Component

Human Nrf2 nuclear accumulation

Human Nrf2 nuclear accumulation. Species, exposure and limitations are retained in each linked claim.

2 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 increased nuclear Nrf2 accumulation.

    Mangiferin → Human Nrf2 nuclear accumulation source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/mangiferin-research/25380307.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "057a534a2074c49c824120d8e49fba7f4bde4d9d9b8bf15ef78f994083fdc8ea", "start_char": 0, "end_char": 1636, "text_sha256": "057a534a2074c49c824120d8e49fba7f4bde4d9d9b8bf15ef78f994083fdc8ea"}
    experimental_model
    Isolated human cord-blood mononuclear cells
    exposure
    Mangiferin and etoposide; concentration not specified in indexed abstract
    limitations
    Ex vivo DNA-damage and signaling assays; not evidence of clinical chemotherapy protection.
    nutrient_topic
    Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
    organism
    Homo sapiens
    plain_language
    More of the regulator reached the nuclear compartment.
    primary_references
    [mangiferin-p25380307] Mangiferin activates the Nrf2-ARE pathway and reduces etoposide-induced DNA damage in human umbilical cord mononuclear blood cells. (2015). https://pubmed.ncbi.nlm.nih.gov/25380307/ DOI: 10.3109/13880209.2014.927890
    tissue_or_cell_type
    Cord-blood mononuclear cells

    Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 562–573

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated human cord-blood mononuclear cells · source_derived_draft · unverified_draft

    ### mangiferin-nrf2-nuclear Mangiferin increased nuclear Nrf2 accumulation. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: More of the regulator reached the nuclear compartment. organism: Homo sapiens tissue_or_cell_type: Cord-blood mononuclear cells experimental_model: Isolated human cord-blood mononuclear cells limitations: Ex vivo DNA-damage and signaling assays; not evidence of clinical chemotherapy protection. exposure: Mangiferin and etoposide; concentration not specified in indexed abstract evidence_span: {"source_cache": "artifacts/mangiferin-research/25380307.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "057a534a2074c49c824120d8e49fba7f4bde4d9d9b8bf15ef78f994083fdc8ea", "start_char": 0, "end_char": 1636, "text_sha256": "057a534a2074c49c824120d8e49fba7f4bde4d9d9b8bf15ef78f994083fdc8ea"} [mangiferin-p25380307] Mangiferin activates the Nrf2-ARE pathway and reduces etoposide-induced DNA damage in human umbilical cord mononuclear blood cells. (2015). https://pubmed.ncbi.nlm.nih.gov/25380307/ DOI: 10.3109/13880209.2014.927890
    Complete structured claim and evidence

  2. Zeaxanthin increased nuclear Nrf2 in ARPE-19 cells.

    Dietary (3R,3-prime-R)-zeaxanthin → Human Nrf2 nuclear accumulation 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
    It activated part of the cell’s own defense response.
    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 366–377

    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-location Zeaxanthin increased nuclear Nrf2 in ARPE-19 cells. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: It activated part of the cell’s own defense response. 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.

    Evidence, AI assistance and curation standards