Component

Human glutathione S-transferase A1

Human glutathione S-transferase A1. Species, exposure and limitations are retained in each linked claim.

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 it acts on

  1. GSTA1 showed only low-affinity xanthophyll binding in the comparison.

    Human glutathione S-transferase A1 → Dietary (3R,3-prime-R)-zeaxanthin source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/zeaxanthin-research/15355982.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6365b1d54aafda71be4dbf6c8e5252fa6ce0af3b808d9af6fe07c37ae188ea92", "start_char": 0, "end_char": 1907, "text_sha256": "6365b1d54aafda71be4dbf6c8e5252fa6ce0af3b808d9af6fe07c37ae188ea92"}
    experimental_model
    Human macular protein purification and recombinant binding
    exposure
    Equilibrium binding and immunocytochemistry
    limitations
    Binding affinity is assay-specific and does not quantify uptake or clinical benefit.
    nutrient_topic
    Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
    organism
    Human tissue/proteins
    plain_language
    Membership in the GST family does not guarantee selective binding.
    primary_references
    [zeaxanthin-p15355982] Identification and characterization of a Pi isoform of glutathione S-transferase (GSTP1) as a zeaxanthin-binding protein in the macula of the human eye. (2004). https://pubmed.ncbi.nlm.nih.gov/15355982/ DOI: 10.1074/jbc.m405334200
    tissue_or_cell_type
    Macula and purified proteins

    Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 236–247

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human macular protein purification and recombinant binding · source_derived_draft · unverified_draft

    ### zeaxanthin-gsta1-low GSTA1 showed only low-affinity xanthophyll binding in the comparison. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Membership in the GST family does not guarantee selective binding. organism: Human tissue/proteins tissue_or_cell_type: Macula and purified proteins experimental_model: Human macular protein purification and recombinant binding limitations: Binding affinity is assay-specific and does not quantify uptake or clinical benefit. exposure: Equilibrium binding and immunocytochemistry evidence_span: {"source_cache": "artifacts/zeaxanthin-research/15355982.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6365b1d54aafda71be4dbf6c8e5252fa6ce0af3b808d9af6fe07c37ae188ea92", "start_char": 0, "end_char": 1907, "text_sha256": "6365b1d54aafda71be4dbf6c8e5252fa6ce0af3b808d9af6fe07c37ae188ea92"} [zeaxanthin-p15355982] Identification and characterization of a Pi isoform of glutathione S-transferase (GSTP1) as a zeaxanthin-binding protein in the macula of the human eye. (2004). https://pubmed.ncbi.nlm.nih.gov/15355982/ DOI: 10.1074/jbc.m405334200
    Complete structured claim and evidence

What acts on it

  1. No significant GSTA1 transcriptional increase was detected in the phytochemical comparisons including DIM.

    3,3'-Diindolylmethane / DIM → Human glutathione S-transferase A1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/dim-research/15672752.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ccf97f305e0f4d5b98b172cef3a0875729e44b8f65420d87a6d725ec7207ca63", "start_char": 0, "end_char": 1560, "text_sha256": "ccf97f305e0f4d5b98b172cef3a0875729e44b8f65420d87a6d725ec7207ca63"}
    experimental_model
    Quantitative gene expression and protein assessment
    exposure
    DIM 10-50 micromolar
    limitations
    Cell-culture concentrations; fold mRNA induction is not the fold change in drug clearance in people.
    nutrient_topic
    Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. · 3,3'-Diindolylmethane / DIM
    organism
    Primary human hepatocytes
    plain_language
    An enzyme response does not imply that every detoxification pathway rises together.
    primary_references
    [dim-p15672752] Phytochemical-induced changes in gene expression of carcinogen-metabolizing enzymes in cultured human primary hepatocytes. (2004). https://pubmed.ncbi.nlm.nih.gov/15672752/ DOI: 10.1080/00498250412331285481
    tissue_or_cell_type
    CYP and phase-II enzyme expression

    Diindolylmethane (DIM): formation, receptor signaling, metabolism and drug interactions (2026-09-17) · lines 415–426

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Quantitative gene expression and protein assessment · source_derived_draft · unverified_draft

    ### dim-hepatocyte-gsta1-null No significant GSTA1 transcriptional increase was detected in the phytochemical comparisons including DIM. Condition category: normal nutrient_topic: Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. plain_language: An enzyme response does not imply that every detoxification pathway rises together. organism: Primary human hepatocytes tissue_or_cell_type: CYP and phase-II enzyme expression experimental_model: Quantitative gene expression and protein assessment limitations: Cell-culture concentrations; fold mRNA induction is not the fold change in drug clearance in people. exposure: DIM 10-50 micromolar evidence_span: {"source_cache": "artifacts/dim-research/15672752.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ccf97f305e0f4d5b98b172cef3a0875729e44b8f65420d87a6d725ec7207ca63", "start_char": 0, "end_char": 1560, "text_sha256": "ccf97f305e0f4d5b98b172cef3a0875729e44b8f65420d87a6d725ec7207ca63"} [dim-p15672752] Phytochemical-induced changes in gene expression of carcinogen-metabolizing enzymes in cultured human primary hepatocytes. (2004). https://pubmed.ncbi.nlm.nih.gov/15672752/ DOI: 10.1080/00498250412331285481
    Complete structured claim and evidence

  2. Parallel differentiated Caco-2 experiments assigned GSTA1 induction to sulforaphane; perfusion with mixed extract increased GSTA1 mRNA 2.0-fold.

