Component

Alpha-tocopherol-13′-carboxychromanol

Long-chain terminal carboxylate metabolite of alpha-tocopherol, alpha-T-13′-COOH; not a tocotrienol metabolite.

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.

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.

Recorded relationships

What it acts on

  1. Alpha-tocopherol-13′-carboxychromanol inhibited 5-LO product formation in activated human polymorphonuclear leukocytes with an IC50 of approximately 0.08 µM, compared with 0.27 µM for isolated recombinant human 5-LO.

    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    Primary human PMNL and recombinant enzyme, Table 1
    exposure
    10 min compound pretreatment at 37°C; PMNL in PBS pH 7.4, 1 mg/mL glucose and 1 mM CaCl2, stimulated with 2.5 µM A23187 and/or 20 µM arachidonic acid for 10 min; IC50 80 nM.
    limitations
    Potency cannot be equated with oral vitamin E dosing. The activated leukocyte IC50 differs greatly from parent alpha-tocopherol and from other laboratories’ assay results.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Homo sapiens
    plain_language
    The alpha-tocopherol metabolite reduced leukotriene-pathway enzyme output in isolated human immune cells.
    primary_references
    [pein2018] Endogenous metabolites of vitamin E limit inflammation by targeting 5-lipoxygenase. (2018). https://pubmed.ncbi.nlm.nih.gov/30237488/ DOI: 10.1038/s41467-018-06158-5
    tissue_or_cell_type
    Isolated blood polymorphonuclear leukocytes and cell-free enzyme

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 1011–1022

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primary human PMNL and recombinant enzyme, Table 1 · source_derived_draft · unverified_draft

    ### e-sig-alpha-acid-leukocyte-lox Alpha-tocopherol-13′-carboxychromanol inhibited 5-LO product formation in activated human polymorphonuclear leukocytes with an IC50 of approximately 0.08 µM, compared with 0.27 µM for isolated recombinant human 5-LO. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: The alpha-tocopherol metabolite reduced leukotriene-pathway enzyme output in isolated human immune cells. organism: Homo sapiens tissue_or_cell_type: Isolated blood polymorphonuclear leukocytes and cell-free enzyme experimental_model: Primary human PMNL and recombinant enzyme, Table 1 limitations: Potency cannot be equated with oral vitamin E dosing. The activated leukocyte IC50 differs greatly from parent alpha-tocopherol and from other laboratories’ assay results. exposure: 10 min compound pretreatment at 37°C; PMNL in PBS pH 7.4, 1 mg/mL glucose and 1 mM CaCl2, stimulated with 2.5 µM A23187 and/or 20 µM arachidonic acid for 10 min; IC50 80 nM. cross_nutrient: false [pein2018] Endogenous metabolites of vitamin E limit inflammation by targeting 5-lipoxygenase. (2018). https://pubmed.ncbi.nlm.nih.gov/30237488/ DOI: 10.1038/s41467-018-06158-5
    Complete structured claim and evidence

In the sources

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    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards