Component

Fetal blood ascorbate concentration

Fetal blood ascorbate concentration

1 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. Maternal prenatal ascorbic-acid supplementation did not raise fetal blood ascorbate in SVCT2-null mouse fetuses.

    L-Ascorbate → Fetal blood ascorbate concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    SVCT2-null mouse embryos, newborns and embryonic fibroblasts
    exposure
    Prenatal maternal supplementation with SVCT2-null fetuses
    limitations
    Supports a placental transport role but is not a placenta-specific deletion; dose is not resolved in the accessible abstract.
    nutrient_topic
    Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C
    organism
    Mus musculus
    plain_language
    Increasing maternal supply did not overcome the fetus’s missing SVCT2 machinery.
    primary_references
    [sotiriou2002] Ascorbic-acid transporter Slc23a1 is essential for vitamin C transport into the brain and for perinatal survival. (2002). https://pubmed.ncbi.nlm.nih.gov/11984597/ DOI: 10.1038/0502-514
    tissue_or_cell_type
    Placenta/fetal blood
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 234–245

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · SVCT2-null mouse embryos, newborns and embryonic fibroblasts · source_derived_draft · unverified_draft

    ### vc-transport-svct2-prenatal-nonrescue Maternal prenatal ascorbic-acid supplementation did not raise fetal blood ascorbate in SVCT2-null mouse fetuses. Condition category: machinery_impairment nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: Increasing maternal supply did not overcome the fetus’s missing SVCT2 machinery. organism: Mus musculus tissue_or_cell_type: Placenta/fetal blood experimental_model: SVCT2-null mouse embryos, newborns and embryonic fibroblasts limitations: Supports a placental transport role but is not a placenta-specific deletion; dose is not resolved in the accessible abstract. exposure: Prenatal maternal supplementation with SVCT2-null fetuses cross_nutrient: false [sotiriou2002] Ascorbic-acid transporter Slc23a1 is essential for vitamin C transport into the brain and for perinatal survival. (2002). https://pubmed.ncbi.nlm.nih.gov/11984597/ DOI: 10.1038/0502-514
    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