Myricetin 3′-O-sulfate → Human organic anion transporting polypeptide 2B1 / SLCO2B1 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Human transporter-overexpressing cells.
limitations
Probe-substrate potency is not a measured clinical drug interaction.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
Transport competition can depend on the metabolite.
primary_references
Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 164–170
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human transporter-overexpressing cells. · source_derived_draft · unverified_draft
## myricetin-sulfate-slco2b1 Transport competition can depend on the metabolite. The sulfate inhibited human SLCO2B1 transport in vitro, IC50 0.3 micromolar. Model: Human transporter-overexpressing cells. Limitations: Probe-substrate potency is not a measured clinical drug interaction. Evidence access: Primary full text Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021
Complete structured claim and evidence
The sulfate bound human serum albumin with high affinity and moderately displaced the Site I marker warfarin in vitro.
Myricetin 3′-O-sulfate → Human serum albumin source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Albumin fluorescence and ultrafiltration assays.
limitations
Not demonstrated displacement toxicity or a change in patient anticoagulation.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
Carrier binding changes the freely available fraction.
primary_references
Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 172–178
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Albumin fluorescence and ultrafiltration assays. · source_derived_draft · unverified_draft
## myricetin-sulfate-albumin Carrier binding changes the freely available fraction. The sulfate bound human serum albumin with high affinity and moderately displaced the Site I marker warfarin in vitro. Model: Albumin fluorescence and ultrafiltration assays. Limitations: Not demonstrated displacement toxicity or a change in patient anticoagulation. Evidence access: Primary full text Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021
Complete structured claim and evidence
At 20 micromolar, the sulfate did not inhibit diclofenac hydroxylation in the human CYP2C9 assay.
Myricetin 3′-O-sulfate → Human cytochrome P450 2C9 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Recombinant human enzymes; 5 micromolar substrate.
limitations
Restricted substrate, concentration and preparation; earlier CYP2C9 assays gave different potency.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
A transporter interaction does not imply strong CYP inhibition.
primary_references
Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 180–186
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Recombinant human enzymes; 5 micromolar substrate. · source_derived_draft · unverified_draft
## myricetin-sulfate-cyp2c9 A transporter interaction does not imply strong CYP inhibition. At 20 micromolar, the sulfate did not inhibit diclofenac hydroxylation in the human CYP2C9 assay. Model: Recombinant human enzymes; 5 micromolar substrate. Limitations: Restricted substrate, concentration and preparation; earlier CYP2C9 assays gave different potency. Evidence access: Primary full text Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021
Complete structured claim and evidence
At 20 micromolar, the sulfate did not significantly inhibit mephenytoin hydroxylation in the human CYP2C19 assay.
Myricetin 3′-O-sulfate → Human cytochrome P450 2C19 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Recombinant human enzymes; 5 micromolar substrate.
limitations
Restricted substrate, concentration and preparation; earlier CYP2C9 assays gave different potency.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
A transporter interaction does not imply strong CYP inhibition.
primary_references
Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 188–194
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Recombinant human enzymes; 5 micromolar substrate. · source_derived_draft · unverified_draft
## myricetin-sulfate-cyp2c19 A transporter interaction does not imply strong CYP inhibition. At 20 micromolar, the sulfate did not significantly inhibit mephenytoin hydroxylation in the human CYP2C19 assay. Model: Recombinant human enzymes; 5 micromolar substrate. Limitations: Restricted substrate, concentration and preparation; earlier CYP2C9 assays gave different potency. Evidence access: Primary full text Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021
Complete structured claim and evidence
At 20 micromolar, the sulfate reduced testosterone hydroxylation by less than 10% in the human CYP3A4 assay.
Myricetin 3′-O-sulfate → Human cytochrome P450 3A4 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Recombinant human enzymes; 5 micromolar substrate.
limitations
Restricted substrate, concentration and preparation; earlier CYP2C9 assays gave different potency.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
A transporter interaction does not imply strong CYP inhibition.
primary_references
Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 196–202
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Recombinant human enzymes; 5 micromolar substrate. · source_derived_draft · unverified_draft
## myricetin-sulfate-cyp3a4 A transporter interaction does not imply strong CYP inhibition. At 20 micromolar, the sulfate reduced testosterone hydroxylation by less than 10% in the human CYP3A4 assay. Model: Recombinant human enzymes; 5 micromolar substrate. Limitations: Restricted substrate, concentration and preparation; earlier CYP2C9 assays gave different potency. Evidence access: Primary full text Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021
Complete structured claim and evidence
Myricetin 3′-O-sulfate was a substrate of human SLCO1B1.
Human OATP1B1 / SLCO1B1 → Myricetin 3′-O-sulfate source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Overexpressing-cell uptake with flavonoid fluorescence method.
limitations
Not a quantified human tissue delivery rate.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
The sulfate is transported, not simply inactive waste.
primary_references
Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021
transport_effect
raises Recorded as a substrate in the OATP1B1 uptake assay.
transport_pool
the hepatocyte-model cell in the uptake assay Recorded as a substrate in the OATP1B1 uptake assay.
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 204–210
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Overexpressing-cell uptake with flavonoid fluorescence method. · source_derived_draft · unverified_draft
## myricetin-sulfate-uptake-slco1b1 The sulfate is transported, not simply inactive waste. Myricetin 3′-O-sulfate was a substrate of human SLCO1B1. Model: Overexpressing-cell uptake with flavonoid fluorescence method. Limitations: Not a quantified human tissue delivery rate. Evidence access: Primary full text Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021
Complete structured claim and evidence
Myricetin 3′-O-sulfate was a substrate of human SLCO2B1.
Human organic anion transporting polypeptide 2B1 / SLCO2B1 → Myricetin 3′-O-sulfate source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Overexpressing-cell uptake with flavonoid fluorescence method.
limitations
Not a quantified human tissue delivery rate.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
The sulfate is transported, not simply inactive waste.
primary_references
Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021
transport_effect
raises Recorded as a substrate in the OATP2B1 uptake assay.
transport_pool
the expressing cell Recorded as a substrate in the OATP2B1 uptake assay.
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 212–218
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Overexpressing-cell uptake with flavonoid fluorescence method. · source_derived_draft · unverified_draft
## myricetin-sulfate-uptake-slco2b1 The sulfate is transported, not simply inactive waste. Myricetin 3′-O-sulfate was a substrate of human SLCO2B1. Model: Overexpressing-cell uptake with flavonoid fluorescence method. Limitations: Not a quantified human tissue delivery rate. Evidence access: Primary full text Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021
Complete structured claim and evidence
An earlier CYP assay reported myricetin inhibition of CYP2C9 with IC50 13 micromolar.
Myricetin → Human cytochrome P450 2C9 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Enzyme activity testing accompanying a rat carvedilol study.
limitations
Later recombinant diclofenac assay showed no inhibition at 20 micromolar. Assay differences require matched replication; not a universal clinical interaction.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
An earlier enzyme assay reported greater inhibition.
primary_references
Effects of myricetin on the bioavailability of carvedilol in rats. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22132944/ · DOI 10.3109/13880209.2011.611141
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 220–226
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Enzyme activity testing accompanying a rat carvedilol study. · source_derived_draft · unverified_draft
## myricetin-cyp2c9-earlier An earlier enzyme assay reported greater inhibition. An earlier CYP assay reported myricetin inhibition of CYP2C9 with IC50 13 micromolar. Model: Enzyme activity testing accompanying a rat carvedilol study. Limitations: Later recombinant diclofenac assay showed no inhibition at 20 micromolar. Assay differences require matched replication; not a universal clinical interaction. Evidence access: Primary abstract Effects of myricetin on the bioavailability of carvedilol in rats. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22132944/ · DOI 10.3109/13880209.2011.611141
Complete structured claim and evidence
Myricetin inhibited CYP2D6 in the tested enzyme assay, IC50 57 micromolar.
Myricetin → Human cytochrome P450 2D6 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Enzyme activity assay.
limitations
High in-vitro concentration; no human clearance change established.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
Different CYP enzymes have different measured sensitivities.
primary_references
Effects of myricetin on the bioavailability of carvedilol in rats. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22132944/ · DOI 10.3109/13880209.2011.611141
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 228–234
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Enzyme activity assay. · source_derived_draft · unverified_draft
## myricetin-cyp2d6 Different CYP enzymes have different measured sensitivities. Myricetin inhibited CYP2D6 in the tested enzyme assay, IC50 57 micromolar. Model: Enzyme activity assay. Limitations: High in-vitro concentration; no human clearance change established. Evidence access: Primary abstract Effects of myricetin on the bioavailability of carvedilol in rats. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22132944/ · DOI 10.3109/13880209.2011.611141
Complete structured claim and evidence
Myricetin increased rhodamine-123 accumulation in P-glycoprotein-overexpressing human MCF-7/ADR cells.
Myricetin → Human P-glycoprotein / ABCB1 / MDR1 supersededungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Drug-resistant human breast-cell model.
limitations
Functional probe result, not proof of selective direct binding or human intestinal inhibition.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
Less export can increase intracellular probe retention.
primary_references
Effects of myricetin on the bioavailability of carvedilol in rats. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22132944/ · DOI 10.3109/13880209.2011.611141
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 236–242
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Drug-resistant human breast-cell model. · source_derived_draft · unverified_draft
## myricetin-pgp-efflux Less export can increase intracellular probe retention. Myricetin increased rhodamine-123 accumulation in P-glycoprotein-overexpressing human MCF-7/ADR cells. Model: Drug-resistant human breast-cell model. Limitations: Functional probe result, not proof of selective direct binding or human intestinal inhibition. Evidence access: Primary abstract Effects of myricetin on the bioavailability of carvedilol in rats. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22132944/ · DOI 10.3109/13880209.2011.611141
Complete structured claim and evidence
Coadministered myricetin increased oral carvedilol AUC by 52.0–85.1% in the reported rat comparisons.
Myricetin → Carvedilol source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Rat oral versus intravenous carvedilol pharmacokinetics.
limitations
CYP and P-gp contributions were proposed, not separately proven; no human dose adjustment follows.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
A whole-animal drug exposure change was observed.
primary_references
Effects of myricetin on the bioavailability of carvedilol in rats. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22132944/ · DOI 10.3109/13880209.2011.611141
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 244–250
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat oral versus intravenous carvedilol pharmacokinetics. · source_derived_draft · unverified_draft
## myricetin-carvedilol-rat A whole-animal drug exposure change was observed. Coadministered myricetin increased oral carvedilol AUC by 52.0–85.1% in the reported rat comparisons. Model: Rat oral versus intravenous carvedilol pharmacokinetics. Limitations: CYP and P-gp contributions were proposed, not separately proven; no human dose adjustment follows. Evidence access: Primary abstract Effects of myricetin on the bioavailability of carvedilol in rats. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22132944/ · DOI 10.3109/13880209.2011.611141
Complete structured claim and evidence
Myricetin inhibited NADPH-reduced recombinant rat TrxR1, IC50 0.62 micromolar after the reported preincubation.
Myricetin → Rat thioredoxin reductase 1 / Txnrd1 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract and publisher methods/results
experimental_model
Recombinant rat TrxR; one-hour preincubation and DTNB assay.
limitations
Enzyme potency differs from cellular exposure; not human dietary selenium depletion.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
A selenium-containing defense enzyme can be inhibited.
primary_references
Inhibition of Mammalian thioredoxin reductase by some flavonoids: implications for myricetin and quercetin anticancer activity. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16618767/ · DOI 10.1158/0008-5472.CAN-05-3310
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 252–258
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Recombinant rat TrxR; one-hour preincubation and DTNB assay. · source_derived_draft · unverified_draft
## myricetin-txnrd-inhibition A selenium-containing defense enzyme can be inhibited. Myricetin inhibited NADPH-reduced recombinant rat TrxR1, IC50 0.62 micromolar after the reported preincubation. Model: Recombinant rat TrxR; one-hour preincubation and DTNB assay. Limitations: Enzyme potency differs from cellular exposure; not human dietary selenium depletion. Evidence access: Primary abstract and publisher methods/results Inhibition of Mammalian thioredoxin reductase by some flavonoids: implications for myricetin and quercetin anticancer activity. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16618767/ · DOI 10.1158/0008-5472.CAN-05-3310
Complete structured claim and evidence
Myricetin inhibition was time- and NADPH-dependent and involved the reduced C-terminal Cys-Sec-Gly active site.
Myricetin → Rat thioredoxin reductase 1 / Txnrd1 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract and publisher methods/results
experimental_model
Rat TrxR biochemical experiments.
limitations
Semiquinone mediation was proposed; do not treat the precise intermediate as directly proven.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
The enzyme’s chemical state affects vulnerability.
primary_references
Inhibition of Mammalian thioredoxin reductase by some flavonoids: implications for myricetin and quercetin anticancer activity. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16618767/ · DOI 10.1158/0008-5472.CAN-05-3310
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 260–266
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat TrxR biochemical experiments. · source_derived_draft · unverified_draft
## myricetin-txnrd-active-site The enzyme’s chemical state affects vulnerability. Myricetin inhibition was time- and NADPH-dependent and involved the reduced C-terminal Cys-Sec-Gly active site. Model: Rat TrxR biochemical experiments. Limitations: Semiquinone mediation was proposed; do not treat the precise intermediate as directly proven. Evidence access: Primary abstract and publisher methods/results Inhibition of Mammalian thioredoxin reductase by some flavonoids: implications for myricetin and quercetin anticancer activity. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16618767/ · DOI 10.1158/0008-5472.CAN-05-3310
Complete structured claim and evidence
Superoxide enhanced myricetin-mediated TrxR inhibition, while anaerobic conditions attenuated it.