    Sulforaphane / SFN, stereochemistry specified per study → Human glutathione S-transferase A1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/sulforaphane-research/12756216.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "98a56e8d1e84bffe3a4213eb3619d52869f85d999355d0e0f487d412149101af", "start_char": 0, "end_char": 1816, "text_sha256": "98a56e8d1e84bffe3a4213eb3619d52869f85d999355d0e0f487d412149101af"}
    experimental_model
    Human jejunal perfusion and parallel Caco-2 experiments
    exposure
    Dietary-concentration onion/broccoli extract perfusion
    limitations
    Human perfusion used a mixture; isolated Caco-2 comparisons help distinguish components. Local permeability is not systemic oral bioavailability.
    nutrient_topic
    Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study
    organism
    Human intestinal segment and human intestinal cell line
    plain_language
    The mixture and the isolated-component experiment provide different levels of attribution.
    primary_references
    [sulforaphane-p12756216] Absorption/metabolism of sulforaphane and quercetin, and regulation of phase II enzymes, in human jejunum in vivo. (2003). https://pubmed.ncbi.nlm.nih.gov/12756216/ DOI: 10.1124/dmd.31.6.805
    tissue_or_cell_type
    Absorption, luminal return and gene expression

    Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 411–422

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human jejunal perfusion and parallel Caco-2 experiments · source_derived_draft · unverified_draft

    ### sulforaphane-gsta1-induction Parallel differentiated Caco-2 experiments assigned GSTA1 induction to sulforaphane; perfusion with mixed extract increased GSTA1 mRNA 2.0-fold. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The mixture and the isolated-component experiment provide different levels of attribution. organism: Human intestinal segment and human intestinal cell line tissue_or_cell_type: Absorption, luminal return and gene expression experimental_model: Human jejunal perfusion and parallel Caco-2 experiments limitations: Human perfusion used a mixture; isolated Caco-2 comparisons help distinguish components. Local permeability is not systemic oral bioavailability. exposure: Dietary-concentration onion/broccoli extract perfusion evidence_span: {"source_cache": "artifacts/sulforaphane-research/12756216.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "98a56e8d1e84bffe3a4213eb3619d52869f85d999355d0e0f487d412149101af", "start_char": 0, "end_char": 1816, "text_sha256": "98a56e8d1e84bffe3a4213eb3619d52869f85d999355d0e0f487d412149101af"} [sulforaphane-p12756216] Absorption/metabolism of sulforaphane and quercetin, and regulation of phase II enzymes, in human jejunum in vivo. (2003). https://pubmed.ncbi.nlm.nih.gov/12756216/ DOI: 10.1124/dmd.31.6.805
    Complete structured claim and evidence

  3. Fisetin reduced GSTA1 mRNA and protein in proliferating human Caco-2 cells.

    Fisetin → Human glutathione S-transferase A1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human colorectal adenocarcinoma cell culture.
    limitations
    Cell state matters; the proposed binding-site location was based on modeling.
    nutrient_topic
    Fisetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Fisetin
    plain_language
    Expression and direct enzyme inhibition are separate observations.
    primary_references
    The Interaction of the Flavonoid Fisetin with Human Glutathione Transferase A1-1. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33806779/ · DOI 10.3390/metabo11030190

    Fisetin: metabolism, cell-state responses and cross-nutrient mechanisms (2026-09-19) · lines 96–102

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human colorectal adenocarcinoma cell culture. · source_derived_draft · unverified_draft

    ## fisetin-gsta1-expression Expression and direct enzyme inhibition are separate observations. Fisetin reduced GSTA1 mRNA and protein in proliferating human Caco-2 cells. Model: Human colorectal adenocarcinoma cell culture. Limitations: Cell state matters; the proposed binding-site location was based on modeling. Evidence access: Primary abstract The Interaction of the Flavonoid Fisetin with Human Glutathione Transferase A1-1. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33806779/ · DOI 10.3390/metabo11030190
    Complete structured claim and evidence

  4. Fisetin reversibly inhibited purified human GSTA1-1 with IC50 1.2 +/- 0.1 micromolar; inhibition was mixed toward glutathione and noncompetitive toward CDNB.

    Fisetin → Human glutathione S-transferase A1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Purified human enzyme kinetics.
    limitations
    CDNB probe assay, not proven human chemosensitization or global detoxification failure.
    nutrient_topic
    Fisetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Fisetin
    plain_language
    A compound that supports a glutathione pool can also inhibit an enzyme using it.
    primary_references
    The Interaction of the Flavonoid Fisetin with Human Glutathione Transferase A1-1. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33806779/ · DOI 10.3390/metabo11030190

    Fisetin: metabolism, cell-state responses and cross-nutrient mechanisms (2026-09-19) · lines 88–94

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Purified human enzyme kinetics. · source_derived_draft · unverified_draft

    ## fisetin-gsta1-inhibition A compound that supports a glutathione pool can also inhibit an enzyme using it. Fisetin reversibly inhibited purified human GSTA1-1 with IC50 1.2 +/- 0.1 micromolar; inhibition was mixed toward glutathione and noncompetitive toward CDNB. Model: Purified human enzyme kinetics. Limitations: CDNB probe assay, not proven human chemosensitization or global detoxification failure. Evidence access: Primary abstract The Interaction of the Flavonoid Fisetin with Human Glutathione Transferase A1-1. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33806779/ · DOI 10.3390/metabo11030190
    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