Component
Microsomal tocopherol omega-hydroxylation
NADPH-dependent initial side-chain oxidation in liver 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
Rat liver microsomes formed initial alpha- and gamma-tocopherol side-chain oxidation products with NADPH but not without it.
Experimental context and source evidence
- cross_nutrient
- true
- experimental_model
- Cofactor omission/addition; Figure 6
- exposure
- 0.5 mM NADPH; reaction followed for 80 minutes.
- limitations
- Direct NADPH dependence; no dietary niacin or riboflavin shortage, universal supplement combination or magnesium requirement was tested.
- nutrient_topic
- Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
- organism
- Rattus norvegicus
- plain_language
- The initial microsomal oxidation required a reducing cofactor.
- primary_references
- [sontag2002] Cytochrome P450 omega-hydroxylase pathway of tocopherol catabolism. Novel mechanism of regulation of vitamin E status. (2002). https://pubmed.ncbi.nlm.nih.gov/11997390/ DOI: 10.1074/jbc.m201466200
- tissue_or_cell_type
- Liver microsomes
Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 441–452
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cofactor omission/addition; Figure 6 · source_derived_draft · unverified_draft
### ve-transport-nadph-microsomal-oxidation Rat liver microsomes formed initial alpha- and gamma-tocopherol side-chain oxidation products with NADPH but not without it. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: The initial microsomal oxidation required a reducing cofactor. organism: Rattus norvegicus tissue_or_cell_type: Liver microsomes experimental_model: Cofactor omission/addition; Figure 6 limitations: Direct NADPH dependence; no dietary niacin or riboflavin shortage, universal supplement combination or magnesium requirement was tested. exposure: 0.5 mM NADPH; reaction followed for 80 minutes. cross_nutrient: true [sontag2002] Cytochrome P450 omega-hydroxylase pathway of tocopherol catabolism. Novel mechanism of regulation of vitamin E status. (2002). https://pubmed.ncbi.nlm.nih.gov/11997390/ DOI: 10.1074/jbc.m201466200
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.