Superoxide radical anion → Rat thioredoxin reductase 1 / Txnrd1 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract and publisher methods/results
experimental_model
Cell-free mammalian TrxR study.
limitations
This does not show that lowering oxygen or adding antioxidants benefits patients.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
Oxygen chemistry changes the inhibitory response.
primary_references
Inhibition of Mammalian thioredoxin reductase by some flavonoids: implications for myricetin and quercetin anticancer activity. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16618767/ · DOI 10.1158/0008-5472.CAN-05-3310
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 268–274
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Cell-free mammalian TrxR study. · source_derived_draft · unverified_draft
## myricetin-txnrd-oxygen Oxygen chemistry changes the inhibitory response. Superoxide enhanced myricetin-mediated TrxR inhibition, while anaerobic conditions attenuated it. Model: Cell-free mammalian TrxR study. Limitations: This does not show that lowering oxygen or adding antioxidants benefits patients. Evidence access: Primary abstract and publisher methods/results Inhibition of Mammalian thioredoxin reductase by some flavonoids: implications for myricetin and quercetin anticancer activity. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16618767/ · DOI 10.1158/0008-5472.CAN-05-3310
Complete structured claim and evidence
Myricetin above 50 micromolar reduced thioredoxin reductase activity in A549-cell lysates.
Myricetin → Human A549 thioredoxin reductase activity; isoform unresolved source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human lung cancer cells.
limitations
Do not substitute the purified-enzyme IC50 for a cellular or clinical dose.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
The cell experiment required a different concentration range.
primary_references
Inhibition of Mammalian thioredoxin reductase by some flavonoids: implications for myricetin and quercetin anticancer activity. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16618767/ · DOI 10.1158/0008-5472.CAN-05-3310
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 276–282
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human lung cancer cells. · source_derived_draft · unverified_draft
## myricetin-a549-trxr The cell experiment required a different concentration range. Myricetin above 50 micromolar reduced thioredoxin reductase activity in A549-cell lysates. Model: Human lung cancer cells. Limitations: Do not substitute the purified-enzyme IC50 for a cellular or clinical dose. Evidence access: Primary abstract Inhibition of Mammalian thioredoxin reductase by some flavonoids: implications for myricetin and quercetin anticancer activity. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16618767/ · DOI 10.1158/0008-5472.CAN-05-3310
Complete structured claim and evidence
Myricetin treatment coincided with oxidation of thioredoxin in A549 cells.
Myricetin → Human A549 thioredoxin oxidation source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human A549 culture.
limitations
Concurrent measurements do not establish selective TrxR causation or cancer treatment efficacy.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
A downstream redox protein became more oxidized.
primary_references
Inhibition of Mammalian thioredoxin reductase by some flavonoids: implications for myricetin and quercetin anticancer activity. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16618767/ · DOI 10.1158/0008-5472.CAN-05-3310
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 284–290
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human A549 culture. · source_derived_draft · unverified_draft
## myricetin-a549-trx-oxidation A downstream redox protein became more oxidized. Myricetin treatment coincided with oxidation of thioredoxin in A549 cells. Model: Human A549 culture. Limitations: Concurrent measurements do not establish selective TrxR causation or cancer treatment efficacy. Evidence access: Primary abstract Inhibition of Mammalian thioredoxin reductase by some flavonoids: implications for myricetin and quercetin anticancer activity. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16618767/ · DOI 10.1158/0008-5472.CAN-05-3310
Complete structured claim and evidence
Myricetin reduced IL-10-positive B-cell frequencies and IL-10 secretion after 72-hour CpGC stimulation without reducing B-cell viability.
Myricetin → Human IL-10-positive regulatory B-cell differentiation source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Primary human B cells; methods specify 10 micromolar myricetin.
limitations
Extended Data figure caption in retrieved text says 10 mM, conflicting with methods; use methods dose provisionally and retain the reporting discrepancy. D9-only results are not assigned to myricetin.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
An immune-suppressing B-cell population also depends on redox machinery.
primary_references
Thioredoxin is a metabolic rheostat controlling regulatory B cells. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38553615/ · DOI 10.1038/s41590-024-01798-w
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 292–298
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Primary human B cells; methods specify 10 micromolar myricetin. · source_derived_draft · unverified_draft
## myricetin-breg-myricetin An immune-suppressing B-cell population also depends on redox machinery. Myricetin reduced IL-10-positive B-cell frequencies and IL-10 secretion after 72-hour CpGC stimulation without reducing B-cell viability. Model: Primary human B cells; methods specify 10 micromolar myricetin. Limitations: Extended Data figure caption in retrieved text says 10 mM, conflicting with methods; use methods dose provisionally and retain the reporting discrepancy. D9-only results are not assigned to myricetin. Evidence access: Primary full text Thioredoxin is a metabolic rheostat controlling regulatory B cells. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38553615/ · DOI 10.1038/s41590-024-01798-w
Complete structured claim and evidence
CRISPR–Cas9 silencing of TXNRD1 reduced IL-10-positive B-cell frequencies after CpGC stimulation.
TXNRD1 → Human IL-10-positive regulatory B-cell differentiation source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary full text
experimental_model
Primary human B cells; 72-hour stimulation.
limitations
Supports machinery dependence, not selective drug targeting or evidence that a supplement causes autoimmunity.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
Removing one component weakens the same immune program.
primary_references
Thioredoxin is a metabolic rheostat controlling regulatory B cells. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38553615/ · DOI 10.1038/s41590-024-01798-w
trigger_kind
machinery_impairment Imported condition classification; unverified.
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 300–306
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Primary human B cells; 72-hour stimulation. · source_derived_draft · unverified_draft
## myricetin-breg-silencing-txnrd1 Removing one component weakens the same immune program. CRISPR–Cas9 silencing of TXNRD1 reduced IL-10-positive B-cell frequencies after CpGC stimulation. Model: Primary human B cells; 72-hour stimulation. Limitations: Supports machinery dependence, not selective drug targeting or evidence that a supplement causes autoimmunity. Evidence access: Primary full text Thioredoxin is a metabolic rheostat controlling regulatory B cells. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38553615/ · DOI 10.1038/s41590-024-01798-w
Complete structured claim and evidence
CRISPR–Cas9 silencing of TXN1 reduced IL-10-positive B-cell frequencies after CpGC stimulation.
TXN1 → Human IL-10-positive regulatory B-cell differentiation source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary full text
experimental_model
Primary human B cells; 72-hour stimulation.
limitations
Supports machinery dependence, not selective drug targeting or evidence that a supplement causes autoimmunity.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
Removing one component weakens the same immune program.
primary_references
Thioredoxin is a metabolic rheostat controlling regulatory B cells. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38553615/ · DOI 10.1038/s41590-024-01798-w
trigger_kind
machinery_impairment Imported condition classification; unverified.
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 308–314
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Primary human B cells; 72-hour stimulation. · source_derived_draft · unverified_draft
## myricetin-breg-silencing-txn1 Removing one component weakens the same immune program. CRISPR–Cas9 silencing of TXN1 reduced IL-10-positive B-cell frequencies after CpGC stimulation. Model: Primary human B cells; 72-hour stimulation. Limitations: Supports machinery dependence, not selective drug targeting or evidence that a supplement causes autoimmunity. Evidence access: Primary full text Thioredoxin is a metabolic rheostat controlling regulatory B cells. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38553615/ · DOI 10.1038/s41590-024-01798-w
Complete structured claim and evidence
A 1.77-angstrom crystal structure showed myricetin covalently attached to catalytic Cys145 of SARS-CoV-2 Mpro.
Myricetin → SARS-CoV-2 main protease / Mpro / 3CLpro source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Purified viral protease crystallography and enzyme screen.
limitations
Not proof of antiviral efficacy after eating myricetin or taking a supplement.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
This target has structural evidence, not docking alone.
primary_references
Identification of Inhibitors of SARS-CoV-2 3CL-Pro Enzymatic Activity Using a Small Molecule in Vitro Repurposing Screen. · 2021 · https://pubmed.ncbi.nlm.nih.gov/35287429/ · DOI 10.1021/acsptsci.0c00216
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 316–322
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Purified viral protease crystallography and enzyme screen. · source_derived_draft · unverified_draft
## myricetin-mpro-adduct This target has structural evidence, not docking alone. A 1.77-angstrom crystal structure showed myricetin covalently attached to catalytic Cys145 of SARS-CoV-2 Mpro. Model: Purified viral protease crystallography and enzyme screen. Limitations: Not proof of antiviral efficacy after eating myricetin or taking a supplement. Evidence access: Primary full text Identification of Inhibitors of SARS-CoV-2 3CL-Pro Enzymatic Activity Using a Small Molecule in Vitro Repurposing Screen. · 2021 · https://pubmed.ncbi.nlm.nih.gov/35287429/ · DOI 10.1021/acsptsci.0c00216
Complete structured claim and evidence
Reduced glutathione prevented myricetin–Mpro conjugate formation and canceled the inhibitory effect in the tested assay.
GSH → SARS-CoV-2 main protease / Mpro / 3CLpro source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary full text
experimental_model
Purified viral protease; product chromatography, mass spectrometry and quinone staining.
limitations
Cell-free competition does not quantify GSH consumption or establish antiviral benefit in vivo.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
A cellular antioxidant can intercept a reaction that inhibits another protein.
primary_references
Food phytochemicals, epigallocatechin gallate and myricetin, covalently bind to the active site of the coronavirus main protease in vitro. · 2021 · https://pubmed.ncbi.nlm.nih.gov/35425933/ · DOI 10.1016/j.arres.2021.100021
trigger_kind
machinery_impairment Imported condition classification; unverified.
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 324–330
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Purified viral protease; product chromatography, mass spectrometry and quinone staining. · source_derived_draft · unverified_draft
## myricetin-mpro-gsh A cellular antioxidant can intercept a reaction that inhibits another protein. Reduced glutathione prevented myricetin–Mpro conjugate formation and canceled the inhibitory effect in the tested assay. Model: Purified viral protease; product chromatography, mass spectrometry and quinone staining. Limitations: Cell-free competition does not quantify GSH consumption or establish antiviral benefit in vivo. Evidence access: Primary full text Food phytochemicals, epigallocatechin gallate and myricetin, covalently bind to the active site of the coronavirus main protease in vitro. · 2021 · https://pubmed.ncbi.nlm.nih.gov/35425933/ · DOI 10.1016/j.arres.2021.100021
Complete structured claim and evidence
Myricetin at 5–10 micrograms/mL increased ROS under 0.5 mM CuSO4 exposure.
Myricetin → Human SH-SY5Y ROS under copper exposure source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Human SH-SY5Y cells, 24 hours; 10 micrograms/mL myricetin is about 31.4 micromolar.
limitations
High copper cell-culture challenge; not evidence that ordinary copper foods plus myricetin cause neuronal injury.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
Copper changes the outcome of this redox-active compound.
primary_references
Neurotoxic Effect of Flavonol Myricetin in the Presence of Excess Copper. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33562817/ · DOI 10.3390/molecules26040845
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 332–338
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human SH-SY5Y cells, 24 hours; 10 micrograms/mL myricetin is about 31.4 micromolar. · source_derived_draft · unverified_draft
## myricetin-copper-ros Copper changes the outcome of this redox-active compound. Myricetin at 5–10 micrograms/mL increased ROS under 0.5 mM CuSO4 exposure. Model: Human SH-SY5Y cells, 24 hours; 10 micrograms/mL myricetin is about 31.4 micromolar. Limitations: High copper cell-culture challenge; not evidence that ordinary copper foods plus myricetin cause neuronal injury. Evidence access: Primary full text Neurotoxic Effect of Flavonol Myricetin in the Presence of Excess Copper. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33562817/ · DOI 10.3390/molecules26040845
Complete structured claim and evidence
With 0.5 mM CuSO4 and 10 micrograms/mL myricetin, ATP content fell to 43% of untreated control.
Myricetin → Human SH-SY5Y ATP content under copper exposure source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Human SH-SY5Y cells, 24 hours; 10 micrograms/mL myricetin is about 31.4 micromolar.
limitations
High copper cell-culture challenge; not evidence that ordinary copper foods plus myricetin cause neuronal injury.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
Copper changes the outcome of this redox-active compound.
primary_references
Neurotoxic Effect of Flavonol Myricetin in the Presence of Excess Copper. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33562817/ · DOI 10.3390/molecules26040845
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 340–346
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human SH-SY5Y cells, 24 hours; 10 micrograms/mL myricetin is about 31.4 micromolar. · source_derived_draft · unverified_draft
## myricetin-copper-atp Copper changes the outcome of this redox-active compound. With 0.5 mM CuSO4 and 10 micrograms/mL myricetin, ATP content fell to 43% of untreated control. Model: Human SH-SY5Y cells, 24 hours; 10 micrograms/mL myricetin is about 31.4 micromolar. Limitations: High copper cell-culture challenge; not evidence that ordinary copper foods plus myricetin cause neuronal injury. Evidence access: Primary full text Neurotoxic Effect of Flavonol Myricetin in the Presence of Excess Copper. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33562817/ · DOI 10.3390/molecules26040845
Complete structured claim and evidence
Myricetin exacerbated copper-associated cell death, corroborated by metabolic and trypan-blue measurements.
