Component

Delta-tocopherol

Delta tocopherol congener with a saturated side chain; distinct from delta-tocotrienol and its carboxychromanol metabolites.

3 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. Delta-tocopherol at 50 µM diminished A23187-triggered extracellular calcium entry in differentiated HL-60 cells, monitored with fluo-4 after calcium was added to calcium-free buffer.

    Delta-tocopherol → Stimulus-induced calcium influx source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    true
    experimental_model
    DMSO-differentiated human HL-60 neutrophil-like cells; fluo-4 fluorescence
    exposure
    2 µM fluo-4 AM loading; 50 µM delta-tocopherol for 10 min; A23187 0.5 µM before extracellular calcium addition.
    limitations
    Methods and figure caption disagree on added calcium units (mM versus µM). No specific calcium channel was identified; membrane stabilization remains a proposed explanation.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Homo sapiens
    plain_language
    Delta-tocopherol reduced calcium entry caused by an experimental ion carrier in this cell model.
    primary_references
    [jiang2011] Natural forms of vitamin E and 13'-carboxychromanol, a long-chain vitamin E metabolite, inhibit leukotriene generation from stimulated neutrophils by blocking calcium influx and suppressing 5-lipoxygenase activity, respectively. (2011). https://pubmed.ncbi.nlm.nih.gov/21169551/ DOI: 10.4049/jimmunol.1002342
    tissue_or_cell_type
    Neutrophil-like leukemia-derived cell culture

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 894–905

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · DMSO-differentiated human HL-60 neutrophil-like cells; fluo-4 fluorescence · source_derived_draft · unverified_draft

    ### e-sig-delta-calcium-influx Delta-tocopherol at 50 µM diminished A23187-triggered extracellular calcium entry in differentiated HL-60 cells, monitored with fluo-4 after calcium was added to calcium-free buffer. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Delta-tocopherol reduced calcium entry caused by an experimental ion carrier in this cell model. organism: Homo sapiens tissue_or_cell_type: Neutrophil-like leukemia-derived cell culture experimental_model: DMSO-differentiated human HL-60 neutrophil-like cells; fluo-4 fluorescence limitations: Methods and figure caption disagree on added calcium units (mM versus µM). No specific calcium channel was identified; membrane stabilization remains a proposed explanation. exposure: 2 µM fluo-4 AM loading; 50 µM delta-tocopherol for 10 min; A23187 0.5 µM before extracellular calcium addition. cross_nutrient: true [jiang2011] Natural forms of vitamin E and 13'-carboxychromanol, a long-chain vitamin E metabolite, inhibit leukotriene generation from stimulated neutrophils by blocking calcium influx and suppressing 5-lipoxygenase activity, respectively. (2011). https://pubmed.ncbi.nlm.nih.gov/21169551/ DOI: 10.4049/jimmunol.1002342
    Complete structured claim and evidence
  2. Delta-tocopherol pretreatment largely prevented A23187-induced redistribution of 5-LOX from cytosolic to nuclear fractions in differentiated HL-60 cells.

    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    DMSO-differentiated human HL-60 neutrophil-like cells; fractionation and immunoblot
    exposure
    50 µM delta-tocopherol for 10 min followed by 2.5 µM A23187 for 15 min.
    limitations
    Fractionation is a localization assay, not proof of direct enzyme inhibition; purified 5-LOX was unaffected by tocopherols at 50 µM in this paper.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Homo sapiens
    plain_language
    Delta-tocopherol kept much of the enzyme from moving to the cell location associated with leukotriene production.
    primary_references
    [jiang2011] Natural forms of vitamin E and 13'-carboxychromanol, a long-chain vitamin E metabolite, inhibit leukotriene generation from stimulated neutrophils by blocking calcium influx and suppressing 5-lipoxygenase activity, respectively. (2011). https://pubmed.ncbi.nlm.nih.gov/21169551/ DOI: 10.4049/jimmunol.1002342
    tissue_or_cell_type
    Neutrophil-like leukemia-derived cell culture

