Component

Glutathione pool in human ARPE-19 cells

Glutathione pool in human ARPE-19 cells. Species, exposure and limitations are retained in each linked claim.

3 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. Mangiferin preserved the glutathione pool during H2O2 exposure.

    Mangiferin → Glutathione pool in human ARPE-19 cells source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/mangiferin-research/38586992.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3568135f9e3471d748a1f42c7ed136800b1cb9d017ebd9aa1522de71b71a72be", "start_char": 0, "end_char": 1792, "text_sha256": "3568135f9e3471d748a1f42c7ed136800b1cb9d017ebd9aa1522de71b71a72be"}
    experimental_model
    Hydrogen-peroxide challenge with pharmacological HO-1 inhibition
    exposure
    Mangiferin before H2O2 exposure
    limitations
    Cell protection is not demonstrated retinal clinical efficacy; GPx isoforms unresolved and expression is not cofactor sufficiency.
    nutrient_topic
    Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
    organism
    Homo sapiens
    plain_language
    A cellular redox buffer was better maintained.
    primary_references
    [mangiferin-p38586992] Activation of Heme Oxygenase-1 by Mangiferin in Human Retinal Pigment Epithelial Cells Contributes to Blocking Oxidative Damage. (2024). https://pubmed.ncbi.nlm.nih.gov/38586992/ DOI: 10.4062/biomolther.2023.175
    tissue_or_cell_type
    ARPE-19 retinal pigment epithelial cells

    Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 601–612

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Hydrogen-peroxide challenge with pharmacological HO-1 inhibition · source_derived_draft · unverified_draft

    ### mangiferin-rpe-gsh Mangiferin preserved the glutathione pool during H2O2 exposure. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A cellular redox buffer was better maintained. organism: Homo sapiens tissue_or_cell_type: ARPE-19 retinal pigment epithelial cells experimental_model: Hydrogen-peroxide challenge with pharmacological HO-1 inhibition limitations: Cell protection is not demonstrated retinal clinical efficacy; GPx isoforms unresolved and expression is not cofactor sufficiency. exposure: Mangiferin before H2O2 exposure evidence_span: {"source_cache": "artifacts/mangiferin-research/38586992.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3568135f9e3471d748a1f42c7ed136800b1cb9d017ebd9aa1522de71b71a72be", "start_char": 0, "end_char": 1792, "text_sha256": "3568135f9e3471d748a1f42c7ed136800b1cb9d017ebd9aa1522de71b71a72be"} [mangiferin-p38586992] Activation of Heme Oxygenase-1 by Mangiferin in Human Retinal Pigment Epithelial Cells Contributes to Blocking Oxidative Damage. (2024). https://pubmed.ncbi.nlm.nih.gov/38586992/ DOI: 10.4062/biomolther.2023.175
    Complete structured claim and evidence

  2. Zeaxanthin increased the measured cellular glutathione pool.

    Dietary (3R,3-prime-R)-zeaxanthin → Glutathione pool in human ARPE-19 cells source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/zeaxanthin-research/24810054.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0f185c805dd5d825445cb40e547b794fbc595388aff6e2d29ac81c2eab8b8348", "start_char": 5813, "end_char": 15716, "text_sha256": "89e6abf1967c10b359cb62d935d5b839cf53acf42576d9db3d463bff9f474e38"}
    experimental_model
    Cell challenge with siRNA and pathway inhibitors
    exposure
    Zeaxanthin commonly 10 micromolar for 24 h; 300 micromolar t-BHP challenge for 6 h; study-specific inhibitors
    limitations
    Pharmacological cell exposures are not dietary concentrations. PI3K/Akt inhibitor evidence is not direct zeaxanthin binding to a kinase. Liposome GSTP1 protection and this cellular GSH-dependent response are different mechanisms.
    nutrient_topic
    Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
    organism
    Human ARPE-19 cell line
    plain_language
    The cells accumulated more glutathione.
    primary_references
    [zeaxanthin-p24810054] Zeaxanthin induces Nrf2-mediated phase II enzymes in protection of cell death. (2014). https://pubmed.ncbi.nlm.nih.gov/24810054/ DOI: 10.1038/cddis.2014.190
    tissue_or_cell_type
    Retinal pigment epithelial model

    Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 431–442

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell challenge with siRNA and pathway inhibitors · source_derived_draft · unverified_draft