Myricetin → Human SH-SY5Y death under copper exposure source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Human SH-SY5Y cells, 24 hours; 10 micrograms/mL myricetin is about 31.4 micromolar.
limitations
High copper cell-culture challenge; not evidence that ordinary copper foods plus myricetin cause neuronal injury.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
Copper changes the outcome of this redox-active compound.
primary_references
Neurotoxic Effect of Flavonol Myricetin in the Presence of Excess Copper. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33562817/ · DOI 10.3390/molecules26040845
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 348–354
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human SH-SY5Y cells, 24 hours; 10 micrograms/mL myricetin is about 31.4 micromolar. · source_derived_draft · unverified_draft
## myricetin-copper-death Copper changes the outcome of this redox-active compound. Myricetin exacerbated copper-associated cell death, corroborated by metabolic and trypan-blue measurements. Model: Human SH-SY5Y cells, 24 hours; 10 micrograms/mL myricetin is about 31.4 micromolar. Limitations: High copper cell-culture challenge; not evidence that ordinary copper foods plus myricetin cause neuronal injury. Evidence access: Primary full text Neurotoxic Effect of Flavonol Myricetin in the Presence of Excess Copper. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33562817/ · DOI 10.3390/molecules26040845
Complete structured claim and evidence
Myricetin did not further reduce the glutathione pool already lowered by copper in this SH-SY5Y experiment.
Myricetin → GSH source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Human cells; 0.5 mM CuSO4, up to 10 micrograms/mL myricetin.
limitations
Do not convert proposed thiol chemistry into measured GSH depletion.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
More injury did not require a further measured fall in glutathione.
primary_references
Neurotoxic Effect of Flavonol Myricetin in the Presence of Excess Copper. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33562817/ · DOI 10.3390/molecules26040845
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 356–362
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human cells; 0.5 mM CuSO4, up to 10 micrograms/mL myricetin. · source_derived_draft · unverified_draft
## myricetin-copper-gsh-null More injury did not require a further measured fall in glutathione. Myricetin did not further reduce the glutathione pool already lowered by copper in this SH-SY5Y experiment. Model: Human cells; 0.5 mM CuSO4, up to 10 micrograms/mL myricetin. Limitations: Do not convert proposed thiol chemistry into measured GSH depletion. Evidence access: Primary full text Neurotoxic Effect of Flavonol Myricetin in the Presence of Excess Copper. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33562817/ · DOI 10.3390/molecules26040845
Complete structured claim and evidence
L-type calcium-channel blockade with 10 micromolar nifedipine exacerbated death during copper/myricetin exposure.
Nifedipine → Human SH-SY5Y death under copper exposure source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary full text
experimental_model
Human SH-SY5Y pharmacological perturbation.
limitations
Channel subtype and causal downstream steps were not resolved; no human medication interaction established.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
Changing calcium entry altered the response.
primary_references
Neurotoxic Effect of Flavonol Myricetin in the Presence of Excess Copper. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33562817/ · DOI 10.3390/molecules26040845
trigger_kind
machinery_impairment Imported condition classification; unverified.
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 364–370
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human SH-SY5Y pharmacological perturbation. · source_derived_draft · unverified_draft
## myricetin-copper-nifedipine Changing calcium entry altered the response. L-type calcium-channel blockade with 10 micromolar nifedipine exacerbated death during copper/myricetin exposure. Model: Human SH-SY5Y pharmacological perturbation. Limitations: Channel subtype and causal downstream steps were not resolved; no human medication interaction established. Evidence access: Primary full text Neurotoxic Effect of Flavonol Myricetin in the Presence of Excess Copper. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33562817/ · DOI 10.3390/molecules26040845
Complete structured claim and evidence
Feeding vitamin-E-deficient rats 100 mg myricetin/kg diet for two weeks did not significantly improve the reported lipid-peroxidation and tissue-damage indices, unlike alpha-tocopherol repletion.
Myricetin → Rat vitamin-E-deficient lipid peroxidation and tissue-injury indices source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_access
Primary full text
experimental_model
Rats first maintained on vitamin-E-deficient diet for ten weeks.
limitations
Dose is per kg of diet, not body weight; does not establish all possible co-supplementation effects.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
Myricetin did not function as a substitute for vitamin E in this model.
primary_references
Antioxidant capacity of flavonoids in hepatic microsomes is not reflected by antioxidant effects in vivo. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22919437/ · DOI 10.1155/2012/165127
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 372–378
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rats first maintained on vitamin-E-deficient diet for ten weeks. · source_derived_draft · unverified_draft
## myricetin-vitamin-e-replacement Myricetin did not function as a substitute for vitamin E in this model. Feeding vitamin-E-deficient rats 100 mg myricetin/kg diet for two weeks did not significantly improve the reported lipid-peroxidation and tissue-damage indices, unlike alpha-tocopherol repletion. Model: Rats first maintained on vitamin-E-deficient diet for ten weeks. Limitations: Dose is per kg of diet, not body weight; does not establish all possible co-supplementation effects. Evidence access: Primary full text Antioxidant capacity of flavonoids in hepatic microsomes is not reflected by antioxidant effects in vivo. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22919437/ · DOI 10.1155/2012/165127
Complete structured claim and evidence
Myricetin reacted with galvinoxyl radicals faster and with greater stoichiometric capacity than alpha-tocopherol, yet failed to protect the tested vitamin-E-deficient microsomes.
Myricetin → Cell-free galvinoxyl radical reduction source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Radical assay and microsomal TBARS comparison; species unresolved in accessed abstract.
limitations
Synthetic lipophilic analogues in this paper are separate compounds; their activity is not assigned to myricetin.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
A chemical antioxidant ranking is not membrane protection.
primary_references
Potential therapeutic antioxidants that combine the radical scavenging ability of myricetin and the lipophilic chain of vitamin E to effectively inhibit microsomal lipid peroxidation. · 2004 · https://pubmed.ncbi.nlm.nih.gov/15080911/ · DOI 10.1016/j.bmc.2004.02.031
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 380–386
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Radical assay and microsomal TBARS comparison; species unresolved in accessed abstract. · source_derived_draft · unverified_draft
## myricetin-radical-versus-membrane A chemical antioxidant ranking is not membrane protection. Myricetin reacted with galvinoxyl radicals faster and with greater stoichiometric capacity than alpha-tocopherol, yet failed to protect the tested vitamin-E-deficient microsomes. Model: Radical assay and microsomal TBARS comparison; species unresolved in accessed abstract. Limitations: Synthetic lipophilic analogues in this paper are separate compounds; their activity is not assigned to myricetin. Evidence access: Primary abstract Potential therapeutic antioxidants that combine the radical scavenging ability of myricetin and the lipophilic chain of vitamin E to effectively inhibit microsomal lipid peroxidation. · 2004 · https://pubmed.ncbi.nlm.nih.gov/15080911/ · DOI 10.1016/j.bmc.2004.02.031
Complete structured claim and evidence
Myricetin aglycone inhibited bovine-milk xanthine oxidase-mediated xanthine oxidation.
Myricetin → Bovine xanthine oxidoreductase / XDH source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract and repository full-text methods
experimental_model
Purified bovine-milk enzyme, chromatographic product analysis.
limitations
Sulfate was more potent than parent in the study. Not demonstrated human urate lowering or thiopurine toxicity.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
One enzyme processes both a natural purine and a medication.
primary_references
Inhibition of xanthine oxidase-catalyzed xanthine and 6-mercaptopurine oxidation by luteolin, naringenin, myricetin, ampelopsin and their conjugated metabolites. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37734263/ · DOI 10.1016/j.biopha.2023.115548
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 388–394
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Purified bovine-milk enzyme, chromatographic product analysis. · source_derived_draft · unverified_draft
## myricetin-xo-parent-xanthine One enzyme processes both a natural purine and a medication. Myricetin aglycone inhibited bovine-milk xanthine oxidase-mediated xanthine oxidation. Model: Purified bovine-milk enzyme, chromatographic product analysis. Limitations: Sulfate was more potent than parent in the study. Not demonstrated human urate lowering or thiopurine toxicity. Evidence access: Primary abstract and repository full-text methods Inhibition of xanthine oxidase-catalyzed xanthine and 6-mercaptopurine oxidation by luteolin, naringenin, myricetin, ampelopsin and their conjugated metabolites. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37734263/ · DOI 10.1016/j.biopha.2023.115548
Complete structured claim and evidence
Myricetin aglycone inhibited bovine-milk xanthine oxidase-mediated 6-mercaptopurine oxidation.
Myricetin → Bovine xanthine oxidoreductase / XDH source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract and repository full-text methods
experimental_model
Purified bovine-milk enzyme, chromatographic product analysis.
limitations
Sulfate was more potent than parent in the study. Not demonstrated human urate lowering or thiopurine toxicity.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
One enzyme processes both a natural purine and a medication.
primary_references
Inhibition of xanthine oxidase-catalyzed xanthine and 6-mercaptopurine oxidation by luteolin, naringenin, myricetin, ampelopsin and their conjugated metabolites. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37734263/ · DOI 10.1016/j.biopha.2023.115548
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 396–402
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Purified bovine-milk enzyme, chromatographic product analysis. · source_derived_draft · unverified_draft
## myricetin-xo-parent-6-mercaptopurine One enzyme processes both a natural purine and a medication. Myricetin aglycone inhibited bovine-milk xanthine oxidase-mediated 6-mercaptopurine oxidation. Model: Purified bovine-milk enzyme, chromatographic product analysis. Limitations: Sulfate was more potent than parent in the study. Not demonstrated human urate lowering or thiopurine toxicity. Evidence access: Primary abstract and repository full-text methods Inhibition of xanthine oxidase-catalyzed xanthine and 6-mercaptopurine oxidation by luteolin, naringenin, myricetin, ampelopsin and their conjugated metabolites. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37734263/ · DOI 10.1016/j.biopha.2023.115548
Complete structured claim and evidence
Myricetin 3′-O-sulfate inhibited bovine-milk xanthine oxidase-mediated xanthine oxidation.
Myricetin 3′-O-sulfate → Bovine xanthine oxidoreductase / XDH source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract and repository full-text methods
experimental_model
Purified bovine-milk enzyme, chromatographic product analysis.
limitations
Sulfate was more potent than parent in the study. Not demonstrated human urate lowering or thiopurine toxicity.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
One enzyme processes both a natural purine and a medication.
primary_references
Inhibition of xanthine oxidase-catalyzed xanthine and 6-mercaptopurine oxidation by luteolin, naringenin, myricetin, ampelopsin and their conjugated metabolites. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37734263/ · DOI 10.1016/j.biopha.2023.115548
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 404–410
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Purified bovine-milk enzyme, chromatographic product analysis. · source_derived_draft · unverified_draft
## myricetin-xo-sulfate-xanthine One enzyme processes both a natural purine and a medication. Myricetin 3′-O-sulfate inhibited bovine-milk xanthine oxidase-mediated xanthine oxidation. Model: Purified bovine-milk enzyme, chromatographic product analysis. Limitations: Sulfate was more potent than parent in the study. Not demonstrated human urate lowering or thiopurine toxicity. Evidence access: Primary abstract and repository full-text methods Inhibition of xanthine oxidase-catalyzed xanthine and 6-mercaptopurine oxidation by luteolin, naringenin, myricetin, ampelopsin and their conjugated metabolites. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37734263/ · DOI 10.1016/j.biopha.2023.115548
Complete structured claim and evidence
Myricetin 3′-O-sulfate inhibited bovine-milk xanthine oxidase-mediated 6-mercaptopurine oxidation.
Myricetin 3′-O-sulfate → Bovine xanthine oxidoreductase / XDH source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract and repository full-text methods
experimental_model
Purified bovine-milk enzyme, chromatographic product analysis.
limitations
Sulfate was more potent than parent in the study. Not demonstrated human urate lowering or thiopurine toxicity.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
One enzyme processes both a natural purine and a medication.
primary_references
Inhibition of xanthine oxidase-catalyzed xanthine and 6-mercaptopurine oxidation by luteolin, naringenin, myricetin, ampelopsin and their conjugated metabolites. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37734263/ · DOI 10.1016/j.biopha.2023.115548
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 412–418
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Purified bovine-milk enzyme, chromatographic product analysis. · source_derived_draft · unverified_draft
## myricetin-xo-sulfate-6-mercaptopurine One enzyme processes both a natural purine and a medication. Myricetin 3′-O-sulfate inhibited bovine-milk xanthine oxidase-mediated 6-mercaptopurine oxidation. Model: Purified bovine-milk enzyme, chromatographic product analysis. Limitations: Sulfate was more potent than parent in the study. Not demonstrated human urate lowering or thiopurine toxicity. Evidence access: Primary abstract and repository full-text methods Inhibition of xanthine oxidase-catalyzed xanthine and 6-mercaptopurine oxidation by luteolin, naringenin, myricetin, ampelopsin and their conjugated metabolites. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37734263/ · DOI 10.1016/j.biopha.2023.115548
Complete structured claim and evidence
Myricetin inhibited anti-IgE-stimulated histamine release from cultured human cord-blood mast cells.
