Component

Ascorbyl radical reduction to ascorbate

Ascorbyl radical reduction to ascorbate

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. Rat liver microsomes reduced ascorbyl radical using NADH, and this activity was insensitive to selenium depletion.

    NADH → Ascorbyl radical reduction to ascorbate source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    true
    experimental_model
    Purified rat liver enzyme, dialyzed cytosol and microsomes from control/selenium-deficient rats
    exposure
    Control and selenium-deficient rat liver microsome assays
    limitations
    Responsible microsomal enzyme was not established in the abstract; do not assign the activity to TXNRD1.
    nutrient_topic
    Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C
    organism
    Rattus norvegicus
    plain_language
    A membrane-associated recycling route remained active despite selenium shortage.
    primary_references
    [may1998] Reduction of the ascorbyl free radical to ascorbate by thioredoxin reductase. (1998). https://pubmed.ncbi.nlm.nih.gov/9722529/ DOI: 10.1074/jbc.273.36.23039
    tissue_or_cell_type
    Liver microsomal fraction
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 442–453

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified rat liver enzyme, dialyzed cytosol and microsomes from control/selenium-deficient rats · source_derived_draft · unverified_draft

    ### vc-transport-microsomal-radical Rat liver microsomes reduced ascorbyl radical using NADH, and this activity was insensitive to selenium depletion. Condition category: nutrient_deficiency nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: A membrane-associated recycling route remained active despite selenium shortage. organism: Rattus norvegicus tissue_or_cell_type: Liver microsomal fraction experimental_model: Purified rat liver enzyme, dialyzed cytosol and microsomes from control/selenium-deficient rats limitations: Responsible microsomal enzyme was not established in the abstract; do not assign the activity to TXNRD1. exposure: Control and selenium-deficient rat liver microsome assays cross_nutrient: true [may1998] Reduction of the ascorbyl free radical to ascorbate by thioredoxin reductase. (1998). https://pubmed.ncbi.nlm.nih.gov/9722529/ DOI: 10.1074/jbc.273.36.23039
    Complete structured claim and evidence
  2. Dialyzed liver cytosol from selenium-deficient rats lost NADPH-dependent ascorbyl-radical reducing activity attributed to thioredoxin reductase.

    Selenium → Ascorbyl radical reduction to ascorbate source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    true
    experimental_model
    Purified rat liver enzyme, dialyzed cytosol and microsomes from control/selenium-deficient rats
    exposure
    Dietary selenium depletion; isolated dialyzed cytosol
    limitations
    Activity assignment also used inhibitor sensitivity; this is a fraction assay, not a direct human outcome.
    nutrient_topic
    Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C
    organism
    Rattus norvegicus
    plain_language
    Selenium deficiency impaired radical recycling in the rat liver’s soluble fraction.
    primary_references
    [may1998] Reduction of the ascorbyl free radical to ascorbate by thioredoxin reductase. (1998). https://pubmed.ncbi.nlm.nih.gov/9722529/ DOI: 10.1074/jbc.273.36.23039
    tissue_or_cell_type
    Liver cytosol
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 429–440

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified rat liver enzyme, dialyzed cytosol and microsomes from control/selenium-deficient rats · source_derived_draft · unverified_draft

    ### vc-transport-selenium-cytosolic-radical Dialyzed liver cytosol from selenium-deficient rats lost NADPH-dependent ascorbyl-radical reducing activity attributed to thioredoxin reductase. Condition category: nutrient_deficiency nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: Selenium deficiency impaired radical recycling in the rat liver’s soluble fraction. organism: Rattus norvegicus tissue_or_cell_type: Liver cytosol experimental_model: Purified rat liver enzyme, dialyzed cytosol and microsomes from control/selenium-deficient rats limitations: Activity assignment also used inhibitor sensitivity; this is a fraction assay, not a direct human outcome. exposure: Dietary selenium depletion; isolated dialyzed cytosol cross_nutrient: true [may1998] Reduction of the ascorbyl free radical to ascorbate by thioredoxin reductase. (1998). https://pubmed.ncbi.nlm.nih.gov/9722529/ DOI: 10.1074/jbc.273.36.23039
    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