Component

Viability of the 2017 mammalian allicin cell-line panel

Viability of the 2017 mammalian allicin cell-line panel. Interpret through the linked study species, preparation, exposure and measured endpoint.

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. Direct allicin exposure reduced mammalian-cell viability or proliferation in a concentration- and cell-type-dependent manner.

    Experimental context and source evidence
    evidence_access
    Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
    experimental_contrast
    {"intervention": "Allicin concentration series", "comparator": "Matched untreated cells in each model", "endpoint": "Direct allicin exposure reduced mammalian-cell viability or proliferation in a concentration- and cell-type-dependent manner.", "effect_direction": "mixed", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Human A549/HUVEC/HT29/MCF7 and mouse 3T3; separate viability, proliferation and apoptosis assays.
    interpretation_status
    Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
    limitations
    Separate species and endpoints; no cancer-selective clinical efficacy or direct measurement of every GSH species.
    plain_language
    Direct allicin exposure reduced mammalian-cell viability or proliferation in a concentration- and cell-type-dependent manner.
    primary_references
    The Effects of Allicin, a Reactive Sulfur Species from Garlic, on a Selection of Mammalian Cell Lines. | 2016 | DOI 10.3390/antiox6010001 | PMID 28035949 | https://pubmed.ncbi.nlm.nih.gov/28035949/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC5384165/ | https://doi.org/10.3390/antiox6010001
    source_locator
    Reviewed reference lines 53-53; exact primary location described in quoted passage where extracted.

    Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 53–53

    Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human A549/HUVEC/HT29/MCF7 and mouse 3T3; separate viability, proliferation and apoptosis assays. · source_derived_draft · unverified_draft

    **Mammalian injury is context-dependent.** Allicin reduced viability or proliferation and altered thiol-associated fluorescence in a panel including human A549, HUVEC, HT29, and MCF7 cells and mouse 3T3 cells. Sensitivity and apoptotic responses differed. Fluorescence changes are not a complete measurement of every glutathione species. Thiol reactivity does not guarantee selective toxicity to microbes or cancer cells. [Gruhlke 2017](https://pmc.ncbi.nlm.nih.gov/articles/PMC5384165/)
    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.