Component

Glutathione redox readout in SAC-treated human colonic cells

Context-specific entity; species, compartment and exposure are stated on each claim.

1 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. The study reported an improved glutathione-related redox ratio with SAC during PhIP exposure.

    Experimental context and source evidence
    acting_entity
    s-allylcysteine
    dose
    Not specified in accessed abstract
    duration
    Not specified in accessed abstract
    evidence_access
    Primary abstract
    experimental_comparison
    SAC with PhIP challenge and corresponding cell controls
    experimental_model
    Normal human colonic mucosal epithelial cells exposed to PhIP
    interpretation_status
    Source-derived research curation; not independent primary verification
    limitations
    The abstract describes the ratio ambiguously as GSH to GSH/GSSG; exact numerator/denominator require full-text clarification. No cysteine donation is inferred.
    nutrient_topic
    S-allylcysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · S-allyl-L-cysteine / SAC
    organism
    Homo sapiens
    plain_language
    The glutathione readout is retained without inventing a precursor flux.
    primary_references
    [35753083] S-Allylcysteine Potently Protects against PhIP-Induced DNA Damage via Nrf2/AhR Signaling Pathway Modulation in Normal Human Colonic Mucosal Epithelial Cells. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35753083/ · DOI 10.1002/mnfr.202101141
    route
    Cell culture
    tissue_or_cell_type
    Normal human colonic mucosal epithelial cells exposed to PhIP

    S-allylcysteine: sulfur signaling, redox responses and cross-nutrient mechanisms (2026-09-20) · lines 176–183

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Normal human colonic mucosal epithelial cells exposed to PhIP · source_derived_draft · unverified_draft

    ## s-allylcysteine-colon-redox The glutathione readout is retained without inventing a precursor flux. The study reported an improved glutathione-related redox ratio with SAC during PhIP exposure. Model: Normal human colonic mucosal epithelial cells exposed to PhIP Limitations: The abstract describes the ratio ambiguously as GSH to GSH/GSSG; exact numerator/denominator require full-text clarification. No cysteine donation is inferred. Evidence access: Primary abstract [35753083] S-Allylcysteine Potently Protects against PhIP-Induced DNA Damage via Nrf2/AhR Signaling Pathway Modulation in Normal Human Colonic Mucosal Epithelial Cells. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35753083/ · DOI 10.1002/mnfr.202101141 Structured context: {"organism": "Homo sapiens", "tissue_or_cell_type": "Normal human colonic mucosal epithelial cells exposed to PhIP", "dose": "Not specified in accessed abstract", "duration": "Not specified in accessed abstract", "route": "Cell culture", "experimental_comparison": "SAC with PhIP challenge and corresponding cell controls", "acting_entity": "s-allylcysteine", "interpretation_status": "Source-derived research curation; not independent primary verification"}
    Complete structured claim and evidence

In the sources

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    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