Component

Erythrocyte glutathione reductase activation coefficient / EGRAC

Measured process or biological entity; consult each linked claim for the experimental scope.

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 acts on it

  1. In G6PD-deficient erythrocytes, glutathione reductase was usually already FAD-saturated despite evidence of low FMN-dependent oxidase activity.

    Glucose-6-phosphate dehydrogenase / G6PD → Erythrocyte glutathione reductase activation coefficient / EGRAC source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    cross_nutrient
    G6PD genotype and distinct flavin pools alter interpretation of B2/B6-linked assays.
    experimental_model
    Human erythrocytes from G6PD deficiency, heterozygous beta-thalassemia and controls.
    exposure
    In-vitro FAD stimulation of glutathione reductase and PNP oxidase activity, with oral-riboflavin response observations.
    limitations
    Human red-cell observation; the proposed faster FMN-to-FAD flux was an interpretation, not a directly measured universal mechanism.
    nutrient_topic
    Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
    organism
    Homo sapiens
    plain_language
    A red-cell FAD saturation test can look adequate while another B2-dependent enzyme system is poorly supplied.
    primary_references
    [b2-anderson1987] Glutathione reductase activity and its relationship to pyridoxine phosphate activity in G6PD deficiency (1987). https://pubmed.ncbi.nlm.nih.gov/3582603/ DOI: 10.1111/j.1600-0609.1987.tb01417.x
    tissue_or_cell_type
    Human clinical setting
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1666–1677

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human erythrocytes from G6PD deficiency, heterozygous beta-thalassemia and controls. · source_derived_draft · unverified_draft

    ### b2-g6pd-fad-assay-limit In G6PD-deficient erythrocytes, glutathione reductase was usually already FAD-saturated despite evidence of low FMN-dependent oxidase activity. Condition category: biomarker_context nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A red-cell FAD saturation test can look adequate while another B2-dependent enzyme system is poorly supplied. organism: Homo sapiens tissue_or_cell_type: Human clinical setting experimental_model: Human erythrocytes from G6PD deficiency, heterozygous beta-thalassemia and controls. limitations: Human red-cell observation; the proposed faster FMN-to-FAD flux was an interpretation, not a directly measured universal mechanism. exposure: In-vitro FAD stimulation of glutathione reductase and PNP oxidase activity, with oral-riboflavin response observations. cross_nutrient: G6PD genotype and distinct flavin pools alter interpretation of B2/B6-linked assays. [b2-anderson1987] Glutathione reductase activity and its relationship to pyridoxine phosphate activity in G6PD deficiency (1987). https://pubmed.ncbi.nlm.nih.gov/3582603/ DOI: 10.1111/j.1600-0609.1987.tb01417.x
    Complete structured claim and evidence

  2. Infants of supplemented mothers had lower activation coefficients; maternal and infant values rose toward placebo levels after supplement withdrawal.

    Human milk riboflavin concentration → Erythrocyte glutathione reductase activation coefficient / EGRAC source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    experimental_model
    Double-blind controlled trial in 60 lactating women from two Gambian villages and their infants.
    exposure
    Maternal 2 mg/day riboflavin or placebo for 12 weeks; background intake about 0.5 mg/day; supplementation-withdrawal observations.
    limitations
    Supports maternal-infant supply responsiveness; not proof of a developmental benefit or an independently measured transport mechanism.
    nutrient_topic
    Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
    organism
    Homo sapiens
    plain_language
    The infant marker improved while maternal B2 was supplied and worsened again after it stopped.
    primary_references
    [b2-bates1982] Riboflavin requirements of lactating Gambian women: a controlled supplementation trial (1982). https://pubmed.ncbi.nlm.nih.gov/7072623/ DOI: 10.1093/ajcn/35.4.701
    tissue_or_cell_type
    Infant erythrocytes in maternal lactation trial
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1777–1787

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind controlled trial in 60 lactating women from two Gambian villages and their infants. · source_derived_draft · unverified_draft