    ### zeaxanthin-gsh-pool Zeaxanthin increased the measured cellular glutathione pool. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The cells accumulated more glutathione. organism: Human ARPE-19 cell line tissue_or_cell_type: Retinal pigment epithelial model experimental_model: Cell challenge with siRNA and pathway inhibitors limitations: Pharmacological cell exposures are not dietary concentrations. PI3K/Akt inhibitor evidence is not direct zeaxanthin binding to a kinase. Liposome GSTP1 protection and this cellular GSH-dependent response are different mechanisms. exposure: Zeaxanthin commonly 10 micromolar for 24 h; 300 micromolar t-BHP challenge for 6 h; study-specific inhibitors evidence_span: {"source_cache": "artifacts/zeaxanthin-research/24810054.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0f185c805dd5d825445cb40e547b794fbc595388aff6e2d29ac81c2eab8b8348", "start_char": 5813, "end_char": 15716, "text_sha256": "89e6abf1967c10b359cb62d935d5b839cf53acf42576d9db3d463bff9f474e38"} [zeaxanthin-p24810054] Zeaxanthin induces Nrf2-mediated phase II enzymes in protection of cell death. (2014). https://pubmed.ncbi.nlm.nih.gov/24810054/ DOI: 10.1038/cddis.2014.190
    Complete structured claim and evidence

  3. Nrf2 knockdown suppressed zeaxanthin-induced glutathione accumulation.

    Experimental human NFE2L2 knockdown → Glutathione pool in human ARPE-19 cells source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/zeaxanthin-research/24810054.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0f185c805dd5d825445cb40e547b794fbc595388aff6e2d29ac81c2eab8b8348", "start_char": 5813, "end_char": 15716, "text_sha256": "89e6abf1967c10b359cb62d935d5b839cf53acf42576d9db3d463bff9f474e38"}
    experimental_model
    Cell challenge with siRNA and pathway inhibitors
    exposure
    Zeaxanthin commonly 10 micromolar for 24 h; 300 micromolar t-BHP challenge for 6 h; study-specific inhibitors
    limitations
    Pharmacological cell exposures are not dietary concentrations. PI3K/Akt inhibitor evidence is not direct zeaxanthin binding to a kinase. Liposome GSTP1 protection and this cellular GSH-dependent response are different mechanisms.
    nutrient_topic
    Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
    organism
    Human ARPE-19 cell line
    plain_language
    Adding pigment could not fully replace the missing regulatory machinery.
    primary_references
    [zeaxanthin-p24810054] Zeaxanthin induces Nrf2-mediated phase II enzymes in protection of cell death. (2014). https://pubmed.ncbi.nlm.nih.gov/24810054/ DOI: 10.1038/cddis.2014.190
    tissue_or_cell_type
    Retinal pigment epithelial model
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 444–455

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell challenge with siRNA and pathway inhibitors · source_derived_draft · unverified_draft

    ### zeaxanthin-nrf2-failure Nrf2 knockdown suppressed zeaxanthin-induced glutathione accumulation. Condition category: machinery_impairment nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Adding pigment could not fully replace the missing regulatory machinery. organism: Human ARPE-19 cell line tissue_or_cell_type: Retinal pigment epithelial model experimental_model: Cell challenge with siRNA and pathway inhibitors limitations: Pharmacological cell exposures are not dietary concentrations. PI3K/Akt inhibitor evidence is not direct zeaxanthin binding to a kinase. Liposome GSTP1 protection and this cellular GSH-dependent response are different mechanisms. exposure: Zeaxanthin commonly 10 micromolar for 24 h; 300 micromolar t-BHP challenge for 6 h; study-specific inhibitors evidence_span: {"source_cache": "artifacts/zeaxanthin-research/24810054.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0f185c805dd5d825445cb40e547b794fbc595388aff6e2d29ac81c2eab8b8348", "start_char": 5813, "end_char": 15716, "text_sha256": "89e6abf1967c10b359cb62d935d5b839cf53acf42576d9db3d463bff9f474e38"} [zeaxanthin-p24810054] Zeaxanthin induces Nrf2-mediated phase II enzymes in protection of cell death. (2014). https://pubmed.ncbi.nlm.nih.gov/24810054/ DOI: 10.1038/cddis.2014.190
    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.

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