Myricetin → Histamine source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human cord-blood-derived mast cells; 15-minute pretreatment, 0.01–100 micromolar tested.
limitations
No oral allergy trial; reduced phosphorylation is not direct kinase inhibition.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
The allergic response involves multiple independently recorded steps.
primary_references
Flavonols inhibit proinflammatory mediator release, intracellular calcium ion levels and protein kinase C theta phosphorylation in human mast cells. · 2005 · https://pubmed.ncbi.nlm.nih.gov/15912140/ · DOI 10.1038/sj.bjp.0706246
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 420–426
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human cord-blood-derived mast cells; 15-minute pretreatment, 0.01–100 micromolar tested. · source_derived_draft · unverified_draft
## myricetin-mast-histamine The allergic response involves multiple independently recorded steps. Myricetin inhibited anti-IgE-stimulated histamine release from cultured human cord-blood mast cells. Model: Human cord-blood-derived mast cells; 15-minute pretreatment, 0.01–100 micromolar tested. Limitations: No oral allergy trial; reduced phosphorylation is not direct kinase inhibition. Evidence access: Primary abstract Flavonols inhibit proinflammatory mediator release, intracellular calcium ion levels and protein kinase C theta phosphorylation in human mast cells. · 2005 · https://pubmed.ncbi.nlm.nih.gov/15912140/ · DOI 10.1038/sj.bjp.0706246
Complete structured claim and evidence
Myricetin inhibited tryptase release from anti-IgE-activated human mast cells.
Myricetin → Human mast-cell tryptase, isoform unresolved source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human cord-blood-derived mast cells; 15-minute pretreatment, 0.01–100 micromolar tested.
limitations
No oral allergy trial; reduced phosphorylation is not direct kinase inhibition.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
The allergic response involves multiple independently recorded steps.
primary_references
Flavonols inhibit proinflammatory mediator release, intracellular calcium ion levels and protein kinase C theta phosphorylation in human mast cells. · 2005 · https://pubmed.ncbi.nlm.nih.gov/15912140/ · DOI 10.1038/sj.bjp.0706246
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 428–434
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human cord-blood-derived mast cells; 15-minute pretreatment, 0.01–100 micromolar tested. · source_derived_draft · unverified_draft
## myricetin-mast-tryptase The allergic response involves multiple independently recorded steps. Myricetin inhibited tryptase release from anti-IgE-activated human mast cells. Model: Human cord-blood-derived mast cells; 15-minute pretreatment, 0.01–100 micromolar tested. Limitations: No oral allergy trial; reduced phosphorylation is not direct kinase inhibition. Evidence access: Primary abstract Flavonols inhibit proinflammatory mediator release, intracellular calcium ion levels and protein kinase C theta phosphorylation in human mast cells. · 2005 · https://pubmed.ncbi.nlm.nih.gov/15912140/ · DOI 10.1038/sj.bjp.0706246
Complete structured claim and evidence
Myricetin suppressed the stimulus-induced intracellular calcium elevation in human mast cells.
Myricetin → Human mast-cell intracellular calcium elevation source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human cord-blood-derived mast cells; 15-minute pretreatment, 0.01–100 micromolar tested.
limitations
No oral allergy trial; reduced phosphorylation is not direct kinase inhibition.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
The allergic response involves multiple independently recorded steps.
primary_references
Flavonols inhibit proinflammatory mediator release, intracellular calcium ion levels and protein kinase C theta phosphorylation in human mast cells. · 2005 · https://pubmed.ncbi.nlm.nih.gov/15912140/ · DOI 10.1038/sj.bjp.0706246
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 436–442
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human cord-blood-derived mast cells; 15-minute pretreatment, 0.01–100 micromolar tested. · source_derived_draft · unverified_draft
## myricetin-mast-calcium The allergic response involves multiple independently recorded steps. Myricetin suppressed the stimulus-induced intracellular calcium elevation in human mast cells. Model: Human cord-blood-derived mast cells; 15-minute pretreatment, 0.01–100 micromolar tested. Limitations: No oral allergy trial; reduced phosphorylation is not direct kinase inhibition. Evidence access: Primary abstract Flavonols inhibit proinflammatory mediator release, intracellular calcium ion levels and protein kinase C theta phosphorylation in human mast cells. · 2005 · https://pubmed.ncbi.nlm.nih.gov/15912140/ · DOI 10.1038/sj.bjp.0706246
Complete structured claim and evidence
Myricetin reduced PKC-theta phosphorylation in the human mast-cell flavonol comparison.
Myricetin → Human protein kinase C theta / PRKCQ source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human cord-blood-derived mast cells; 15-minute pretreatment, 0.01–100 micromolar tested.
limitations
No oral allergy trial; reduced phosphorylation is not direct kinase inhibition.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
The allergic response involves multiple independently recorded steps.
primary_references
Flavonols inhibit proinflammatory mediator release, intracellular calcium ion levels and protein kinase C theta phosphorylation in human mast cells. · 2005 · https://pubmed.ncbi.nlm.nih.gov/15912140/ · DOI 10.1038/sj.bjp.0706246
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 444–450
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human cord-blood-derived mast cells; 15-minute pretreatment, 0.01–100 micromolar tested. · source_derived_draft · unverified_draft
## myricetin-mast-pkc The allergic response involves multiple independently recorded steps. Myricetin reduced PKC-theta phosphorylation in the human mast-cell flavonol comparison. Model: Human cord-blood-derived mast cells; 15-minute pretreatment, 0.01–100 micromolar tested. Limitations: No oral allergy trial; reduced phosphorylation is not direct kinase inhibition. Evidence access: Primary abstract Flavonols inhibit proinflammatory mediator release, intracellular calcium ion levels and protein kinase C theta phosphorylation in human mast cells. · 2005 · https://pubmed.ncbi.nlm.nih.gov/15912140/ · DOI 10.1038/sj.bjp.0706246
Complete structured claim and evidence
Myricetin inhibited MEK1 activity in the mouse JB6 transformation system; GST-MEK1 pull-down supported ATP-noncompetitive binding.
Myricetin → Mouse MEK1 / Map2k1 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Mouse epidermal JB6 P+ cells and GST-MEK1 binding; recombinant construct species not resolved in accessed abstract.
limitations
Cellular node is mouse; do not assume recombinant construct species or selective human inhibition.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
This kinase experiment differs from ATP-competitive targets.
primary_references
Myricetin is a novel natural inhibitor of neoplastic cell transformation and MEK1. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17693661/ · DOI 10.1093/carcin/bgm110
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 452–458
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse epidermal JB6 P+ cells and GST-MEK1 binding; recombinant construct species not resolved in accessed abstract. · source_derived_draft · unverified_draft
## myricetin-mek1 This kinase experiment differs from ATP-competitive targets. Myricetin inhibited MEK1 activity in the mouse JB6 transformation system; GST-MEK1 pull-down supported ATP-noncompetitive binding. Model: Mouse epidermal JB6 P+ cells and GST-MEK1 binding; recombinant construct species not resolved in accessed abstract. Limitations: Cellular node is mouse; do not assume recombinant construct species or selective human inhibition. Evidence access: Primary abstract Myricetin is a novel natural inhibitor of neoplastic cell transformation and MEK1. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17693661/ · DOI 10.1093/carcin/bgm110
Complete structured claim and evidence
Myricetin plus resveratrol inhibited TPA/EGF-induced mouse JB6 transformation additively, not synergistically.
Myricetin → Resveratrol source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Mouse epidermal cells; study compared 10 micromolar myricetin and 20 micromolar resveratrol.
limitations
Assay-specific interaction, not a universal combination verdict.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
Two active compounds did not demonstrate synergy in this test.
primary_references
Myricetin is a novel natural inhibitor of neoplastic cell transformation and MEK1. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17693661/ · DOI 10.1093/carcin/bgm110
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 460–466
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse epidermal cells; study compared 10 micromolar myricetin and 20 micromolar resveratrol. · source_derived_draft · unverified_draft
## myricetin-resveratrol-addition Two active compounds did not demonstrate synergy in this test. Myricetin plus resveratrol inhibited TPA/EGF-induced mouse JB6 transformation additively, not synergistically. Model: Mouse epidermal cells; study compared 10 micromolar myricetin and 20 micromolar resveratrol. Limitations: Assay-specific interaction, not a universal combination verdict. Evidence access: Primary abstract Myricetin is a novel natural inhibitor of neoplastic cell transformation and MEK1. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17693661/ · DOI 10.1093/carcin/bgm110
Complete structured claim and evidence
Myricetin inhibited Fyn kinase activity in mouse epidermal cells and skin; pull-down supported ATP-competitive binding.
Myricetin → Mouse Fyn kinase source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Mouse JB6 P+ cells and UVB-exposed mouse skin.
limitations
No human skin-cancer prevention trial; related papers share investigators.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
A separate kinase connects UVB signaling to downstream responses.
primary_references
Myricetin suppresses UVB-induced skin cancer by targeting Fyn. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18632659/ · DOI 10.1158/0008-5472.CAN-08-0899
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 468–474
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse JB6 P+ cells and UVB-exposed mouse skin. · source_derived_draft · unverified_draft
## myricetin-fyn A separate kinase connects UVB signaling to downstream responses. Myricetin inhibited Fyn kinase activity in mouse epidermal cells and skin; pull-down supported ATP-competitive binding. Model: Mouse JB6 P+ cells and UVB-exposed mouse skin. Limitations: No human skin-cancer prevention trial; related papers share investigators. Evidence access: Primary abstract Myricetin suppresses UVB-induced skin cancer by targeting Fyn. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18632659/ · DOI 10.1158/0008-5472.CAN-08-0899
Complete structured claim and evidence
Myricetin bound Akt in an ATP-competitive binding assay and reduced Akt kinase activity.
Myricetin → Akt assay protein, species and isoform unresolved in accessed abstract source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Biochemical and cellular transformation experiments.
limitations
Do not relabel the unresolved construct as human AKT1; docking is supporting modeling, not an independent experiment.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
Direct binding evidence is recorded without guessing the isoform.
primary_references
Akt is a direct target for myricetin to inhibit cell transformation. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19504174/ · DOI 10.1007/s11010-009-0171-9
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 476–482
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Biochemical and cellular transformation experiments. · source_derived_draft · unverified_draft
## myricetin-akt-binding Direct binding evidence is recorded without guessing the isoform. Myricetin bound Akt in an ATP-competitive binding assay and reduced Akt kinase activity. Model: Biochemical and cellular transformation experiments. Limitations: Do not relabel the unresolved construct as human AKT1; docking is supporting modeling, not an independent experiment. Evidence access: Primary abstract Akt is a direct target for myricetin to inhibit cell transformation. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19504174/ · DOI 10.1007/s11010-009-0171-9
Complete structured claim and evidence
Myricetin inhibited reconstituted human CK2 alpha-prime/beta holoenzyme, IC50 1.18 micromolar.
Myricetin → Human CK2 alpha-prime/beta reconstituted holoenzyme source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Recombinant human subunits; radiolabeled ATP incorporation.
limitations
Not a measured therapeutic human exposure.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
The same canonical kinase can connect multiple flavonoid chapters.
primary_references
Structure-activity relationship of 7 flavonoids on recombinant human protein kinase CK2 holoenzyme. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19197122/
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 484–490
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Recombinant human subunits; radiolabeled ATP incorporation. · source_derived_draft · unverified_draft
## myricetin-ck2 The same canonical kinase can connect multiple flavonoid chapters. Myricetin inhibited reconstituted human CK2 alpha-prime/beta holoenzyme, IC50 1.18 micromolar. Model: Recombinant human subunits; radiolabeled ATP incorporation. Limitations: Not a measured therapeutic human exposure. Evidence access: Primary abstract Structure-activity relationship of 7 flavonoids on recombinant human protein kinase CK2 holoenzyme. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19197122/
Complete structured claim and evidence
Myricetin increased glucose uptake and lipogenesis in isolated rat adipocytes without detected insulin-receptor autophosphorylation or GLUT4 translocation.
Myricetin → Rat adipocyte glucose uptake source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Isolated rat adipocytes; lipogenesis EC50 about 65 micromolar.
limitations
Not a universal insulin mimic; membrane transporter activity and tissue context matter.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
Increased uptake need not mean more GLUT4 moved to the membrane.
primary_references
Insulinomimetic effects of myricetin on lipogenesis and glucose transport in rat adipocytes but not glucose transport translocation. · 1996 · https://pubmed.ncbi.nlm.nih.gov/8619886/ · DOI 10.1016/0006-2952(95)02195-7
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 492–498
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Isolated rat adipocytes; lipogenesis EC50 about 65 micromolar. · source_derived_draft · unverified_draft
## myricetin-adipocyte-uptake Increased uptake need not mean more GLUT4 moved to the membrane. Myricetin increased glucose uptake and lipogenesis in isolated rat adipocytes without detected insulin-receptor autophosphorylation or GLUT4 translocation. Model: Isolated rat adipocytes; lipogenesis EC50 about 65 micromolar. Limitations: Not a universal insulin mimic; membrane transporter activity and tissue context matter. Evidence access: Primary abstract Insulinomimetic effects of myricetin on lipogenesis and glucose transport in rat adipocytes but not glucose transport translocation. · 1996 · https://pubmed.ncbi.nlm.nih.gov/8619886/ · DOI 10.1016/0006-2952(95)02195-7
Complete structured claim and evidence
Fourteen days of injected myricetin improved insulin-stimulated GLUT4 translocation and downstream signaling in fructose-fed rat soleus muscle.
