Component

Male fertility

Reproductive function examined in selenium-restriction and genetic animal models.

2 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 acts on it

  1. Selenium restriction can impair male fertility in animal models.

    Selenium → Male fertility source_derived_draftsource_reported: Strong genetic and animal-model evidence as reported by the supplied reference; unverified source synthesis.
    Experimental context and source evidence
    availability_state
    Selenium restriction affects sperm biology; genetic disruption of delivery or GPX4 provides related but distinct evidence.
    experimental_scope
    Animal dietary-restriction and genetic models; the experiments address related mechanisms with different perturbations.
    limitations
    Genetic loss is not an ordinary dietary-deficiency phenotype. No human plasma threshold or guaranteed fertility outcome is established.
    trigger_kind
    nutrient_deficiency

    Selenium deficiency: a mechanism-first reference · lines 420–430

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

    4.5 Male fertility GPX4 has a distinctive role in sperm: during maturation, a structural form contributes to the mitochondrial sheath. Selenium restriction and disruption of the SELENOP–ApoER2/LRP8 pathway can impair male fertility in animal models. SELENOP delivery / GPX4 biology disrupted ↓ mitochondrial-sheath and membrane defects ↓ reduced sperm motility and fertility in experimental models Evidence: strong genetic and animal-model evidence; translation to a specific human plasma selenium threshold is not established.
    Complete structured claim and evidence
  2. Male Txnrd3-knockout mice showed impaired reproductive performance and reduced fertilization in the reported assays.

    TXNRD3 → Male fertility source_derived_draftliterature_reviewed:direct_experimental
    Experimental context and source evidence
    experimental_model
    Txnrd3-knockout mice, sperm thiol assays and in-vitro fertilization.
    limitations
    This experiment-specific relationship does not establish a human dietary-deficiency threshold or supplementation benefit.
    organism
    Mouse

    Selenium: literature corrections and mechanism additions · lines 987–996

    Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Txnrd3-knockout mice, sperm thiol assays and in-vitro fertilization. · secondary_verified · secondary_verified

    ## txnrd3-mouse-fertility Removing TXNRD3 impaired fertility in the studied mice. Male Txnrd3-knockout mice showed impaired reproductive performance and reduced fertilization in the reported assays. Experimental model: Txnrd3-knockout mice, sperm thiol assays and in-vitro fertilization. Organism: Mouse Limitations: This experiment-specific relationship does not establish a human dietary-deficiency threshold or supplementation benefit. Primary reference: [Selenoprotein TXNRD3 supports male fertility via the redox regulation of spermatogenesis](https://pmc.ncbi.nlm.nih.gov/articles/PMC9352919/)
    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