Component
CYP4F2-mediated phylloquinone omega-hydroxylation
Initial vitamin K1 side-chain catabolic step measured with recombinant CYP4F2 microsomes.
1 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
Alpha-tocopherol did not increase phylloquinone omega-hydroxylation in CYP4F2 microsomes; the study reported a slight decrease in apparent phylloquinone Vmax.
Experimental context and source evidence
- cross_nutrient
- true
- experimental_model
- Recombinant human CYP4F2 co-substrate kinetics
- exposure
- Labeled phylloquinone 0–50 µM with RRR-alpha-tocopherol 0–50 µM or SRR-alpha-tocopherol 0–100 µM; 30 min, 37 °C, 1 mM NADPH.
- limitations
- Does not exclude other mechanisms of vitamin E–K interaction in animals or humans.
- nutrient_topic
- Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
- organism
- Human protein in insect microsomes
- plain_language
- This assay did not support faster vitamin K1 breakdown caused by alpha-tocopherol.
- primary_references
- [farley2013] ω-Hydroxylation of phylloquinone by CYP4F2 is not increased by α-tocopherol. (2013). https://pubmed.ncbi.nlm.nih.gov/23650179/ DOI: 10.1002/mnfr.201200797
- tissue_or_cell_type
- Microsomal enzyme preparation
Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 467–478
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human CYP4F2 co-substrate kinetics · source_derived_draft · unverified_draft
### ve-transport-alpha-does-not-activate-k1-catabolism Alpha-tocopherol did not increase phylloquinone omega-hydroxylation in CYP4F2 microsomes; the study reported a slight decrease in apparent phylloquinone Vmax. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: This assay did not support faster vitamin K1 breakdown caused by alpha-tocopherol. organism: Human protein in insect microsomes tissue_or_cell_type: Microsomal enzyme preparation experimental_model: Recombinant human CYP4F2 co-substrate kinetics limitations: Does not exclude other mechanisms of vitamin E–K interaction in animals or humans. exposure: Labeled phylloquinone 0–50 µM with RRR-alpha-tocopherol 0–50 µM or SRR-alpha-tocopherol 0–100 µM; 30 min, 37 °C, 1 mM NADPH. cross_nutrient: true [farley2013] ω-Hydroxylation of phylloquinone by CYP4F2 is not increased by α-tocopherol. (2013). https://pubmed.ncbi.nlm.nih.gov/23650179/ DOI: 10.1002/mnfr.201200797
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.