Myricetin → Rat glucose transporter 4 / Slc2a4 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Rats; 1 mg/kg per injection, three injections daily, 14 days.
limitations
Different tissue and exposure from isolated adipocytes; not a scientific contradiction or evidence of oral human efficacy.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
The muscle response involved transporter relocation.
primary_references
Myricetin Ameliorates Defective Post-Receptor Insulin Signaling via β-Endorphin Signaling in the Skeletal Muscles of Fructose-Fed Rats. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21785619/ · DOI 10.1093/ecam/neq017
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 500–506
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rats; 1 mg/kg per injection, three injections daily, 14 days. · source_derived_draft · unverified_draft
## myricetin-muscle-glut4 The muscle response involved transporter relocation. Fourteen days of injected myricetin improved insulin-stimulated GLUT4 translocation and downstream signaling in fructose-fed rat soleus muscle. Model: Rats; 1 mg/kg per injection, three injections daily, 14 days. Limitations: Different tissue and exposure from isolated adipocytes; not a scientific contradiction or evidence of oral human efficacy. Evidence access: Primary abstract Myricetin Ameliorates Defective Post-Receptor Insulin Signaling via β-Endorphin Signaling in the Skeletal Muscles of Fructose-Fed Rats. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21785619/ · DOI 10.1093/ecam/neq017
Complete structured claim and evidence
Mu-opioid-receptor blockade with beta-funaltrexamine inhibited the myricetin-associated improvements in insulin resistance and signaling.
Rat mu-opioid receptor / Oprm1 → Rat myricetin-associated insulin-sensitivity response source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Fructose-fed rats; beta-endorphin elevation measured alongside signaling.
limitations
Pharmacological pathway dependence does not prove direct myricetin binding to the opioid receptor.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
Blocking a receptor disrupted the response to another compound.
primary_references
Myricetin Ameliorates Defective Post-Receptor Insulin Signaling via β-Endorphin Signaling in the Skeletal Muscles of Fructose-Fed Rats. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21785619/ · DOI 10.1093/ecam/neq017
trigger_kind
machinery_impairment Imported condition classification; unverified.
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 508–514
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Fructose-fed rats; beta-endorphin elevation measured alongside signaling. · source_derived_draft · unverified_draft
## myricetin-mor-blockade Blocking a receptor disrupted the response to another compound. Mu-opioid-receptor blockade with beta-funaltrexamine inhibited the myricetin-associated improvements in insulin resistance and signaling. Model: Fructose-fed rats; beta-endorphin elevation measured alongside signaling. Limitations: Pharmacological pathway dependence does not prove direct myricetin binding to the opioid receptor. Evidence access: Primary abstract Myricetin Ameliorates Defective Post-Receptor Insulin Signaling via β-Endorphin Signaling in the Skeletal Muscles of Fructose-Fed Rats. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21785619/ · DOI 10.1093/ecam/neq017
Complete structured claim and evidence
Myricetin reduced high-glucose-associated CDK5 activation in rat INS-1 cells and isolated islets.
Myricetin → Rat cyclin-dependent kinase 5 / Cdk5 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Rat INS-1 cells and rat islets challenged with 30 mM glucose; myricetin 20 micromolar in the cell protocol.
limitations
Direct CDK5 binding was predicted by docking, not established by a binding experiment; expression is not a calcium-pump flux measurement.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
Beta-cell calcium handling and gene regulation are linked.
primary_references
Myricetin Protects Against High Glucose-Induced β-Cell Apoptosis by Attenuating Endoplasmic Reticulum Stress via Inactivation of Cyclin-Dependent Kinase 5. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30688049/ · DOI 10.4093/dmj.2018.0052
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 516–522
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat INS-1 cells and rat islets challenged with 30 mM glucose; myricetin 20 micromolar in the cell protocol. · source_derived_draft · unverified_draft
## myricetin-beta-cell-cdk5 Beta-cell calcium handling and gene regulation are linked. Myricetin reduced high-glucose-associated CDK5 activation in rat INS-1 cells and isolated islets. Model: Rat INS-1 cells and rat islets challenged with 30 mM glucose; myricetin 20 micromolar in the cell protocol. Limitations: Direct CDK5 binding was predicted by docking, not established by a binding experiment; expression is not a calcium-pump flux measurement. Evidence access: Primary abstract Myricetin Protects Against High Glucose-Induced β-Cell Apoptosis by Attenuating Endoplasmic Reticulum Stress via Inactivation of Cyclin-Dependent Kinase 5. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30688049/ · DOI 10.4093/dmj.2018.0052
Complete structured claim and evidence
Myricetin counteracted high-glucose-associated loss of SERCA2b expression in rat beta-cell experiments.
Myricetin → Rat SERCA2b / Atp2a2 isoform source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Rat INS-1 cells and rat islets challenged with 30 mM glucose; myricetin 20 micromolar in the cell protocol.
limitations
Direct CDK5 binding was predicted by docking, not established by a binding experiment; expression is not a calcium-pump flux measurement.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
Beta-cell calcium handling and gene regulation are linked.
primary_references
Myricetin Protects Against High Glucose-Induced β-Cell Apoptosis by Attenuating Endoplasmic Reticulum Stress via Inactivation of Cyclin-Dependent Kinase 5. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30688049/ · DOI 10.4093/dmj.2018.0052
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 524–530
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat INS-1 cells and rat islets challenged with 30 mM glucose; myricetin 20 micromolar in the cell protocol. · source_derived_draft · unverified_draft
## myricetin-beta-cell-serca Beta-cell calcium handling and gene regulation are linked. Myricetin counteracted high-glucose-associated loss of SERCA2b expression in rat beta-cell experiments. Model: Rat INS-1 cells and rat islets challenged with 30 mM glucose; myricetin 20 micromolar in the cell protocol. Limitations: Direct CDK5 binding was predicted by docking, not established by a binding experiment; expression is not a calcium-pump flux measurement. Evidence access: Primary abstract Myricetin Protects Against High Glucose-Induced β-Cell Apoptosis by Attenuating Endoplasmic Reticulum Stress via Inactivation of Cyclin-Dependent Kinase 5. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30688049/ · DOI 10.4093/dmj.2018.0052
Complete structured claim and evidence
Myricetin counteracted the high-glucose-associated reduction in nuclear PDX1 in rat beta-cell experiments.
Myricetin → Rat pancreatic and duodenal homeobox 1 / Pdx1 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Rat INS-1 cells and rat islets challenged with 30 mM glucose; myricetin 20 micromolar in the cell protocol.
limitations
Direct CDK5 binding was predicted by docking, not established by a binding experiment; expression is not a calcium-pump flux measurement.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
Beta-cell calcium handling and gene regulation are linked.
primary_references
Myricetin Protects Against High Glucose-Induced β-Cell Apoptosis by Attenuating Endoplasmic Reticulum Stress via Inactivation of Cyclin-Dependent Kinase 5. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30688049/ · DOI 10.4093/dmj.2018.0052
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 532–538
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat INS-1 cells and rat islets challenged with 30 mM glucose; myricetin 20 micromolar in the cell protocol. · source_derived_draft · unverified_draft
## myricetin-beta-cell-pdx1 Beta-cell calcium handling and gene regulation are linked. Myricetin counteracted the high-glucose-associated reduction in nuclear PDX1 in rat beta-cell experiments. Model: Rat INS-1 cells and rat islets challenged with 30 mM glucose; myricetin 20 micromolar in the cell protocol. Limitations: Direct CDK5 binding was predicted by docking, not established by a binding experiment; expression is not a calcium-pump flux measurement. Evidence access: Primary abstract Myricetin Protects Against High Glucose-Induced β-Cell Apoptosis by Attenuating Endoplasmic Reticulum Stress via Inactivation of Cyclin-Dependent Kinase 5. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30688049/ · DOI 10.4093/dmj.2018.0052
Complete structured claim and evidence
Myricetin altered butyrate-associated gut microbial composition alongside reduced hepatic lipid synthesis and inflammation in high-fat-fed rats.
Myricetin → Rat fecal butyrate-associated microbial composition source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Twelve-week rat supplementation study with fecal transplantation.
limitations
Taxa or fecal concentration do not alone establish production flux, a specific strain enzyme, or butyrate as the sole mediator.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
Gut effects may help explain activity despite limited systemic exposure.
primary_references
Myricetin supplementation decreases hepatic lipid synthesis and inflammation by modulating gut microbiota. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34469716/ · DOI 10.1016/j.celrep.2021.109641
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 540–546
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Twelve-week rat supplementation study with fecal transplantation. · source_derived_draft · unverified_draft
## myricetin-rat-butyrate Gut effects may help explain activity despite limited systemic exposure. Myricetin altered butyrate-associated gut microbial composition alongside reduced hepatic lipid synthesis and inflammation in high-fat-fed rats. Model: Twelve-week rat supplementation study with fecal transplantation. Limitations: Taxa or fecal concentration do not alone establish production flux, a specific strain enzyme, or butyrate as the sole mediator. Evidence access: Primary abstract Myricetin supplementation decreases hepatic lipid synthesis and inflammation by modulating gut microbiota. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34469716/ · DOI 10.1016/j.celrep.2021.109641
Complete structured claim and evidence
Myricetin increased occludin expression and goblet-cell numbers in diabetic mice.
Myricetin → Mouse occludin / Ocln source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
STZ/high-fat-diet mice; 16-week gavage study.
limitations
Parallel changes do not individually establish causal mediation.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
The intestinal barrier changed alongside cardiac outcomes.
primary_references
Myricetin alleviates diabetic cardiomyopathy by regulating gut microbiota and their metabolites. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38472186/ · DOI 10.1038/s41387-024-00268-4
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 548–554
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · STZ/high-fat-diet mice; 16-week gavage study. · source_derived_draft · unverified_draft
## myricetin-mouse-barrier The intestinal barrier changed alongside cardiac outcomes. Myricetin increased occludin expression and goblet-cell numbers in diabetic mice. Model: STZ/high-fat-diet mice; 16-week gavage study. Limitations: Parallel changes do not individually establish causal mediation. Evidence access: Primary full text Myricetin alleviates diabetic cardiomyopathy by regulating gut microbiota and their metabolites. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38472186/ · DOI 10.1038/s41387-024-00268-4
Complete structured claim and evidence
Transferring gut contents from myricetin-treated donors improved recipient cardiac/barrier measurements and reduced TLR4/MyD88-pathway protein readouts.
Gut contents from myricetin-treated diabetic mice → Mouse cardiac and barrier response to conditioned gut-content transplantation source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Diabetic mouse donor/recipient transplantation; parent myricetin checked by HPLC in transplant material.
limitations
Does not isolate one bacterium or metabolite as sufficient; absence of detected parent does not exclude all carried metabolites.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
A transferable gut-associated effect was tested.
primary_references
Myricetin alleviates diabetic cardiomyopathy by regulating gut microbiota and their metabolites. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38472186/ · DOI 10.1038/s41387-024-00268-4
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 556–562
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Diabetic mouse donor/recipient transplantation; parent myricetin checked by HPLC in transplant material. · source_derived_draft · unverified_draft
## myricetin-mouse-fmt A transferable gut-associated effect was tested. Transferring gut contents from myricetin-treated donors improved recipient cardiac/barrier measurements and reduced TLR4/MyD88-pathway protein readouts. Model: Diabetic mouse donor/recipient transplantation; parent myricetin checked by HPLC in transplant material. Limitations: Does not isolate one bacterium or metabolite as sufficient; absence of detected parent does not exclude all carried metabolites. Evidence access: Primary full text Myricetin alleviates diabetic cardiomyopathy by regulating gut microbiota and their metabolites. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38472186/ · DOI 10.1038/s41387-024-00268-4
Complete structured claim and evidence
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
Myricetin treatment lowered nocturnal serum melatonin in rats.
Myricetin → Rat nocturnal serum melatonin source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Rat circadian experiment.
limitations
No established human sleep effect or melatonin supplement interaction.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
A biochemical pathway change was accompanied by a hormone measurement.
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 572–578
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat circadian experiment. · source_derived_draft · unverified_draft
## myricetin-rat-melatonin A biochemical pathway change was accompanied by a hormone measurement. Myricetin treatment lowered nocturnal serum melatonin in rats. Model: Rat circadian experiment. Limitations: No established human sleep effect or melatonin supplement interaction. 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
NMR located myricetin binding between DnaK subdomains IB/IIB; binding impaired interaction with DnaJ.
Myricetin → Escherichia coli DnaK chaperone source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Reconstituted E. coli chaperones and NMR.
limitations
Do not generalize directly to human HSP70.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
A compound can inhibit a protein partnership rather than the catalytic site.
primary_references
Chemical screens against a reconstituted multiprotein complex: myricetin blocks DnaJ regulation of DnaK through an allosteric mechanism. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21338918/ · DOI 10.1016/j.chembiol.2010.12.010
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 580–586
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Reconstituted E. coli chaperones and NMR. · source_derived_draft · unverified_draft
## myricetin-dnak-binding A compound can inhibit a protein partnership rather than the catalytic site. NMR located myricetin binding between DnaK subdomains IB/IIB; binding impaired interaction with DnaJ. Model: Reconstituted E. coli chaperones and NMR. Limitations: Do not generalize directly to human HSP70. Evidence access: Primary full text Chemical screens against a reconstituted multiprotein complex: myricetin blocks DnaJ regulation of DnaK through an allosteric mechanism. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21338918/ · DOI 10.1016/j.chembiol.2010.12.010
Complete structured claim and evidence
Myricetin blocked DnaJ-stimulated DnaK ATPase activity with little effect on intrinsic or GrpE-stimulated turnover.
