Component
Luteolin monoglucuronides, position unresolved in study
Context-specific entity; species, compartment and exposure are stated on each claim.
7 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
What acts on it
Ko143 inhibition of ABCG2 reduced luteolin-monoglucuronide efflux and increased intracellular retention.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- UGT1A9-expressing human HeLa cells.
- limitations
- Pharmacological inhibition; diglucuronide compensation was proposed, not proven in patients.
- nutrient_topic
- Luteolin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Luteolin / 3′,4′,5,7-tetrahydroxyflavone
- plain_language
- Blocking export changes where metabolites accumulate.
- primary_references
- Breast cancer resistance protein-mediated efflux of luteolin glucuronides in HeLa cells overexpressing UDP-glucuronosyltransferase 1A9. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24092055/ · DOI 10.1007/s11095-013-1207-0
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 84–90
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · UGT1A9-expressing human HeLa cells. · source_derived_draft · unverified_draft
## luteolin-abcg2-blockade Blocking export changes where metabolites accumulate. Ko143 inhibition of ABCG2 reduced luteolin-monoglucuronide efflux and increased intracellular retention. Model: UGT1A9-expressing human HeLa cells. Limitations: Pharmacological inhibition; diglucuronide compensation was proposed, not proven in patients. Evidence access: Primary abstract Breast cancer resistance protein-mediated efflux of luteolin glucuronides in HeLa cells overexpressing UDP-glucuronosyltransferase 1A9. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24092055/ · DOI 10.1007/s11095-013-1207-0
Complete structured claim and evidenceLPS-treated rats showed increased plasma beta-glucuronidase activity and a higher free-luteolin/monoglucuronide ratio.
Experimental context and source evidence
- availability_state
- biomarker_context Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Rat intravenous LPS experiment.
- limitations
- Association supports deconjugation; not a universal human targeting mechanism.
- nutrient_topic
- Luteolin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Luteolin / 3′,4′,5,7-tetrahydroxyflavone
- plain_language
- Inflammatory state altered measured forms.
- primary_references
- Deglucuronidation of a flavonoid, luteolin monoglucuronide, during inflammation. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11717168/
- trigger_kind
- biomarker_context Imported condition classification; unverified.
Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 164–170
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Rat intravenous LPS experiment. · source_derived_draft · unverified_draft
## luteolin-rat-deconjugation Inflammatory state altered measured forms. LPS-treated rats showed increased plasma beta-glucuronidase activity and a higher free-luteolin/monoglucuronide ratio. Model: Rat intravenous LPS experiment. Limitations: Association supports deconjugation; not a universal human targeting mechanism. Evidence access: Primary abstract Deglucuronidation of a flavonoid, luteolin monoglucuronide, during inflammation. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11717168/
Complete structured claim and evidenceRats given luteolin aglycone or the tested glucosides predominantly contained glucuronides in plasma and organs.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Rat oral aglycone and green-pepper-leaf glucosides.
- limitations
- Species and administered form affect exposure. The glucuronide pool is not a single positional isomer.
- nutrient_topic
- Luteolin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Luteolin / 3′,4′,5,7-tetrahydroxyflavone
- plain_language
- Rat metabolism cannot be copied directly onto humans.
- primary_references
- Absorption and Metabolism of Luteolin in Rats and Humans in Relation to in Vitro Anti-inflammatory Effects. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30280574/ · DOI 10.1021/acs.jafc.8b03273
Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 20–26
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Rat oral aglycone and green-pepper-leaf glucosides. · source_derived_draft · unverified_draft
## luteolin-rat-glucuronides Rat metabolism cannot be copied directly onto humans. Rats given luteolin aglycone or the tested glucosides predominantly contained glucuronides in plasma and organs. Model: Rat oral aglycone and green-pepper-leaf glucosides. Limitations: Species and administered form affect exposure. The glucuronide pool is not a single positional isomer. Evidence access: Primary abstract Absorption and Metabolism of Luteolin in Rats and Humans in Relation to in Vitro Anti-inflammatory Effects. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30280574/ · DOI 10.1021/acs.jafc.8b03273
Complete structured claim and evidence
Where it participates (unsigned role)
Supernatants from activated human neutrophils converted luteolin monoglucuronide to free luteolin, consistent with released beta-glucuronidase.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Ionomycin/cytochalasin-B-stimulated human neutrophils; HPLC.
- limitations
- Position of the monoglucuronide is not resolved in the abstract.
- nutrient_topic
- Luteolin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Luteolin / 3′,4′,5,7-tetrahydroxyflavone
- plain_language
- Inflamed cells can locally regenerate the unconjugated molecule.
