Component

GPX3

Extracellular glutathione peroxidase whose activity is selenium-responsive and can plateau.

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 it acts on

  1. Gpx3-deficient mice showed increased platelet responsiveness.

    GPX3 → Platelet activation source_derived_draftliterature_reviewed:direct_experimental
    Experimental context and source evidence
    cell_type
    platelets and plasma
    experimental_model
    Gpx3 knockout
    limitations
    Not a selenium-supplementation trial.
    organism
    mouse

    Selenium: literature corrections and mechanism additions · lines 690–700

    Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Gpx3 knockout · secondary_verified · secondary_verified

    ## gpx3-loss-increases-platelet-activation GPX3 loss made platelets more reactive in this model. Gpx3-deficient mice showed increased platelet responsiveness. Organism: mouse Cell type: platelets and plasma Experimental model: Gpx3 knockout Limitations: Not a selenium-supplementation trial. Primary reference: [Glutathione Peroxidase-3 Deficiency Promotes Platelet-dependent Thrombosis in vivo](https://pmc.ncbi.nlm.nih.gov/articles/PMC3107543/)
    Complete structured claim and evidence

  2. Gpx3 deficiency increased platelet-dependent thrombosis after experimental vascular provocation.

    GPX3 → Arterial thrombosis source_derived_draftliterature_reviewed:direct_experimental
    Experimental context and source evidence
    cell_type
    arterial injury model
    experimental_model
    Gpx3 knockout
    limitations
    Does not establish a human selenium cutoff.
    organism
    mouse

    Selenium: literature corrections and mechanism additions · lines 702–712

    Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Gpx3 knockout · secondary_verified · secondary_verified

    ## gpx3-loss-increases-provoked-thrombosis GPX3-deficient mice formed more thrombus after vascular injury. Gpx3 deficiency increased platelet-dependent thrombosis after experimental vascular provocation. Organism: mouse Cell type: arterial injury model Experimental model: Gpx3 knockout Limitations: Does not establish a human selenium cutoff. Primary reference: [Glutathione Peroxidase-3 Deficiency Promotes Platelet-dependent Thrombosis in vivo](https://pmc.ncbi.nlm.nih.gov/articles/PMC3107543/)
    Complete structured claim and evidence

  3. Purified human plasma glutathione peroxidase reduced hydrogen peroxide using glutathione.

    GPX3 → Hydrogen peroxide source_derived_draftliterature_reviewed:direct_experimental
    Experimental context and source evidence
    cell_type
    plasma
    experimental_model
    Purified enzyme kinetics
    limitations
    Assay glutathione availability does not define every physiological electron donor.
    organism
    human

    Selenium: literature corrections and mechanism additions · lines 678–688

    Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Purified enzyme kinetics · secondary_verified · secondary_verified

    ## gpx3-reduces-extracellular-peroxide GPX3 can remove peroxide outside cells. Purified human plasma glutathione peroxidase reduced hydrogen peroxide using glutathione. Organism: human Cell type: plasma Experimental model: Purified enzyme kinetics Limitations: Assay glutathione availability does not define every physiological electron donor. Primary reference: [Characterization of the major hydroperoxide-reducing activity of human plasma. Purification and properties of a selenium-dependent glutathione peroxidase.](https://www.sciencedirect.com/science/article/pii/S0021925818453926)
    Complete structured claim and evidence

  4. Redox and platelet measurements support GPX3 preservation of NO-mediated platelet restraint.

    GPX3 → NO source_derived_draftliterature_reviewed:supported_interpretation
    Experimental context and source evidence
    cell_type
    plasma and platelets
    experimental_model
    Gpx3 knockout
    limitations
    Individual oxidant intermediates were not fully isolated.
    organism
    mouse

    Selenium: literature corrections and mechanism additions · lines 714–724

    Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Gpx3 knockout · secondary_verified · secondary_verified

    ## gpx3-supports-no-platelet-restraint GPX3 may help preserve nitric oxide's platelet-inhibitory signal. Redox and platelet measurements support GPX3 preservation of NO-mediated platelet restraint. Organism: mouse Cell type: plasma and platelets Experimental model: Gpx3 knockout Limitations: Individual oxidant intermediates were not fully isolated. Primary reference: [Glutathione Peroxidase-3 Deficiency Promotes Platelet-dependent Thrombosis in vivo](https://pmc.ncbi.nlm.nih.gov/articles/PMC3107543/)
    Complete structured claim and evidence

What acts on it

  1. GPX3 activity can plateau as selenium supply increases, making it less informative near that plateau.

    Selenium → GPX3 source_derived_draftsource_reported: Human intervention for biomarker plateaus; supplied-source interpretation of measurement limits.
    Experimental context and source evidence
    availability_state
    A selenium-responsive circulating biomarker approaches a plateau in a particular study or individual context.
    experimental_scope
    Human intervention dose-response observations and biomarker interpretation.
    limitations
    Study-specific plateaus cannot be mapped to GPX1 NMD, thyroid or immune failure, GPX4 loss, or an absolute antioxidant-to-pro-oxidant switch. Plasma and whole-blood values are not interchangeable.
    trigger_kind
    biomarker_context

    Selenium deficiency: a mechanism-first reference · lines 577–583

    Supplied selenium deficiency reference · supports · Supplied reference; verify the primary study and experimental context. · source_derived_draft · unverified_draft

    GPX3 activity Selenium-responsive and can plateau Functional extracellular GPX activity Becomes less informative once activity is near plateau
    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