Myricetin → Escherichia coli DnaK chaperone source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Purified bacterial DnaK/DnaJ/GrpE system.
limitations
Not demonstrated infection treatment or host chaperone inhibition.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
The same enzyme responds differently to its partner.
primary_references
Chemical screens against a reconstituted multiprotein complex: myricetin blocks DnaJ regulation of DnaK through an allosteric mechanism. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21338918/ · DOI 10.1016/j.chembiol.2010.12.010
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 588–594
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Purified bacterial DnaK/DnaJ/GrpE system. · source_derived_draft · unverified_draft
## myricetin-dnaj-atpase The same enzyme responds differently to its partner. Myricetin blocked DnaJ-stimulated DnaK ATPase activity with little effect on intrinsic or GrpE-stimulated turnover. Model: Purified bacterial DnaK/DnaJ/GrpE system. Limitations: Not demonstrated infection treatment or host chaperone inhibition. Evidence access: Primary full text Chemical screens against a reconstituted multiprotein complex: myricetin blocks DnaJ regulation of DnaK through an allosteric mechanism. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21338918/ · DOI 10.1016/j.chembiol.2010.12.010
Complete structured claim and evidence
Myricetin reduced S. aureus Hla production at tested concentrations without inhibiting bacterial growth.
Myricetin → Staphylococcus aureus alpha-hemolysin / Hla source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
S. aureus cultures, toxin and growth measurements.
limitations
Not an antibiotic replacement in patients.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
Reducing virulence differs from killing the bacterium.
primary_references
A Natural Dietary Flavone Myricetin as an α-Hemolysin Inhibitor for Controlling Staphylococcus aureus Infection. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32793508/ · DOI 10.3389/fcimb.2020.00330
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 596–602
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · S. aureus cultures, toxin and growth measurements. · source_derived_draft · unverified_draft
## myricetin-hla-production Reducing virulence differs from killing the bacterium. Myricetin reduced S. aureus Hla production at tested concentrations without inhibiting bacterial growth. Model: S. aureus cultures, toxin and growth measurements. Limitations: Not an antibiotic replacement in patients. Evidence access: Primary full text A Natural Dietary Flavone Myricetin as an α-Hemolysin Inhibitor for Controlling Staphylococcus aureus Infection. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32793508/ · DOI 10.3389/fcimb.2020.00330
Complete structured claim and evidence
Myricetin interfered with deoxycholate-induced Hla oligomerization and reduced hemolytic activity.
Myricetin → Staphylococcus aureus alpha-hemolysin / Hla source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Purified toxin assembly and hemolysis assays.
limitations
Molecular specificity and clinically achievable exposure remain open.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
Toxin molecules need to assemble to form effective pores.
primary_references
A Natural Dietary Flavone Myricetin as an α-Hemolysin Inhibitor for Controlling Staphylococcus aureus Infection. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32793508/ · DOI 10.3389/fcimb.2020.00330
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 604–610
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Purified toxin assembly and hemolysis assays. · source_derived_draft · unverified_draft
## myricetin-hla-oligomers Toxin molecules need to assemble to form effective pores. Myricetin interfered with deoxycholate-induced Hla oligomerization and reduced hemolytic activity. Model: Purified toxin assembly and hemolysis assays. Limitations: Molecular specificity and clinically achievable exposure remain open. Evidence access: Primary full text A Natural Dietary Flavone Myricetin as an α-Hemolysin Inhibitor for Controlling Staphylococcus aureus Infection. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32793508/ · DOI 10.3389/fcimb.2020.00330
Complete structured claim and evidence
Myricetin inhibited human IAPP aggregation and disaggregated preformed fibrils in biophysical experiments.
Myricetin → Human islet amyloid polypeptide / IAPP source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Synthetic human IAPP; associated rat INS-1E cell-protection experiments.
limitations
Molecular-dynamics binding pose is a prediction; not evidence of human diabetes treatment.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
A secreted peptide has another experimentally tested interaction.
primary_references
Myricetin protects pancreatic β-cells from human islet amyloid polypeptide (hIAPP) induced cytotoxicity and restores islet function. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33544469/ · DOI 10.1515/hsz-2020-0176
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 612–618
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Synthetic human IAPP; associated rat INS-1E cell-protection experiments. · source_derived_draft · unverified_draft
## myricetin-iapp A secreted peptide has another experimentally tested interaction. Myricetin inhibited human IAPP aggregation and disaggregated preformed fibrils in biophysical experiments. Model: Synthetic human IAPP; associated rat INS-1E cell-protection experiments. Limitations: Molecular-dynamics binding pose is a prediction; not evidence of human diabetes treatment. Evidence access: Primary abstract Myricetin protects pancreatic β-cells from human islet amyloid polypeptide (hIAPP) induced cytotoxicity and restores islet function. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33544469/ · DOI 10.1515/hsz-2020-0176
Complete structured claim and evidence
Myricetin promoted ROS-independent NLRP3 ubiquitination in the reported inflammasome experiment.
Myricetin → NLRP3 in the myricetin ubiquitination assay; cell species unresolved in abstract source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Cellular inflammasome experiments with mouse sepsis/peritonitis validation.
limitations
Cell species and chain topology are unresolved in the accessed abstract; do not infer degradation or assign human protein identity.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
A protein modification can change assembly of an inflammatory complex.
primary_references
Myricetin inhibits NLRP3 inflammasome activation via reduction of ROS-dependent ubiquitination of ASC and promotion of ROS-independent NLRP3 ubiquitination. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30594691/ · DOI 10.1016/j.taap.2018.12.019
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 620–626
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Cellular inflammasome experiments with mouse sepsis/peritonitis validation. · source_derived_draft · unverified_draft
## myricetin-nlrp3-ubiquitination A protein modification can change assembly of an inflammatory complex. Myricetin promoted ROS-independent NLRP3 ubiquitination in the reported inflammasome experiment. Model: Cellular inflammasome experiments with mouse sepsis/peritonitis validation. Limitations: Cell species and chain topology are unresolved in the accessed abstract; do not infer degradation or assign human protein identity. Evidence access: Primary abstract Myricetin inhibits NLRP3 inflammasome activation via reduction of ROS-dependent ubiquitination of ASC and promotion of ROS-independent NLRP3 ubiquitination. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30594691/ · DOI 10.1016/j.taap.2018.12.019
Complete structured claim and evidence
Myricetin reduced ROS-dependent ASC ubiquitination and reduced ASC–NLRP3 interaction and ASC oligomerization.
Myricetin → ASC/PYCARD in the myricetin ubiquitination assay; cell species unresolved in abstract source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Cellular inflammasome assembly assays.
limitations
No specific E3 ligase or ubiquitin-chain linkage established by the accessed abstract.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
The two proteins did not show the same ubiquitination direction.
primary_references
Myricetin inhibits NLRP3 inflammasome activation via reduction of ROS-dependent ubiquitination of ASC and promotion of ROS-independent NLRP3 ubiquitination. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30594691/ · DOI 10.1016/j.taap.2018.12.019
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 628–634
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Cellular inflammasome assembly assays. · source_derived_draft · unverified_draft
## myricetin-asc-ubiquitination The two proteins did not show the same ubiquitination direction. Myricetin reduced ROS-dependent ASC ubiquitination and reduced ASC–NLRP3 interaction and ASC oligomerization. Model: Cellular inflammasome assembly assays. Limitations: No specific E3 ligase or ubiquitin-chain linkage established by the accessed abstract. Evidence access: Primary abstract Myricetin inhibits NLRP3 inflammasome activation via reduction of ROS-dependent ubiquitination of ASC and promotion of ROS-independent NLRP3 ubiquitination. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30594691/ · DOI 10.1016/j.taap.2018.12.019
Complete structured claim and evidence
Myricetin increased hepatic Nrf2 expression in mice challenged with LPS/D-galactosamine.
Myricetin → Mouse Nrf2 / Nfe2l2 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Mouse chemically induced fulminant hepatitis.
limitations
Not universal Nrf2 activation or evidence of clinical hepatoprotection. The abstract calls myricetin a glycoside; this collection retains its correct aglycone identity.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
A defense regulator increased in this liver-injury model.
primary_references
The hepatoprotective effect of myricetin against lipopolysaccharide and D-galactosamine-induced fulminant hepatitis. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31712142/ · DOI 10.1016/j.ijbiomac.2019.11.075
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 636–642
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse chemically induced fulminant hepatitis. · source_derived_draft · unverified_draft
## myricetin-mouse-nrf2 A defense regulator increased in this liver-injury model. Myricetin increased hepatic Nrf2 expression in mice challenged with LPS/D-galactosamine. Model: Mouse chemically induced fulminant hepatitis. Limitations: Not universal Nrf2 activation or evidence of clinical hepatoprotection. The abstract calls myricetin a glycoside; this collection retains its correct aglycone identity. Evidence access: Primary abstract The hepatoprotective effect of myricetin against lipopolysaccharide and D-galactosamine-induced fulminant hepatitis. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31712142/ · DOI 10.1016/j.ijbiomac.2019.11.075
Complete structured claim and evidence
Myricetin increased hepatic HO-1 expression in the LPS/D-galactosamine mouse model.
Myricetin → Mouse heme oxygenase 1 / Hmox1 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Mouse liver-injury experiment.
limitations
Expression is not proof of direct binding or enzyme flux; accessed in-vitro knockout details do not resolve cell species.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
A downstream defense enzyme also changed.
primary_references
The hepatoprotective effect of myricetin against lipopolysaccharide and D-galactosamine-induced fulminant hepatitis. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31712142/ · DOI 10.1016/j.ijbiomac.2019.11.075
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 644–650
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse liver-injury experiment. · source_derived_draft · unverified_draft
## myricetin-mouse-ho1 A downstream defense enzyme also changed. Myricetin increased hepatic HO-1 expression in the LPS/D-galactosamine mouse model. Model: Mouse liver-injury experiment. Limitations: Expression is not proof of direct binding or enzyme flux; accessed in-vitro knockout details do not resolve cell species. Evidence access: Primary abstract The hepatoprotective effect of myricetin against lipopolysaccharide and D-galactosamine-induced fulminant hepatitis. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31712142/ · DOI 10.1016/j.ijbiomac.2019.11.075
Complete structured claim and evidence
The 2009 screen reported potent myricetin inhibition of human APE1; radiotracer follow-up placed IC50 below 0.5 micromolar.
Myricetin → Human AP endonuclease 1 / APE1 / APEX1 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Purified enzyme and fluorescent/radiolabeled abasic-DNA incision assays.
limitations
Potency and target specificity were subsequently challenged by aggregation-controlled work; preserve this as a disputed result.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
An early study identified a candidate DNA-repair inhibitor.
primary_references
Identification and characterization of inhibitors of human apurinic/apyrimidinic endonuclease APE1. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19484131/ · DOI 10.1371/journal.pone.0005740
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 652–658
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Purified enzyme and fluorescent/radiolabeled abasic-DNA incision assays. · source_derived_draft · unverified_draft
## myricetin-ape1-original An early study identified a candidate DNA-repair inhibitor. The 2009 screen reported potent myricetin inhibition of human APE1; radiotracer follow-up placed IC50 below 0.5 micromolar. Model: Purified enzyme and fluorescent/radiolabeled abasic-DNA incision assays. Limitations: Potency and target specificity were subsequently challenged by aggregation-controlled work; preserve this as a disputed result. Evidence access: Primary full text Identification and characterization of inhibitors of human apurinic/apyrimidinic endonuclease APE1. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19484131/ · DOI 10.1371/journal.pone.0005740
Complete structured claim and evidence
In 2023, myricetin showed only weak APE1 inhibition at 0.33 mM with detergent/BSA, preventing an IC50 estimate; inhibition was much stronger without those additives.
Myricetin → Human AP endonuclease 1 / APE1 / APEX1 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Human APE1 delta-N38; UHPLC product assay and dynamic light scattering.
limitations
Authors propose nonspecific aggregation as an explanation for earlier potency. This is not a demonstrated explanation for every target in this chapter.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
Controlling compound aggregation changed the conclusion.
primary_references
Characterizing inhibitors of human AP endonuclease 1. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36652434/ · DOI 10.1371/journal.pone.0280526
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 660–666
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human APE1 delta-N38; UHPLC product assay and dynamic light scattering. · source_derived_draft · unverified_draft
## myricetin-ape1-reassessment Controlling compound aggregation changed the conclusion. In 2023, myricetin showed only weak APE1 inhibition at 0.33 mM with detergent/BSA, preventing an IC50 estimate; inhibition was much stronger without those additives. Model: Human APE1 delta-N38; UHPLC product assay and dynamic light scattering. Limitations: Authors propose nonspecific aggregation as an explanation for earlier potency. This is not a demonstrated explanation for every target in this chapter. Evidence access: Primary full text Characterizing inhibitors of human AP endonuclease 1. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36652434/ · DOI 10.1371/journal.pone.0280526
Complete structured claim and evidence
Myricetin formed aggregates at 0.33 mM and above; 0.05% Brij35 or centrifugation disrupted or removed them.
Myricetin → Myricetin colloidal aggregates in APE1 assay buffer source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Dynamic light scattering under the specified buffer conditions.
limitations
Threshold is buffer-specific; not a biological aggregation threshold.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
The assay solution itself can create an apparent target effect.
primary_references
Characterizing inhibitors of human AP endonuclease 1. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36652434/ · DOI 10.1371/journal.pone.0280526
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 668–674
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Dynamic light scattering under the specified buffer conditions. · source_derived_draft · unverified_draft
## myricetin-ape1-aggregation The assay solution itself can create an apparent target effect. Myricetin formed aggregates at 0.33 mM and above; 0.05% Brij35 or centrifugation disrupted or removed them. Model: Dynamic light scattering under the specified buffer conditions. Limitations: Threshold is buffer-specific; not a biological aggregation threshold. Evidence access: Primary full text Characterizing inhibitors of human AP endonuclease 1. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36652434/ · DOI 10.1371/journal.pone.0280526
Complete structured claim and evidence
Omitting MgCl2 abolished detectable APE1 incision in the 2023 control reactions.
