Component
Apoptosis in SAC-treated HCC827/NCI-H1975 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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What acts on it
SAC at 20 mM for 72 hours increased apoptosis in the tested lung cancer cells.
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
- A cell-death endpoint is not a demonstrated cancer treatment in humans.
- nutrient_topic
- S-allylcysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · S-allyl-L-cysteine / SAC
- organism
- Homo sapiens
- plain_language
- Cell death was measured alongside signaling changes.
- 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 329–336
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-apoptosis Cell death was measured alongside signaling changes. SAC at 20 mM for 72 hours increased apoptosis in the tested lung cancer cells. Model: HCC827 and NCI-H1975 lung cancer cells Limitations: A cell-death endpoint is not a demonstrated cancer treatment in humans. 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
The events it takes part in
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Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
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Open hypotheses
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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.