Component

Glutathione efflux from vanadate-exposed human erythrocytes

Context-specific entity; species, compartment and exposure are stated on each claim.

3 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. DIDS inhibited the intracellular thiol decrease and extracellular increase during vanadate exposure, supporting an anion-transport-dependent step.

    Human erythrocyte anion exchanger 1 / SLC4A1 → Glutathione efflux from vanadate-exposed human erythrocytes source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Human erythrocytes; DIDS pharmacological intervention.
    limitations
    DIDS is an inhibitor, not itself an exchanger; pharmacology does not establish a unique SLC4A1 transport substrate or route.
    nutrient_topic
    Vanadium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Vanadium
    plain_language
    Membrane transport can gate the redox response.
    primary_references
    Efflux of glutathione and glutathione complexes from human erythrocytes in response to vanadate. · 2013 · https://pubmed.ncbi.nlm.nih.gov/22824382/ · DOI 10.1016/j.bcmd.2012.07.001
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vanadium: speciation, phosphate-sensitive enzymes and cross-nutrient mechanisms (2026-09-19) · lines 166–172

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human erythrocytes; DIDS pharmacological intervention. · source_derived_draft · unverified_draft

    ## vanadium-anion-exchanger-block Membrane transport can gate the redox response. DIDS inhibited the intracellular thiol decrease and extracellular increase during vanadate exposure, supporting an anion-transport-dependent step. Model: Human erythrocytes; DIDS pharmacological intervention. Limitations: DIDS is an inhibitor, not itself an exchanger; pharmacology does not establish a unique SLC4A1 transport substrate or route. Evidence access: Primary abstract Efflux of glutathione and glutathione complexes from human erythrocytes in response to vanadate. · 2013 · https://pubmed.ncbi.nlm.nih.gov/22824382/ · DOI 10.1016/j.bcmd.2012.07.001
    Complete structured claim and evidence

  2. Vanadate exposure depleted intracellular nonprotein sulfhydryls while increasing extracellular glutathione in human erythrocytes.

    Vanadate(V), protonation/speciation dependent → Glutathione efflux from vanadate-exposed human erythrocytes source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Isolated human erythrocytes; millimolar vanadate exposures up to four hours.
    limitations
    High ex-vivo concentrations; nonprotein sulfhydryl assays are not exclusively glutathione measurements.
    nutrient_topic
    Vanadium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Vanadium
    plain_language
    Loss of an intracellular thiol pool can include export rather than only oxidation.
    primary_references
    Efflux of glutathione and glutathione complexes from human erythrocytes in response to vanadate. · 2013 · https://pubmed.ncbi.nlm.nih.gov/22824382/ · DOI 10.1016/j.bcmd.2012.07.001

    Vanadium: speciation, phosphate-sensitive enzymes and cross-nutrient mechanisms (2026-09-19) · lines 158–164

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Isolated human erythrocytes; millimolar vanadate exposures up to four hours. · source_derived_draft · unverified_draft

    ## vanadium-erythrocyte-gsh Loss of an intracellular thiol pool can include export rather than only oxidation. Vanadate exposure depleted intracellular nonprotein sulfhydryls while increasing extracellular glutathione in human erythrocytes. Model: Isolated human erythrocytes; millimolar vanadate exposures up to four hours. Limitations: High ex-vivo concentrations; nonprotein sulfhydryl assays are not exclusively glutathione measurements. Evidence access: Primary abstract Efflux of glutathione and glutathione complexes from human erythrocytes in response to vanadate. · 2013 · https://pubmed.ncbi.nlm.nih.gov/22824382/ · DOI 10.1016/j.bcmd.2012.07.001
    Complete structured claim and evidence

  3. MK571 reduced glutathione efflux during erythrocyte vanadate exposure, suggesting involvement of an MRP-family exporter.

    MRP-inhibitor experiment in human erythrocytes → Glutathione efflux from vanadate-exposed human erythrocytes source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Human erythrocyte inhibitor experiment.
    limitations
    The accessed study does not identify a specific ABCC isoform; no invented transporter assignment.
    nutrient_topic
    Vanadium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Vanadium
    plain_language
    An exporter can contribute to loss of cellular glutathione.
    primary_references
    Efflux of glutathione and glutathione complexes from human erythrocytes in response to vanadate. · 2013 · https://pubmed.ncbi.nlm.nih.gov/22824382/ · DOI 10.1016/j.bcmd.2012.07.001
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vanadium: speciation, phosphate-sensitive enzymes and cross-nutrient mechanisms (2026-09-19) · lines 174–180

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human erythrocyte inhibitor experiment. · source_derived_draft · unverified_draft

    ## vanadium-mrp-efflux-block An exporter can contribute to loss of cellular glutathione. MK571 reduced glutathione efflux during erythrocyte vanadate exposure, suggesting involvement of an MRP-family exporter. Model: Human erythrocyte inhibitor experiment. Limitations: The accessed study does not identify a specific ABCC isoform; no invented transporter assignment. Evidence access: Primary abstract Efflux of glutathione and glutathione complexes from human erythrocytes in response to vanadate. · 2013 · https://pubmed.ncbi.nlm.nih.gov/22824382/ · DOI 10.1016/j.bcmd.2012.07.001
    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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