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 907–918

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · DMSO-differentiated human HL-60 neutrophil-like cells; fractionation and immunoblot · source_derived_draft · unverified_draft

    ### e-sig-delta-lox-translocation Delta-tocopherol pretreatment largely prevented A23187-induced redistribution of 5-LOX from cytosolic to nuclear fractions in differentiated HL-60 cells. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Delta-tocopherol kept much of the enzyme from moving to the cell location associated with leukotriene production. organism: Homo sapiens tissue_or_cell_type: Neutrophil-like leukemia-derived cell culture experimental_model: DMSO-differentiated human HL-60 neutrophil-like cells; fractionation and immunoblot limitations: Fractionation is a localization assay, not proof of direct enzyme inhibition; purified 5-LOX was unaffected by tocopherols at 50 µM in this paper. exposure: 50 µM delta-tocopherol for 10 min followed by 2.5 µM A23187 for 15 min. cross_nutrient: false [jiang2011] Natural forms of vitamin E and 13'-carboxychromanol, a long-chain vitamin E metabolite, inhibit leukotriene generation from stimulated neutrophils by blocking calcium influx and suppressing 5-lipoxygenase activity, respectively. (2011). https://pubmed.ncbi.nlm.nih.gov/21169551/ DOI: 10.4049/jimmunol.1002342
    Complete structured claim and evidence
  3. Delta-tocopherol at 50 µM inhibited LTB4 production stimulated by S1P or LPA in differentiated HL-60 cells, but did not inhibit the response to fMLP under the tested conditions.

    Delta-tocopherol → Leukotriene B4 source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    DMSO-differentiated human HL-60 neutrophil-like cells
    exposure
    10 min pretreatment; S1P 50 µM, LPA 100 µM or fMLP 1 µM for 10 min.
    limitations
    Stimulus specificity precludes a universal anti-inflammatory claim. High-dose lipid stimuli and transformed cells limit extrapolation.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Homo sapiens
    plain_language
    Delta-tocopherol reduced leukotriene output only for some ways of activating these cells.
    primary_references
    [jiang2011] Natural forms of vitamin E and 13'-carboxychromanol, a long-chain vitamin E metabolite, inhibit leukotriene generation from stimulated neutrophils by blocking calcium influx and suppressing 5-lipoxygenase activity, respectively. (2011). https://pubmed.ncbi.nlm.nih.gov/21169551/ DOI: 10.4049/jimmunol.1002342
    tissue_or_cell_type
    Neutrophil-like leukemia-derived cell culture

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 881–892

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · DMSO-differentiated human HL-60 neutrophil-like cells · source_derived_draft · unverified_draft

    ### e-sig-delta-ltb4-stimulus Delta-tocopherol at 50 µM inhibited LTB4 production stimulated by S1P or LPA in differentiated HL-60 cells, but did not inhibit the response to fMLP under the tested conditions. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Delta-tocopherol reduced leukotriene output only for some ways of activating these cells. organism: Homo sapiens tissue_or_cell_type: Neutrophil-like leukemia-derived cell culture experimental_model: DMSO-differentiated human HL-60 neutrophil-like cells limitations: Stimulus specificity precludes a universal anti-inflammatory claim. High-dose lipid stimuli and transformed cells limit extrapolation. exposure: 10 min pretreatment; S1P 50 µM, LPA 100 µM or fMLP 1 µM for 10 min. cross_nutrient: false [jiang2011] Natural forms of vitamin E and 13'-carboxychromanol, a long-chain vitamin E metabolite, inhibit leukotriene generation from stimulated neutrophils by blocking calcium influx and suppressing 5-lipoxygenase activity, respectively. (2011). https://pubmed.ncbi.nlm.nih.gov/21169551/ DOI: 10.4049/jimmunol.1002342
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

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

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