Mg2+ → Human AP endonuclease 1 / APE1 / APEX1 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Human APE1 delta-N38; standard reaction initiated with 2 mM MgCl2.
limitations
Does not prove myricetin inhibits by magnesium chelation or causes magnesium deficiency.
nutrient_topic
Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
plain_language
The repair enzyme also has a mineral-dependent assay requirement.
primary_references
Characterizing inhibitors of human AP endonuclease 1. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36652434/ · DOI 10.1371/journal.pone.0280526
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 676–682
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human APE1 delta-N38; standard reaction initiated with 2 mM MgCl2. · source_derived_draft · unverified_draft
## myricetin-ape1-magnesium The repair enzyme also has a mineral-dependent assay requirement. Omitting MgCl2 abolished detectable APE1 incision in the 2023 control reactions. Model: Human APE1 delta-N38; standard reaction initiated with 2 mM MgCl2. Limitations: Does not prove myricetin inhibits by magnesium chelation or causes magnesium deficiency. Evidence access: Primary full text Characterizing inhibitors of human AP endonuclease 1. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36652434/ · DOI 10.1371/journal.pone.0280526
Complete structured claim and evidence
TXNRD1 recharges thioredoxin so it can reduce other proteins.
Cytosolic TXNRD1 uses NADPH-derived reducing equivalents to reduce oxidized thioredoxin through its flavin and C-terminal redox centers.
TXNRD1 → TXN1 source_derived_draftliterature_reviewed:direct_experimental
Experimental context and source evidence
experimental_model
Purified rat liver cytosolic thioredoxin reductase and recombinant active-site variants.
limitations
This experiment-specific relationship does not establish a human dietary-deficiency threshold or supplementation benefit.
organism
Rat protein and recombinant enzyme assays
Selenium: literature corrections and mechanism additions · lines 965–974
Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Purified rat liver cytosolic thioredoxin reductase and recombinant active-site variants. · secondary_verified · secondary_verified
## txnrd1-reduces-txn1 TXNRD1 recharges thioredoxin so it can reduce other proteins. Cytosolic TXNRD1 uses NADPH-derived reducing equivalents to reduce oxidized thioredoxin through its flavin and C-terminal redox centers. Experimental model: Purified rat liver cytosolic thioredoxin reductase and recombinant active-site variants. Organism: Rat protein and recombinant enzyme assays Limitations: This experiment-specific relationship does not establish a human dietary-deficiency threshold or supplementation benefit. Primary reference: [Mammalian thioredoxin reductase: C-terminal redox center and selenium-to-sulfur substitution](https://pmc.ncbi.nlm.nih.gov/articles/PMC15961/)
Complete structured claim and evidence
The rat TXNRD1 Sec498Cys structure showed conserved FAD- and NADPH-binding architecture around the N-terminal redox center.
FAD → Rat thioredoxin reductase 1 / Txnrd1 source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
B2-FAD and nicotinamide cofactors provide the upstream side of a selenium-containing reductase.
evidence_location
Abstract
experimental_model
Rat TXNRD1 Sec498Cys recombinant mutant with NADP+, 3.0-A crystallography and substrate-docking interpretation.
exposure
Purified-enzyme assay
limitations
Structure used a Sec-to-Cys mutant and oxidized NADP+; direct atom-level conclusions about wild-type selenium chemistry are limited.
nutrient_topic
Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
organism
Rattus norvegicus protein expressed recombinantly
plain_language
Thioredoxin reductase has a flavin input side.
primary_references
[sandalova2001] Three-dimensional structure of a mammalian thioredoxin reductase: implications for mechanism and evolution of a selenocysteine-dependent enzyme. (2001). https://pubmed.ncbi.nlm.nih.gov/11481439/ DOI: 10.1073/pnas.171178698
tissue_or_cell_type
Purified recombinant enzyme; no intact tissue
Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1346–1358
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat TXNRD1 Sec498Cys recombinant mutant with NADP+, 3.0-A crystallography and substrate-docking interpretation. · source_derived_draft · unverified_draft
### b2-txnrd1-fad-nadph-architecture The rat TXNRD1 Sec498Cys structure showed conserved FAD- and NADPH-binding architecture around the N-terminal redox center. Condition category: normal nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Thioredoxin reductase has a flavin input side. organism: Rattus norvegicus protein expressed recombinantly tissue_or_cell_type: Purified recombinant enzyme; no intact tissue experimental_model: Rat TXNRD1 Sec498Cys recombinant mutant with NADP+, 3.0-A crystallography and substrate-docking interpretation. limitations: Structure used a Sec-to-Cys mutant and oxidized NADP+; direct atom-level conclusions about wild-type selenium chemistry are limited. exposure: Purified-enzyme assay cross_nutrient: B2-FAD and nicotinamide cofactors provide the upstream side of a selenium-containing reductase. evidence_location: Abstract [sandalova2001] Three-dimensional structure of a mammalian thioredoxin reductase: implications for mechanism and evolution of a selenocysteine-dependent enzyme. (2001). https://pubmed.ncbi.nlm.nih.gov/11481439/ DOI: 10.1073/pnas.171178698
Complete structured claim and evidence
Replacing rat TXNRD1 Sec498 with cysteine lowered thioredoxin-reduction kcat about 100-fold; serine substitution and terminal truncation lacked detectable activity.
Rat TXNRD1 Sec498Cys protein → Thioredoxin proteins source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
B2-derived FAD cannot replace the selenium-containing catalytic residue.
evidence_location
Abstract
experimental_model
Rat TXNRD1 Sec498Cys, Sec498Ser and C-terminal truncation expressed in E. coli; FAD analysis, NADPH titration and thioredoxin assays.
exposure
Purified-enzyme assay
limitations
Assay-substrate species is unresolved in accessible source details; engineered proteins do not establish dietary B2-by-selenium synergy.
nutrient_topic
Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
organism
Rattus norvegicus protein expressed in Escherichia coli
plain_language
Flavin retention did not preserve efficient thioredoxin reduction.
primary_references
[zhong2000] Essential role of selenium in the catalytic activities of mammalian thioredoxin reductase revealed by characterization of recombinant enzymes with selenocysteine mutations. (2000). https://pubmed.ncbi.nlm.nih.gov/10849437/ DOI: 10.1074/jbc.m000690200
tissue_or_cell_type
Purified recombinant enzyme; no intact tissue
trigger_kind
machinery_impairment Imported condition classification; unverified.
Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1388–1400
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat TXNRD1 Sec498Cys, Sec498Ser and C-terminal truncation expressed in E. coli; FAD analysis, NADPH titration and thioredoxin assays. · source_derived_draft · unverified_draft
### b2-txnrd-sec498cys-turnover Replacing rat TXNRD1 Sec498 with cysteine lowered thioredoxin-reduction kcat about 100-fold; serine substitution and terminal truncation lacked detectable activity. Condition category: machinery_impairment nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Flavin retention did not preserve efficient thioredoxin reduction. organism: Rattus norvegicus protein expressed in Escherichia coli tissue_or_cell_type: Purified recombinant enzyme; no intact tissue experimental_model: Rat TXNRD1 Sec498Cys, Sec498Ser and C-terminal truncation expressed in E. coli; FAD analysis, NADPH titration and thioredoxin assays. limitations: Assay-substrate species is unresolved in accessible source details; engineered proteins do not establish dietary B2-by-selenium synergy. exposure: Purified-enzyme assay cross_nutrient: B2-derived FAD cannot replace the selenium-containing catalytic residue. evidence_location: Abstract [zhong2000] Essential role of selenium in the catalytic activities of mammalian thioredoxin reductase revealed by characterization of recombinant enzymes with selenocysteine mutations. (2000). https://pubmed.ncbi.nlm.nih.gov/10849437/ DOI: 10.1074/jbc.m000690200
Complete structured claim and evidence
Purified rat liver thioredoxin reductase reduced DHA using NADPH, with apparent DHA Km 2.5 mM and turnover 90 min−1.
Rat thioredoxin reductase 1 / Txnrd1 → Dehydroascorbic acid source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
experimental_model
Purified rat liver thioredoxin reductase/thioredoxin and selenium-deficient rat liver
exposure
Purified enzyme plus NADPH and DHA
limitations
Biochemical capacity; not the same as cellular rate at low DHA concentration.
nutrient_topic
Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C
organism
Rattus norvegicus
plain_language
Thioredoxin reductase provides another route for recovering reduced vitamin C.
primary_references
[may1997] Reduction of dehydroascorbate to ascorbate by the selenoenzyme thioredoxin reductase. (1997). https://pubmed.ncbi.nlm.nih.gov/9278416/ DOI: 10.1074/jbc.272.36.22607
tissue_or_cell_type
Purified liver enzyme
Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 377–388
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified rat liver thioredoxin reductase/thioredoxin and selenium-deficient rat liver · source_derived_draft · unverified_draft
### vc-transport-txnrd-dha Purified rat liver thioredoxin reductase reduced DHA using NADPH, with apparent DHA Km 2.5 mM and turnover 90 min−1. Condition category: normal nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: Thioredoxin reductase provides another route for recovering reduced vitamin C. organism: Rattus norvegicus tissue_or_cell_type: Purified liver enzyme experimental_model: Purified rat liver thioredoxin reductase/thioredoxin and selenium-deficient rat liver limitations: Biochemical capacity; not the same as cellular rate at low DHA concentration. exposure: Purified enzyme plus NADPH and DHA cross_nutrient: true [may1997] Reduction of dehydroascorbate to ascorbate by the selenoenzyme thioredoxin reductase. (1997). https://pubmed.ncbi.nlm.nih.gov/9278416/ DOI: 10.1074/jbc.272.36.22607
Complete structured claim and evidence
Purified rat liver thioredoxin reductase decreased ascorbyl radical measured by electron paramagnetic resonance while consuming NADPH; DHA controls could not explain the signal.
Rat thioredoxin reductase 1 / Txnrd1 → Ascorbyl radical source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
experimental_model
Purified rat liver enzyme, dialyzed cytosol and microsomes from control/selenium-deficient rats
exposure
Low-micromolar ascorbyl radical generated by ascorbate oxidase
limitations
Purified assay; radical and DHA reduction are distinct reactions.
nutrient_topic
Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C
organism
Rattus norvegicus
plain_language
The reductase can also recycle the one-electron vitamin C radical.
primary_references
[may1998] Reduction of the ascorbyl free radical to ascorbate by thioredoxin reductase. (1998). https://pubmed.ncbi.nlm.nih.gov/9722529/ DOI: 10.1074/jbc.273.36.23039
tissue_or_cell_type
Purified liver enzyme
Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 416–427
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified rat liver enzyme, dialyzed cytosol and microsomes from control/selenium-deficient rats · source_derived_draft · unverified_draft
### vc-transport-txnrd-radical Purified rat liver thioredoxin reductase decreased ascorbyl radical measured by electron paramagnetic resonance while consuming NADPH; DHA controls could not explain the signal. Condition category: normal nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: The reductase can also recycle the one-electron vitamin C radical. organism: Rattus norvegicus tissue_or_cell_type: Purified liver enzyme experimental_model: Purified rat liver enzyme, dialyzed cytosol and microsomes from control/selenium-deficient rats limitations: Purified assay; radical and DHA reduction are distinct reactions. exposure: Low-micromolar ascorbyl radical generated by ascorbate oxidase cross_nutrient: true [may1998] Reduction of the ascorbyl free radical to ascorbate by thioredoxin reductase. (1998). https://pubmed.ncbi.nlm.nih.gov/9722529/ DOI: 10.1074/jbc.273.36.23039
Complete structured claim and evidence
Dialyzed liver cytosol from selenium-deficient rats lost NADPH-dependent ascorbyl-radical reducing activity attributed to thioredoxin reductase.
Selenium → Ascorbyl radical reduction to ascorbate source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
true
experimental_model
Purified rat liver enzyme, dialyzed cytosol and microsomes from control/selenium-deficient rats
exposure
Dietary selenium depletion; isolated dialyzed cytosol
limitations
Activity assignment also used inhibitor sensitivity; this is a fraction assay, not a direct human outcome.
nutrient_topic
Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C
organism
Rattus norvegicus
plain_language
Selenium deficiency impaired radical recycling in the rat liver’s soluble fraction.
primary_references
[may1998] Reduction of the ascorbyl free radical to ascorbate by thioredoxin reductase. (1998). https://pubmed.ncbi.nlm.nih.gov/9722529/ DOI: 10.1074/jbc.273.36.23039
tissue_or_cell_type
Liver cytosol
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 429–440
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified rat liver enzyme, dialyzed cytosol and microsomes from control/selenium-deficient rats · source_derived_draft · unverified_draft
### vc-transport-selenium-cytosolic-radical Dialyzed liver cytosol from selenium-deficient rats lost NADPH-dependent ascorbyl-radical reducing activity attributed to thioredoxin reductase. Condition category: nutrient_deficiency nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: Selenium deficiency impaired radical recycling in the rat liver’s soluble fraction. organism: Rattus norvegicus tissue_or_cell_type: Liver cytosol experimental_model: Purified rat liver enzyme, dialyzed cytosol and microsomes from control/selenium-deficient rats limitations: Activity assignment also used inhibitor sensitivity; this is a fraction assay, not a direct human outcome. exposure: Dietary selenium depletion; isolated dialyzed cytosol cross_nutrient: true [may1998] Reduction of the ascorbyl free radical to ascorbate by thioredoxin reductase. (1998). https://pubmed.ncbi.nlm.nih.gov/9722529/ DOI: 10.1074/jbc.273.36.23039
Complete structured claim and evidence
Purified mammalian thioredoxin reductases, including enzyme from human placenta, catalyzed NADPH-dependent lipoic-acid reduction.
