Component

Plasma membrane repair

Resealing after a membrane disruption; measured by exclusion of extracellular dye after controlled injury.

5 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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 acts on it

  1. Loading C2C12 cells with 200 µM alpha-tocopherol for 18 hours reduced FM1-43 entry after laser injury in calcium-containing buffer, consistent with faster membrane resealing.

    All-rac-alpha-tocopherol → Plasma membrane repair source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    true
    evidence_location
    Figure 1a–b
    experimental_model
    Laser wounding and time-resolved dye exclusion
    exposure
    200 µM racemic alpha-tocopherol (96% pure) for 18 h, washed; 1.2 mM extracellular calcium.
    limitations
    Pharmacologic cell loading; not a dietary intake equivalent.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Mus musculus
    plain_language
    Vitamin E loading helped cultured muscle-line cells close laser-induced membrane wounds.
    primary_references
    [ver-howard2011] Promotion of plasma membrane repair by vitamin E. (2011). https://pubmed.ncbi.nlm.nih.gov/22186893/ DOI: 10.1038/ncomms1594
    tissue_or_cell_type
    C2C12 myoblasts

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 662–674

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Laser wounding and time-resolved dye exclusion · source_derived_draft · unverified_draft

    ### ver-c2c12-membrane-repair Loading C2C12 cells with 200 µM alpha-tocopherol for 18 hours reduced FM1-43 entry after laser injury in calcium-containing buffer, consistent with faster membrane resealing. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin E loading helped cultured muscle-line cells close laser-induced membrane wounds. organism: Mus musculus tissue_or_cell_type: C2C12 myoblasts experimental_model: Laser wounding and time-resolved dye exclusion limitations: Pharmacologic cell loading; not a dietary intake equivalent. exposure: 200 µM racemic alpha-tocopherol (96% pure) for 18 h, washed; 1.2 mM extracellular calcium. cross_nutrient: true evidence_location: Figure 1a–b [ver-howard2011] Promotion of plasma membrane repair by vitamin E. (2011). https://pubmed.ncbi.nlm.nih.gov/22186893/ DOI: 10.1038/ncomms1594
    Complete structured claim and evidence

  2. Following 11 months on vitamin E-stripped chow, rat flexor digitorum brevis fibers displayed continued dye influx after controlled laser injury; normal chow and alpha-tocopherol-add-back controls resealed more effectively.

    Alpha-tocopherol → Plasma membrane repair source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    false
    evidence_location
    Methods; Figure 3
    experimental_model
    Dietary depletion with chow and add-back controls; laser assay
    exposure
    Male Sprague-Dawley rats started diets at 4 weeks; assay at 11-month diet interval.
    limitations
    Long-term rat dietary deprivation and controlled wound assays; not evidence that ordinary supplementation improves muscle performance in replete people.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Rattus norvegicus
    plain_language
    Long-term vitamin E deprivation impaired muscle-fiber wound repair in rats.
    primary_references
    [ver-labazi2015] The antioxidant requirement for plasma membrane repair in skeletal muscle. (2015). https://pubmed.ncbi.nlm.nih.gov/25843658/ DOI: 10.1016/j.freeradbiomed.2015.03.016
    tissue_or_cell_type
    Flexor digitorum brevis muscle
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 704–716

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dietary depletion with chow and add-back controls; laser assay · source_derived_draft · unverified_draft

    ### ver-diet-e-muscle-repair-failure Following 11 months on vitamin E-stripped chow, rat flexor digitorum brevis fibers displayed continued dye influx after controlled laser injury; normal chow and alpha-tocopherol-add-back controls resealed more effectively. Condition category: nutrient_deficiency nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Long-term vitamin E deprivation impaired muscle-fiber wound repair in rats. organism: Rattus norvegicus tissue_or_cell_type: Flexor digitorum brevis muscle experimental_model: Dietary depletion with chow and add-back controls; laser assay limitations: Long-term rat dietary deprivation and controlled wound assays; not evidence that ordinary supplementation improves muscle performance in replete people. exposure: Male Sprague-Dawley rats started diets at 4 weeks; assay at 11-month diet interval. cross_nutrient: false evidence_location: Methods; Figure 3 [ver-labazi2015] The antioxidant requirement for plasma membrane repair in skeletal muscle. (2015). https://pubmed.ncbi.nlm.nih.gov/25843658/ DOI: 10.1016/j.freeradbiomed.2015.03.016
    Complete structured claim and evidence

  3. In mouse embryonic fibroblasts subjected to 48-hour inducible Gpx4 deletion, 200 µM alpha-tocopherol supplementation for the preceding 24 hours prevented the pronounced laser-wound repair defect.

