Component

All-rac-alpha-tocopheryl acetate

Synthetic alpha-tocopherol acetate stereoisomer mixture; DL-alpha-tocopheryl acetate in the liver rescue diet. Acetate ester formulation used in SELECT; hydrolysis and tissue retention separate formulation from active tocopherol.

4 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. In the SELECT secondary analysis, vitamin E alone increased total prostate-cancer risk by 63% among men below the 40th percentile of baseline toenail selenium; a significant effect was not found above that split.

    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    cross_nutrient
    true
    experimental_model
    Secondary case-cohort analysis nested within SELECT; 1739 total cases and 3117 sampled cohort members
    exposure
    Trial supplementation analyzed by baseline toenail selenium; E-alone comparison used below versus at/above the 40th percentile.
    limitations
    Exploratory subgroup thresholds are cohort percentiles, not deficiency thresholds; baseline selenium was not randomized. Does not justify adding selenium to make high-dose vitamin E safe.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Homo sapiens
    plain_language
    Baseline selenium measurements helped identify different trial outcomes, but did not establish a safe supplement combination.
    primary_references
    [e-clin-select2014] Baseline selenium status and effects of selenium and vitamin e supplementation on prostate cancer risk. (2014). https://pubmed.ncbi.nlm.nih.gov/24563519/ DOI: 10.1093/jnci/djt456
    tissue_or_cell_type
    Prostate and toenail selenium biomarker
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 1310–1321

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Secondary case-cohort analysis nested within SELECT; 1739 total cases and 3117 sampled cohort members · source_derived_draft · unverified_draft

    ### e-clin-select-baseline-selenium In the SELECT secondary analysis, vitamin E alone increased total prostate-cancer risk by 63% among men below the 40th percentile of baseline toenail selenium; a significant effect was not found above that split. Condition category: biomarker_context nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Baseline selenium measurements helped identify different trial outcomes, but did not establish a safe supplement combination. organism: Homo sapiens tissue_or_cell_type: Prostate and toenail selenium biomarker experimental_model: Secondary case-cohort analysis nested within SELECT; 1739 total cases and 3117 sampled cohort members limitations: Exploratory subgroup thresholds are cohort percentiles, not deficiency thresholds; baseline selenium was not randomized. Does not justify adding selenium to make high-dose vitamin E safe. exposure: Trial supplementation analyzed by baseline toenail selenium; E-alone comparison used below versus at/above the 40th percentile. cross_nutrient: true [e-clin-select2014] Baseline selenium status and effects of selenium and vitamin e supplementation on prostate cancer risk. (2014). https://pubmed.ncbi.nlm.nih.gov/24563519/ DOI: 10.1093/jnci/djt456
    Complete structured claim and evidence
  2. SELECT did not demonstrate prostate-cancer prevention with vitamin E plus selenium (HR 1.05, 99% CI 0.89–1.22 versus placebo).

    Experimental context and source evidence
    cross_nutrient
    true
    experimental_model
    SELECT randomized factorial prevention trial; 34887 men in primary analysis, 35533 originally randomized
    exposure
    All-rac-alpha-tocopheryl acetate 400 IU/day; selenium arm 200 micrograms/day selenium as L-selenomethionine; supplements stopped in 2008, follow-up continued to July 2011.
    limitations
    Trial-specific formulation, dose and population; does not establish the effect of food intake or of every vitamin E form. Group results cannot identify an intracellular mechanism. The nonsignificant combination estimate is not proof that selenium mechanistically neutralizes vitamin E-associated harm.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Homo sapiens
    plain_language
    Adding selenium did not demonstrate a prostate-cancer prevention benefit.
    primary_references
    [e-clin-select2011] Vitamin E and the risk of prostate cancer: the Selenium and Vitamin E Cancer Prevention Trial (SELECT). (2011). https://pubmed.ncbi.nlm.nih.gov/21990298/ DOI: 10.1001/jama.2011.1437
    tissue_or_cell_type
    Prostate and whole-person outcomes

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 1297–1308

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · SELECT randomized factorial prevention trial; 34887 men in primary analysis, 35533 originally randomized · source_derived_draft · unverified_draft

    ### e-clin-select-combination-boundary SELECT did not demonstrate prostate-cancer prevention with vitamin E plus selenium (HR 1.05, 99% CI 0.89–1.22 versus placebo). Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Adding selenium did not demonstrate a prostate-cancer prevention benefit. organism: Homo sapiens tissue_or_cell_type: Prostate and whole-person outcomes experimental_model: SELECT randomized factorial prevention trial; 34887 men in primary analysis, 35533 originally randomized limitations: Trial-specific formulation, dose and population; does not establish the effect of food intake or of every vitamin E form. Group results cannot identify an intracellular mechanism. The nonsignificant combination estimate is not proof that selenium mechanistically neutralizes vitamin E-associated harm. exposure: All-rac-alpha-tocopheryl acetate 400 IU/day; selenium arm 200 micrograms/day selenium as L-selenomethionine; supplements stopped in 2008, follow-up continued to July 2011. cross_nutrient: true [e-clin-select2011] Vitamin E and the risk of prostate cancer: the Selenium and Vitamin E Cancer Prevention Trial (SELECT). (2011). https://pubmed.ncbi.nlm.nih.gov/21990298/ DOI: 10.1001/jama.2011.1437
    Complete structured claim and evidence
  3. In SELECT, vitamin E alone increased prostate-cancer incidence relative to placebo (HR 1.17, 99% CI 1.004–1.36); the absolute increase was 1.6 cases per 1000 person-years.