Mammalian thioredoxin reductases, isoform unspecified → Lipoic acid source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/ala-research/8769129.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9ba6524ef04fdc03c0a6d108325b8a96fe7ad0748be4d7056e694b5afa2a8499", "start_char": 0, "end_char": 1307, "text_sha256": "9ba6524ef04fdc03c0a6d108325b8a96fe7ad0748be4d7056e694b5afa2a8499"}
experimental_model
Purified mammalian thioredoxin reductase assays
exposure
NADPH-dependent lipoate/lipoamide reduction
limitations
Isoform identity was not resolved as a specific human TXNRD gene in the indexed abstract; assay rate comparisons are not tissue-wide flux rankings.
nutrient_topic
Alpha-lipoic acid research collection; topical membership is not evidence of a direct dietary effect. · Lipoic acid
organism
Human placenta, calf tissues and rat liver
plain_language
The thioredoxin system provides another route to DHLA.
primary_references
[ala-p8769129] Efficient reduction of lipoamide and lipoic acid by mammalian thioredoxin reductase. (1996). https://pubmed.ncbi.nlm.nih.gov/8769129/ DOI: 10.1006/bbrc.1996.1165
tissue_or_cell_type
Purified thioredoxin reductases
Alpha-lipoic acid: cofactor assembly, redox signaling and nutrient interactions (2026-09-17) · lines 754–765
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified mammalian thioredoxin reductase assays · source_derived_draft · unverified_draft
### ala-thioredoxin-reductase-dhla Purified mammalian thioredoxin reductases, including enzyme from human placenta, catalyzed NADPH-dependent lipoic-acid reduction. Condition category: normal nutrient_topic: Alpha-lipoic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: The thioredoxin system provides another route to DHLA. organism: Human placenta, calf tissues and rat liver tissue_or_cell_type: Purified thioredoxin reductases experimental_model: Purified mammalian thioredoxin reductase assays limitations: Isoform identity was not resolved as a specific human TXNRD gene in the indexed abstract; assay rate comparisons are not tissue-wide flux rankings. exposure: NADPH-dependent lipoate/lipoamide reduction evidence_span: {"source_cache": "artifacts/ala-research/8769129.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9ba6524ef04fdc03c0a6d108325b8a96fe7ad0748be4d7056e694b5afa2a8499", "start_char": 0, "end_char": 1307, "text_sha256": "9ba6524ef04fdc03c0a6d108325b8a96fe7ad0748be4d7056e694b5afa2a8499"} [ala-p8769129] Efficient reduction of lipoamide and lipoic acid by mammalian thioredoxin reductase. (1996). https://pubmed.ncbi.nlm.nih.gov/8769129/ DOI: 10.1006/bbrc.1996.1165
Complete structured claim and evidence
Purified PHGPX (GPX4) with glutathione reduced phospholipid hydroperoxides within photooxidized human erythrocyte ghost membranes to alcohol products without prior phospholipase cleavage.
GPX4 → Phospholipid hydroperoxides source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
evidence_location
Primary abstract
experimental_model
Rose-bengal photoperoxidation followed by enzyme treatment
exposure
GSH/PHGPX after photooxidation.
limitations
Purified-enzyme preparation; distinguishes peroxide removal from vitamin E radical trapping.
nutrient_topic
Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
organism
Human-derived cell-free membranes
plain_language
GPX4 removed peroxide groups from membrane phospholipids using glutathione.
primary_references
[ver-thomas1990] Protective action of phospholipid hydroperoxide glutathione peroxidase against membrane-damaging lipid peroxidation. In situ reduction of phospholipid and cholesterol hydroperoxides. (1990). https://pubmed.ncbi.nlm.nih.gov/2294113/ DOI: 10.1016/s0021-9258(19)40252-4
tissue_or_cell_type
Erythrocyte ghosts
Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 550–562
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rose-bengal photoperoxidation followed by enzyme treatment · source_derived_draft · unverified_draft
### ver-gpx4-pl-hydroperoxide-reduction Purified PHGPX (GPX4) with glutathione reduced phospholipid hydroperoxides within photooxidized human erythrocyte ghost membranes to alcohol products without prior phospholipase cleavage. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: GPX4 removed peroxide groups from membrane phospholipids using glutathione. organism: Human-derived cell-free membranes tissue_or_cell_type: Erythrocyte ghosts experimental_model: Rose-bengal photoperoxidation followed by enzyme treatment limitations: Purified-enzyme preparation; distinguishes peroxide removal from vitamin E radical trapping. exposure: GSH/PHGPX after photooxidation. cross_nutrient: true evidence_location: Primary abstract [ver-thomas1990] Protective action of phospholipid hydroperoxide glutathione peroxidase against membrane-damaging lipid peroxidation. In situ reduction of phospholipid and cholesterol hydroperoxides. (1990). https://pubmed.ncbi.nlm.nih.gov/2294113/ DOI: 10.1016/s0021-9258(19)40252-4
Complete structured claim and evidence
MOCOS defects in type II xanthinuria support its role in supplying the terminal sulfur required by XDH and AOX1.
Human molybdenum cofactor sulfurase / MOCOS → Human xanthine oxidoreductase / XDH source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/molybdenum-research/11302742.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8f595c96d16b055cd6b9611c4d036626222ffb084ec778f840255cac57ecdfb3", "start_char": 0, "end_char": 1011, "text_sha256": "8f595c96d16b055cd6b9611c4d036626222ffb084ec778f840255cac57ecdfb3"}
experimental_model
Gene identification in two type II xanthinuria patients and comparison subjects
exposure
MOCOS Arg419 stop mutation
limitations
Genetic evidence for terminal sulfuration; type II xanthinuria is different from loss of all Moco synthesis.
nutrient_topic
Molybdenum research collection; topical membership is not evidence of a direct dietary effect. · Molybdenum
organism
Homo sapiens
plain_language
Two molybdenum enzymes need an additional sulfur-activation step.
primary_references
[mo-p11302742] Mutation of human molybdenum cofactor sulfurase gene is responsible for classical xanthinuria type II. (2001). https://pubmed.ncbi.nlm.nih.gov/11302742/ DOI: 10.1006/bbrc.2001.4719
tissue_or_cell_type
Liver cDNA and patient genetics
Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 521–532
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Gene identification in two type II xanthinuria patients and comparison subjects · source_derived_draft · unverified_draft
### mo-mocos-sulfuration MOCOS defects in type II xanthinuria support its role in supplying the terminal sulfur required by XDH and AOX1. Condition category: normal nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: Two molybdenum enzymes need an additional sulfur-activation step. organism: Homo sapiens tissue_or_cell_type: Liver cDNA and patient genetics experimental_model: Gene identification in two type II xanthinuria patients and comparison subjects limitations: Genetic evidence for terminal sulfuration; type II xanthinuria is different from loss of all Moco synthesis. exposure: MOCOS Arg419 stop mutation evidence_span: {"source_cache": "artifacts/molybdenum-research/11302742.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8f595c96d16b055cd6b9611c4d036626222ffb084ec778f840255cac57ecdfb3", "start_char": 0, "end_char": 1011, "text_sha256": "8f595c96d16b055cd6b9611c4d036626222ffb084ec778f840255cac57ecdfb3"} [mo-p11302742] Mutation of human molybdenum cofactor sulfurase gene is responsible for classical xanthinuria type II. (2001). https://pubmed.ncbi.nlm.nih.gov/11302742/ DOI: 10.1006/bbrc.2001.4719
Complete structured claim and evidence
Recombinant human XDH/XOR catalyzed conversion of xanthine to urate.
Human xanthine oxidoreductase / XDH → Xanthine source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/molybdenum-research/37713777.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "30e93ea24784120403bef1dfe72cf46411f1af88946b9cc1cba3d4c45a367bf9", "start_char": 0, "end_char": 1655, "text_sha256": "30e93ea24784120403bef1dfe72cf46411f1af88946b9cc1cba3d4c45a367bf9"}
experimental_model
Recombinant human XDH variants with urate, superoxide and NO assays
exposure
Xanthine, oxygen and inorganic nitrite assays
limitations
The 2023 Fig. 6E corrigendum corrects a displayed panel; authors state data and conclusions are unchanged. Enzyme activity is not a clinical benefit or dietary response.
nutrient_topic
Molybdenum research collection; topical membership is not evidence of a direct dietary effect. · Molybdenum
organism
Homo sapiens protein
plain_language
The purine-breakdown pathway uses a molybdenum enzyme to make urate.
primary_references
[mo-p37713777] Natural mutations of human XDH promote the nitrite (NO2-)-reductase capacity of xanthine oxidoreductase: A novel mechanism to promote redox health? (2023). https://pubmed.ncbi.nlm.nih.gov/37713777/ DOI: 10.1016/j.redox.2023.102864
tissue_or_cell_type
Purified human enzyme
Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 742–753
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human XDH variants with urate, superoxide and NO assays · source_derived_draft · unverified_draft
### mo-xdh-xanthine Recombinant human XDH/XOR catalyzed conversion of xanthine to urate. Condition category: normal nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: The purine-breakdown pathway uses a molybdenum enzyme to make urate. organism: Homo sapiens protein tissue_or_cell_type: Purified human enzyme experimental_model: Recombinant human XDH variants with urate, superoxide and NO assays limitations: The 2023 Fig. 6E corrigendum corrects a displayed panel; authors state data and conclusions are unchanged. Enzyme activity is not a clinical benefit or dietary response. exposure: Xanthine, oxygen and inorganic nitrite assays evidence_span: {"source_cache": "artifacts/molybdenum-research/37713777.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "30e93ea24784120403bef1dfe72cf46411f1af88946b9cc1cba3d4c45a367bf9", "start_char": 0, "end_char": 1655, "text_sha256": "30e93ea24784120403bef1dfe72cf46411f1af88946b9cc1cba3d4c45a367bf9"} [mo-p37713777] Natural mutations of human XDH promote the nitrite (NO2-)-reductase capacity of xanthine oxidoreductase: A novel mechanism to promote redox health? (2023). https://pubmed.ncbi.nlm.nih.gov/37713777/ DOI: 10.1016/j.redox.2023.102864
Complete structured claim and evidence
The XDH form transfers purine-derived electrons through its iron-sulfur centers and FAD to NAD+, producing NADH.
Human xanthine oxidoreductase / XDH → NAD+ source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/molybdenum-research/37713777.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a8092b2aa7328b59f0275dd8a37d2a2dbb5abb2a32236d0cab5fffcc1ddc671d", "start_char": 0, "end_char": 1579, "text_sha256": "18325172be489f8f4beae16c04dbc4f49f94c87186321e32aede61f27089c7c4"}
experimental_model
Recombinant human XDH variants with urate, superoxide and NO assays
exposure
Xanthine, oxygen and inorganic nitrite assays
limitations
Canonical electron-transfer mechanism stated in this primary article; not an experiment on dietary B2 or niacin depletion.
nutrient_topic
Molybdenum research collection; topical membership is not evidence of a direct dietary effect. · Molybdenum
organism
Homo sapiens protein
plain_language
Riboflavin-derived FAD, iron-sulfur centers and niacin-derived NAD work alongside molybdenum.
primary_references
[mo-p37713777] Natural mutations of human XDH promote the nitrite (NO2-)-reductase capacity of xanthine oxidoreductase: A novel mechanism to promote redox health? (2023). https://pubmed.ncbi.nlm.nih.gov/37713777/ DOI: 10.1016/j.redox.2023.102864
tissue_or_cell_type
Purified human enzyme
Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 768–779
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human XDH variants with urate, superoxide and NO assays · source_derived_draft · unverified_draft
### mo-xdh-nad The XDH form transfers purine-derived electrons through its iron-sulfur centers and FAD to NAD+, producing NADH. Condition category: normal nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: Riboflavin-derived FAD, iron-sulfur centers and niacin-derived NAD work alongside molybdenum. organism: Homo sapiens protein tissue_or_cell_type: Purified human enzyme experimental_model: Recombinant human XDH variants with urate, superoxide and NO assays limitations: Canonical electron-transfer mechanism stated in this primary article; not an experiment on dietary B2 or niacin depletion. exposure: Xanthine, oxygen and inorganic nitrite assays evidence_span: {"source_cache": "artifacts/molybdenum-research/37713777.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a8092b2aa7328b59f0275dd8a37d2a2dbb5abb2a32236d0cab5fffcc1ddc671d", "start_char": 0, "end_char": 1579, "text_sha256": "18325172be489f8f4beae16c04dbc4f49f94c87186321e32aede61f27089c7c4"} [mo-p37713777] Natural mutations of human XDH promote the nitrite (NO2-)-reductase capacity of xanthine oxidoreductase: A novel mechanism to promote redox health? (2023). https://pubmed.ncbi.nlm.nih.gov/37713777/ DOI: 10.1016/j.redox.2023.102864
Complete structured claim and evidence
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

Availability and dependencies

Each situation shows the normal role first, then what the sources report under a specific condition. A shortfall in the diet, a fault in the machinery, and a low blood reading are kept separate because they are not the same thing.

Vitamin E deficiency: myricetin did not replace alpha-tocopherol

Condition: nutrient_deficiency · Vitamin E deficiency followed by two-week dietary replacement.