Component

Lipid oxidative damage in SAC-treated lung cancer 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. SAC at 20 mM for 72 hours increased lipid oxidative damage in both tested lung cancer lines.

    Experimental context and source evidence
    acting_entity
    s-allylcysteine
    dose
    10 or 20 mM SAC; mechanistic endpoints 20 mM
    duration
    24, 48 or 72 hours; mechanistic endpoints 72 hours
    evidence_access
    Primary abstract
    experimental_comparison
    SAC; BEAS-2B and A549 comparator cell lines also studied
    experimental_model
    HCC827 and NCI-H1975 lung cancer cells
    interpretation_status
    Source-derived research curation; not independent primary verification
    limitations
    Does not establish that usual dietary exposure produces this tissue concentration.
    nutrient_topic
    S-allylcysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · S-allyl-L-cysteine / SAC
    organism
    Homo sapiens
    plain_language
    Oxidative injury increased under this exposure.
    primary_references
    [33136700] S-allylcysteine induces cytotoxic effects in two human lung cancer cell lines via induction of oxidative damage, downregulation of Nrf2 and NF-κB, and apoptosis. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33136700/ · DOI 10.1097/CAD.0000000000001015
    route
    Cell culture
    tissue_or_cell_type
    HCC827 and NCI-H1975 lung cancer cells

    S-allylcysteine: sulfur signaling, redox responses and cross-nutrient mechanisms (2026-09-20) · lines 320–327

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · HCC827 and NCI-H1975 lung cancer cells · source_derived_draft · unverified_draft

    ## s-allylcysteine-lung-oxidative-injury Oxidative injury increased under this exposure. SAC at 20 mM for 72 hours increased lipid oxidative damage in both tested lung cancer lines. Model: HCC827 and NCI-H1975 lung cancer cells Limitations: Does not establish that usual dietary exposure produces this tissue concentration. Evidence access: Primary abstract [33136700] S-allylcysteine induces cytotoxic effects in two human lung cancer cell lines via induction of oxidative damage, downregulation of Nrf2 and NF-κB, and apoptosis. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33136700/ · DOI 10.1097/CAD.0000000000001015 Structured context: {"organism": "Homo sapiens", "tissue_or_cell_type": "HCC827 and NCI-H1975 lung cancer cells", "dose": "10 or 20 mM SAC; mechanistic endpoints 20 mM", "duration": "24, 48 or 72 hours; mechanistic endpoints 72 hours", "route": "Cell culture", "experimental_comparison": "SAC; BEAS-2B and A549 comparator cell lines also studied", "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