    ### b2-milk-infant-marker-response Infants of supplemented mothers had lower activation coefficients; maternal and infant values rose toward placebo levels after supplement withdrawal. Condition category: nutrient_deficiency nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The infant marker improved while maternal B2 was supplied and worsened again after it stopped. organism: Homo sapiens tissue_or_cell_type: Infant erythrocytes in maternal lactation trial experimental_model: Double-blind controlled trial in 60 lactating women from two Gambian villages and their infants. limitations: Supports maternal-infant supply responsiveness; not proof of a developmental benefit or an independently measured transport mechanism. exposure: Maternal 2 mg/day riboflavin or placebo for 12 weeks; background intake about 0.5 mg/day; supplementation-withdrawal observations. [b2-bates1982] Riboflavin requirements of lactating Gambian women: a controlled supplementation trial (1982). https://pubmed.ncbi.nlm.nih.gov/7072623/ DOI: 10.1093/ajcn/35.4.701
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Maternal supplementation increased breast-milk riboflavin and improved maternal status compared with placebo in the Gambian lactation trial.

    Riboflavin (vitamin B2) → Human milk riboflavin concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    experimental_model
    Double-blind controlled trial in 60 lactating women from two Gambian villages and their infants.
    exposure
    Maternal 2 mg/day riboflavin or placebo for 12 weeks; background intake about 0.5 mg/day; supplementation-withdrawal observations.
    limitations
    Nutritionally constrained population; no direct mammary transporter assay in this trial.
    nutrient_topic
    Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
    organism
    Homo sapiens
    plain_language
    The mother’s B2 supply affected the vitamin delivered in milk.
    primary_references
    [b2-bates1982] Riboflavin requirements of lactating Gambian women: a controlled supplementation trial (1982). https://pubmed.ncbi.nlm.nih.gov/7072623/ DOI: 10.1093/ajcn/35.4.701
    tissue_or_cell_type
    Maternal blood and human milk
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1765–1775

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind controlled trial in 60 lactating women from two Gambian villages and their infants. · source_derived_draft · unverified_draft

    ### b2-maternal-milk-response Maternal supplementation increased breast-milk riboflavin and improved maternal status compared with placebo in the Gambian lactation trial. Condition category: nutrient_deficiency nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The mother’s B2 supply affected the vitamin delivered in milk. organism: Homo sapiens tissue_or_cell_type: Maternal blood and human milk experimental_model: Double-blind controlled trial in 60 lactating women from two Gambian villages and their infants. limitations: Nutritionally constrained population; no direct mammary transporter assay in this trial. exposure: Maternal 2 mg/day riboflavin or placebo for 12 weeks; background intake about 0.5 mg/day; supplementation-withdrawal observations. [b2-bates1982] Riboflavin requirements of lactating Gambian women: a controlled supplementation trial (1982). https://pubmed.ncbi.nlm.nih.gov/7072623/ DOI: 10.1093/ajcn/35.4.701
    Complete structured claim and evidence

  2. Erythrocyte PPO activity and its activation coefficient responded to B2 supplementation and correlated with EGRAC; enzyme activity showed a dose response.

    Riboflavin (vitamin B2) → Erythrocyte pyridoxamine/pyridoxine phosphate oxidase activity source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    cross_nutrient
    A B6-activation enzyme provides a B2-sensitive functional assay.
    experimental_model
    Assay-development study using hemolysates from the RIBOFEM riboflavin intervention; same trial registration ISRCTN35811298.
    exposure
    Erythrocyte PPO activity with/without flavin activation; 2 and 4 mg/day supplementation arms. Not independent replication of RIBOFEM.
    limitations
    Assay-development analysis shares samples with RIBOFEM; not independent replication. Proposed utility in G6PD deficiency requires population-specific validation.
    nutrient_topic
    Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
    organism
    Homo sapiens
    plain_language
    An enzyme used to activate B6 can also reveal aspects of B2 status because it needs an FMN cofactor.
    primary_references
    [b2-mushtaq2009] Erythrocyte pyridoxamine phosphate oxidase activity: a potential biomarker of riboflavin status? (2009). https://pubmed.ncbi.nlm.nih.gov/19740970/ DOI: 10.3945/ajcn.2009.28338
    tissue_or_cell_type
    Human clinical setting
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1653–1664