    Experimental context and source evidence
    cross_nutrient
    true
    experimental_model
    SELECT randomized factorial prevention trial; 34887 men in primary analysis, 35533 originally randomized
    exposure
    All-rac-alpha-tocopheryl acetate 400 IU/day; selenium arm 200 micrograms/day selenium as L-selenomethionine; supplements stopped in 2008, follow-up continued to July 2011.
    limitations
    Trial-specific formulation, dose and population; does not establish the effect of food intake or of every vitamin E form. Group results cannot identify an intracellular mechanism.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Homo sapiens
    plain_language
    The tested high-dose vitamin E preparation increased prostate-cancer diagnoses in this trial.
    primary_references
    [e-clin-select2011] Vitamin E and the risk of prostate cancer: the Selenium and Vitamin E Cancer Prevention Trial (SELECT). (2011). https://pubmed.ncbi.nlm.nih.gov/21990298/ DOI: 10.1001/jama.2011.1437
    tissue_or_cell_type
    Prostate and whole-person outcomes

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 1284–1295

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · SELECT randomized factorial prevention trial; 34887 men in primary analysis, 35533 originally randomized · source_derived_draft · unverified_draft

    ### e-clin-select-prostate-incidence In SELECT, vitamin E alone increased prostate-cancer incidence relative to placebo (HR 1.17, 99% CI 1.004–1.36); the absolute increase was 1.6 cases per 1000 person-years. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: The tested high-dose vitamin E preparation increased prostate-cancer diagnoses in this trial. organism: Homo sapiens tissue_or_cell_type: Prostate and whole-person outcomes experimental_model: SELECT randomized factorial prevention trial; 34887 men in primary analysis, 35533 originally randomized limitations: Trial-specific formulation, dose and population; does not establish the effect of food intake or of every vitamin E form. Group results cannot identify an intracellular mechanism. exposure: All-rac-alpha-tocopheryl acetate 400 IU/day; selenium arm 200 micrograms/day selenium as L-selenomethionine; supplements stopped in 2008, follow-up continued to July 2011. cross_nutrient: true [e-clin-select2011] Vitamin E and the risk of prostate cancer: the Selenium and Vitamin E Cancer Prevention Trial (SELECT). (2011). https://pubmed.ncbi.nlm.nih.gov/21990298/ DOI: 10.1001/jama.2011.1437
    Complete structured claim and evidence
  4. Maternal dietary supplementation with 500 IU/kg DL-alpha-tocopheryl acetate through gestation and nursing allowed Alb-Cre;Gpx4fl/fl pups to survive to weaning, whereas liver-specific Gpx4-null pups on standard chow died within 48 hours after birth.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    true
    evidence_location
    Results/Table 2; standard-chow comparison Table 1
    experimental_model
    Alb-Cre conditional Gpx4 deletion and maternal diet
    exposure
    500 IU/kg DL-alpha-tocopheryl acetate during gestation/lactation; weaning at 3 weeks.
    limitations
    Alb-Cre Gpx4 loss is machinery impairment, not selenium deficiency; mouse survival rescue does not establish human substitutability.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Mus musculus
    plain_language
    Extra dietary vitamin E rescued early survival in mice lacking liver GPX4.
    primary_references
    [ver-carlson2016] Glutathione peroxidase 4 and vitamin E cooperatively prevent hepatocellular degeneration. (2016). https://pubmed.ncbi.nlm.nih.gov/27262435/ DOI: 10.1016/j.redox.2016.05.003
    tissue_or_cell_type
    Hepatocytes and whole-animal survival
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 606–618

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Alb-Cre conditional Gpx4 deletion and maternal diet · source_derived_draft · unverified_draft

    ### ver-liver-gpx4-e-rescue Maternal dietary supplementation with 500 IU/kg DL-alpha-tocopheryl acetate through gestation and nursing allowed Alb-Cre;Gpx4fl/fl pups to survive to weaning, whereas liver-specific Gpx4-null pups on standard chow died within 48 hours after birth. Condition category: machinery_impairment nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Extra dietary vitamin E rescued early survival in mice lacking liver GPX4. organism: Mus musculus tissue_or_cell_type: Hepatocytes and whole-animal survival experimental_model: Alb-Cre conditional Gpx4 deletion and maternal diet limitations: Alb-Cre Gpx4 loss is machinery impairment, not selenium deficiency; mouse survival rescue does not establish human substitutability. exposure: 500 IU/kg DL-alpha-tocopheryl acetate during gestation/lactation; weaning at 3 weeks. cross_nutrient: true evidence_location: Results/Table 2; standard-chow comparison Table 1 [ver-carlson2016] Glutathione peroxidase 4 and vitamin E cooperatively prevent hepatocellular degeneration. (2016). https://pubmed.ncbi.nlm.nih.gov/27262435/ DOI: 10.1016/j.redox.2016.05.003
    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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