    Alpha-tocopherol → Plasma membrane repair source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    true
    evidence_location
    Figure 4d; Methods
    experimental_model
    Tamoxifen-inducible Gpx4 deletion with re-expression controls
    exposure
    1 µM tamoxifen for 48 h; 200 µM alpha-tocopherol for 24 h before repair assay.
    limitations
    Genetic GPX4 loss, not nutritional selenium deficiency; repair mechanism downstream of oxidation was not resolved.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Mus musculus
    plain_language
    Vitamin E loading rescued membrane resealing after GPX4 deletion in these fibroblasts.
    primary_references
    [ver-labazi2015] The antioxidant requirement for plasma membrane repair in skeletal muscle. (2015). https://pubmed.ncbi.nlm.nih.gov/25843658/ DOI: 10.1016/j.freeradbiomed.2015.03.016
    tissue_or_cell_type
    Embryonic fibroblasts
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 718–730

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Tamoxifen-inducible Gpx4 deletion with re-expression controls · source_derived_draft · unverified_draft

    ### ver-gpx4-fibroblast-repair-rescue In mouse embryonic fibroblasts subjected to 48-hour inducible Gpx4 deletion, 200 µM alpha-tocopherol supplementation for the preceding 24 hours prevented the pronounced laser-wound repair defect. Condition category: machinery_impairment nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin E loading rescued membrane resealing after GPX4 deletion in these fibroblasts. organism: Mus musculus tissue_or_cell_type: Embryonic fibroblasts experimental_model: Tamoxifen-inducible Gpx4 deletion with re-expression controls limitations: Genetic GPX4 loss, not nutritional selenium deficiency; repair mechanism downstream of oxidation was not resolved. exposure: 1 µM tamoxifen for 48 h; 200 µM alpha-tocopherol for 24 h before repair assay. cross_nutrient: true evidence_location: Figure 4d; Methods [ver-labazi2015] The antioxidant requirement for plasma membrane repair in skeletal muscle. (2015). https://pubmed.ncbi.nlm.nih.gov/25843658/ DOI: 10.1016/j.freeradbiomed.2015.03.016
    Complete structured claim and evidence

  4. Pretreatment of BS-C-1 cells with 200 µM alpha-tocopherol for 24 hours prevented the membrane-repair defect caused by 1 mM hydrogen peroxide during laser injury.

    All-rac-alpha-tocopherol → Plasma membrane repair source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    evidence_location
    Figure 4a–b
    experimental_model
    Oxidant challenge during laser-wound assay
    exposure
    200 µM racemic alpha-tocopherol (96% pure), 24 h; 1 mM H2O2 during injury.
    limitations
    Oxidant and loading concentrations are experimental; no specific fusion protein target was identified.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    African green monkey-derived cell line
    plain_language
    Vitamin E loading protected the repair response against this oxidant challenge.
    primary_references
    [ver-howard2011] Promotion of plasma membrane repair by vitamin E. (2011). https://pubmed.ncbi.nlm.nih.gov/22186893/ DOI: 10.1038/ncomms1594
    tissue_or_cell_type
    BS-C-1 kidney epithelial cells

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 690–702

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Oxidant challenge during laser-wound assay · source_derived_draft · unverified_draft

    ### ver-oxidant-challenged-repair Pretreatment of BS-C-1 cells with 200 µM alpha-tocopherol for 24 hours prevented the membrane-repair defect caused by 1 mM hydrogen peroxide during laser injury. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin E loading protected the repair response against this oxidant challenge. organism: African green monkey-derived cell line tissue_or_cell_type: BS-C-1 kidney epithelial cells experimental_model: Oxidant challenge during laser-wound assay limitations: Oxidant and loading concentrations are experimental; no specific fusion protein target was identified. exposure: 200 µM racemic alpha-tocopherol (96% pure), 24 h; 1 mM H2O2 during injury. cross_nutrient: false evidence_location: Figure 4a–b [ver-howard2011] Promotion of plasma membrane repair by vitamin E. (2011). https://pubmed.ncbi.nlm.nih.gov/22186893/ DOI: 10.1038/ncomms1594
    Complete structured claim and evidence

  5. Alpha-tocopherol-loaded HeLa cells still failed to restrict dye entry after laser injury when extracellular calcium was omitted, despite improved repair in calcium-containing buffer.

    Calcium ion → Plasma membrane repair source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    true
    evidence_location
    Figure 1c
    experimental_model
    Laser wounding with extracellular calcium control
    exposure
    200 µM racemic alpha-tocopherol (96% pure) for 24 h; with versus without added extracellular calcium.
    limitations
    Acute assay calcium removal is not dietary calcium deficiency; does not identify the calcium sensor.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Homo sapiens
    plain_language
    Vitamin E loading did not eliminate the need for extracellular calcium during membrane repair.
    primary_references
    [ver-howard2011] Promotion of plasma membrane repair by vitamin E. (2011). https://pubmed.ncbi.nlm.nih.gov/22186893/ DOI: 10.1038/ncomms1594
    tissue_or_cell_type
    HeLa cells

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 676–688

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Laser wounding with extracellular calcium control · source_derived_draft · unverified_draft

    ### ver-repair-extracellular-calcium Alpha-tocopherol-loaded HeLa cells still failed to restrict dye entry after laser injury when extracellular calcium was omitted, despite improved repair in calcium-containing buffer. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin E loading did not eliminate the need for extracellular calcium during membrane repair. organism: Homo sapiens tissue_or_cell_type: HeLa cells experimental_model: Laser wounding with extracellular calcium control limitations: Acute assay calcium removal is not dietary calcium deficiency; does not identify the calcium sensor. exposure: 200 µM racemic alpha-tocopherol (96% pure) for 24 h; with versus without added extracellular calcium. cross_nutrient: true evidence_location: Figure 1c [ver-howard2011] Promotion of plasma membrane repair by vitamin E. (2011). https://pubmed.ncbi.nlm.nih.gov/22186893/ DOI: 10.1038/ncomms1594
    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.

    Evidence, AI assistance and curation standards