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Assay-development study using hemolysates from the RIBOFEM riboflavin intervention; same trial registration ISRCTN35811298. · source_derived_draft · unverified_draft

    ### b2-ppo-biomarker-response Erythrocyte PPO activity and its activation coefficient responded to B2 supplementation and correlated with EGRAC; enzyme activity showed a dose response. Condition category: biomarker_context nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: An enzyme used to activate B6 can also reveal aspects of B2 status because it needs an FMN cofactor. organism: Homo sapiens tissue_or_cell_type: Human clinical setting experimental_model: Assay-development study using hemolysates from the RIBOFEM riboflavin intervention; same trial registration ISRCTN35811298. limitations: Assay-development analysis shares samples with RIBOFEM; not independent replication. Proposed utility in G6PD deficiency requires population-specific validation. exposure: Erythrocyte PPO activity with/without flavin activation; 2 and 4 mg/day supplementation arms. Not independent replication of RIBOFEM. cross_nutrient: A B6-activation enzyme provides a B2-sensitive functional assay. [b2-mushtaq2009] Erythrocyte pyridoxamine phosphate oxidase activity: a potential biomarker of riboflavin status? (2009). https://pubmed.ncbi.nlm.nih.gov/19740970/ DOI: 10.3945/ajcn.2009.28338
    Complete structured claim and evidence

  3. In RIBOFEM, improvement in B2 status correlated with hemoglobin increase among supplemented women; women with baseline EGRAC >1.65 had the greater hemoglobin response.

    Riboflavin (vitamin B2) → Blood hemoglobin concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    Riboflavin status modifies iron-related hematologic outcomes.
    experimental_model
    RIBOFEM: 123 UK women aged 19-25 randomized with EGRAC >1.40; 119 completed, 117 analyzed after two exclusions; iron-absorption subset 34.
    exposure
    Placebo, 2 or 4 mg/day riboflavin for eight weeks; historical trial regimens.
    limitations
    Baseline-tertile and response associations should not be restated as a uniform hemoglobin benefit in every randomized participant.
    nutrient_topic
    Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
    organism
    Homo sapiens
    plain_language
    Women with poorer starting B2 status tended to gain more hemoglobin when their B2 status improved.
    primary_references
    [b2-powers2011] Correcting a marginal riboflavin deficiency improves hematologic status in young women in the United Kingdom (RIBOFEM) (2011). https://pubmed.ncbi.nlm.nih.gov/21525198/ DOI: 10.3945/ajcn.110.008409
    tissue_or_cell_type
    Human clinical setting
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1552–1563

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · RIBOFEM: 123 UK women aged 19-25 randomized with EGRAC >1.40; 119 completed, 117 analyzed after two exclusions; iron-absorption subset 34. · source_derived_draft · unverified_draft

    ### b2-ribofem-hemoglobin In RIBOFEM, improvement in B2 status correlated with hemoglobin increase among supplemented women; women with baseline EGRAC >1.65 had the greater hemoglobin response. Condition category: nutrient_deficiency nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Women with poorer starting B2 status tended to gain more hemoglobin when their B2 status improved. organism: Homo sapiens tissue_or_cell_type: Human clinical setting experimental_model: RIBOFEM: 123 UK women aged 19-25 randomized with EGRAC >1.40; 119 completed, 117 analyzed after two exclusions; iron-absorption subset 34. limitations: Baseline-tertile and response associations should not be restated as a uniform hemoglobin benefit in every randomized participant. exposure: Placebo, 2 or 4 mg/day riboflavin for eight weeks; historical trial regimens. cross_nutrient: Riboflavin status modifies iron-related hematologic outcomes. [b2-powers2011] Correcting a marginal riboflavin deficiency improves hematologic status in young women in the United Kingdom (RIBOFEM) (2011). https://pubmed.ncbi.nlm.nih.gov/21525198/ DOI: 10.3945/ajcn.110.008409
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

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