Component

Dehydroascorbic acid reduction to ascorbate

Dehydroascorbic acid reduction to ascorbate

3 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. During DHA reduction by human erythrocytes, 5 mM D-glucose maintained GSH and NADH concentrations whereas NADPH still declined; without glucose all three fell.

    Experimental context and source evidence
    cross_nutrient
    true
    experimental_model
    Human volunteer erythrocytes ex vivo
    exposure
    DHA challenge with or without 5 mM glucose
    limitations
    Metabolic support and transporter competition are different processes; this does not imply dietary sugar supplementation is needed.
    nutrient_topic
    Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C
    organism
    Homo sapiens
    plain_language
    Glucose metabolism helped sustain the reducing resources used to recycle vitamin C.
    primary_references
    [may2001] Mechanisms of ascorbic acid recycling in human erythrocytes. (2001). https://pubmed.ncbi.nlm.nih.gov/11687303/ DOI: 10.1016/s0304-4165(01)00188-x
    tissue_or_cell_type
    Erythrocytes

    Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 325–336

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human volunteer erythrocytes ex vivo · source_derived_draft · unverified_draft

    ### vc-transport-rbc-glucose-support During DHA reduction by human erythrocytes, 5 mM D-glucose maintained GSH and NADH concentrations whereas NADPH still declined; without glucose all three fell. Condition category: normal nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: Glucose metabolism helped sustain the reducing resources used to recycle vitamin C. organism: Homo sapiens tissue_or_cell_type: Erythrocytes experimental_model: Human volunteer erythrocytes ex vivo limitations: Metabolic support and transporter competition are different processes; this does not imply dietary sugar supplementation is needed. exposure: DHA challenge with or without 5 mM glucose cross_nutrient: true [may2001] Mechanisms of ascorbic acid recycling in human erythrocytes. (2001). https://pubmed.ncbi.nlm.nih.gov/11687303/ DOI: 10.1016/s0304-4165(01)00188-x
    Complete structured claim and evidence
  2. Diethyl maleate depletion of erythrocyte GSH by 75–90% reduced the combined uptake and conversion of DHA to ascorbate in human cells.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    true
    experimental_model
    Human volunteer erythrocytes ex vivo
    exposure
    Up to 1 mM diethyl maleate ex vivo
    limitations
    Chemical depletion, not dietary deficiency; combined uptake/reduction readout does not isolate membrane transport.
    nutrient_topic
    Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C
    organism
    Homo sapiens
    plain_language
    Depleting glutathione impaired the red cells’ vitamin C recycling capacity.
    primary_references
    [may2001] Mechanisms of ascorbic acid recycling in human erythrocytes. (2001). https://pubmed.ncbi.nlm.nih.gov/11687303/ DOI: 10.1016/s0304-4165(01)00188-x
    tissue_or_cell_type
    Erythrocytes
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 338–349

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human volunteer erythrocytes ex vivo · source_derived_draft · unverified_draft

    ### vc-transport-rbc-gsh-depletion Diethyl maleate depletion of erythrocyte GSH by 75–90% reduced the combined uptake and conversion of DHA to ascorbate in human cells. Condition category: machinery_impairment nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: Depleting glutathione impaired the red cells’ vitamin C recycling capacity. organism: Homo sapiens tissue_or_cell_type: Erythrocytes experimental_model: Human volunteer erythrocytes ex vivo limitations: Chemical depletion, not dietary deficiency; combined uptake/reduction readout does not isolate membrane transport. exposure: Up to 1 mM diethyl maleate ex vivo cross_nutrient: true [may2001] Mechanisms of ascorbic acid recycling in human erythrocytes. (2001). https://pubmed.ncbi.nlm.nih.gov/11687303/ DOI: 10.1016/s0304-4165(01)00188-x
    Complete structured claim and evidence
  3. Adding 2.8 µM rat liver thioredoxin lowered apparent DHA Km of the thioredoxin-reductase system from 2.5 to 0.7 mM without materially increasing turnover.

    Experimental context and source evidence
    cross_nutrient
    true
    experimental_model
    Purified rat liver thioredoxin reductase/thioredoxin and selenium-deficient rat liver
    exposure
    2.8 µM thioredoxin added to NADPH/thioredoxin-reductase assay
    limitations
    Apparent kinetic effect is not proof of a faster whole-body recycling rate.
    nutrient_topic
    Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C
    organism
    Rattus norvegicus
    plain_language
    Thioredoxin improved the system’s apparent affinity for oxidized vitamin C in this assay.
    primary_references
    [may1997] Reduction of dehydroascorbate to ascorbate by the selenoenzyme thioredoxin reductase. (1997). https://pubmed.ncbi.nlm.nih.gov/9278416/ DOI: 10.1074/jbc.272.36.22607
    tissue_or_cell_type
    Purified liver enzymes

    Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 390–401

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified rat liver thioredoxin reductase/thioredoxin and selenium-deficient rat liver · source_derived_draft · unverified_draft

    ### vc-transport-thioredoxin-dha-affinity Adding 2.8 µM rat liver thioredoxin lowered apparent DHA Km of the thioredoxin-reductase system from 2.5 to 0.7 mM without materially increasing turnover. Condition category: normal nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: Thioredoxin improved the system’s apparent affinity for oxidized vitamin C in this assay. organism: Rattus norvegicus tissue_or_cell_type: Purified liver enzymes experimental_model: Purified rat liver thioredoxin reductase/thioredoxin and selenium-deficient rat liver limitations: Apparent kinetic effect is not proof of a faster whole-body recycling rate. exposure: 2.8 µM thioredoxin added to NADPH/thioredoxin-reductase assay cross_nutrient: true [may1997] Reduction of dehydroascorbate to ascorbate by the selenoenzyme thioredoxin reductase. (1997). https://pubmed.ncbi.nlm.nih.gov/9278416/ DOI: 10.1074/jbc.272.36.22607
    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