- primary_references
- Deglucuronidation of a flavonoid, luteolin monoglucuronide, during inflammation. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11717168/
Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 156–162
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Ionomycin/cytochalasin-B-stimulated human neutrophils; HPLC. · source_derived_draft · unverified_draft
## luteolin-neutrophil-release Inflamed cells can locally regenerate the unconjugated molecule. Supernatants from activated human neutrophils converted luteolin monoglucuronide to free luteolin, consistent with released beta-glucuronidase. Model: Ionomycin/cytochalasin-B-stimulated human neutrophils; HPLC. Limitations: Position of the monoglucuronide is not resolved in the abstract. Evidence access: Primary abstract Deglucuronidation of a flavonoid, luteolin monoglucuronide, during inflammation. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11717168/
Complete structured claim and evidenceRecombinant human UGT1A1 efficiently glucuronidated luteolin in the isoenzyme comparison.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human recombinant UGT comparison and microsomes.
- limitations
- Relative activity depends on tissue and conjugation position. Not a claim of equal in-vivo contribution.
- nutrient_topic
- Luteolin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Luteolin / 3′,4′,5,7-tetrahydroxyflavone
- plain_language
- A specific enzyme can attach a glucuronide group.
- primary_references
- Regioselectivity of phase II metabolism of luteolin and quercetin by UDP-glucuronosyl transferases. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12018987/ · DOI 10.1021/tx0101705
Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 28–34
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human recombinant UGT comparison and microsomes. · source_derived_draft · unverified_draft
## luteolin-ugt1a1-formation A specific enzyme can attach a glucuronide group. Recombinant human UGT1A1 efficiently glucuronidated luteolin in the isoenzyme comparison. Model: Human recombinant UGT comparison and microsomes. Limitations: Relative activity depends on tissue and conjugation position. Not a claim of equal in-vivo contribution. Evidence access: Primary abstract Regioselectivity of phase II metabolism of luteolin and quercetin by UDP-glucuronosyl transferases. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12018987/ · DOI 10.1021/tx0101705
Complete structured claim and evidenceRecombinant human UGT1A8 efficiently glucuronidated luteolin in the isoenzyme comparison.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human recombinant UGT comparison and microsomes.
- limitations
- Relative activity depends on tissue and conjugation position. Not a claim of equal in-vivo contribution.
- nutrient_topic
- Luteolin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Luteolin / 3′,4′,5,7-tetrahydroxyflavone
- plain_language
- A specific enzyme can attach a glucuronide group.
- primary_references
- Regioselectivity of phase II metabolism of luteolin and quercetin by UDP-glucuronosyl transferases. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12018987/ · DOI 10.1021/tx0101705
Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 36–42
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human recombinant UGT comparison and microsomes. · source_derived_draft · unverified_draft
## luteolin-ugt1a8-formation A specific enzyme can attach a glucuronide group. Recombinant human UGT1A8 efficiently glucuronidated luteolin in the isoenzyme comparison. Model: Human recombinant UGT comparison and microsomes. Limitations: Relative activity depends on tissue and conjugation position. Not a claim of equal in-vivo contribution. Evidence access: Primary abstract Regioselectivity of phase II metabolism of luteolin and quercetin by UDP-glucuronosyl transferases. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12018987/ · DOI 10.1021/tx0101705
Complete structured claim and evidenceRecombinant human UGT1A9 efficiently glucuronidated luteolin in the isoenzyme comparison.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human recombinant UGT comparison and microsomes.
- limitations
- Relative activity depends on tissue and conjugation position. Not a claim of equal in-vivo contribution.
- nutrient_topic
- Luteolin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Luteolin / 3′,4′,5,7-tetrahydroxyflavone
- plain_language
- A specific enzyme can attach a glucuronide group.
- primary_references
- Regioselectivity of phase II metabolism of luteolin and quercetin by UDP-glucuronosyl transferases. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12018987/ · DOI 10.1021/tx0101705
Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 44–50
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human recombinant UGT comparison and microsomes. · source_derived_draft · unverified_draft
## luteolin-ugt1a9-formation A specific enzyme can attach a glucuronide group. Recombinant human UGT1A9 efficiently glucuronidated luteolin in the isoenzyme comparison. Model: Human recombinant UGT comparison and microsomes. Limitations: Relative activity depends on tissue and conjugation position. Not a claim of equal in-vivo contribution. Evidence access: Primary abstract Regioselectivity of phase II metabolism of luteolin and quercetin by UDP-glucuronosyl transferases. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12018987/ · DOI 10.1021/tx0101705
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.