Component

Mouse pain-related behavior after allicin exposure

Mouse pain-related behavior after allicin exposure. Interpret through the linked study species, preparation, exposure and measured endpoint.

2 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. Loss of mouse-trpa1 reduced but did not abolish allicin-evoked pain-related behavior.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    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_condition
    Wild-type with the same allicin exposure deleted · Mouse Trpa1 ion channel Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_condition
    Wild-type with the same allicin exposure present · Allicin Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_contrast
    {"intervention": "mouse-trpa1 deletion with allicin", "comparator": "Wild-type with the same allicin exposure", "endpoint": "Loss of mouse-trpa1 reduced but did not abolish allicin-evoked pain-related behavior.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "mouse-trpa1", "state": "deleted"}, {"entity_slug": "allicin", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Mouse single-gene knockout compared with its wild-type littermate background.
    interpretation_status
    Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
    limitations
    No double-knockout inference; behavioral assay, not proof of human allergy or burns.
    plain_language
    Loss of mouse-trpa1 reduced but did not abolish allicin-evoked pain-related behavior.
    primary_references
    A single N-terminal cysteine in TRPV1 determines activation by pungent compounds from onion and garlic. | 2008 | DOI 10.1038/nn2056 | PMID 18297068 | https://pubmed.ncbi.nlm.nih.gov/18297068/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC4370189/ | https://doi.org/10.1038/nn2056
    source_locator
    Reviewed reference lines 71-71; exact primary location described in quoted passage where extracted.
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 71–71

    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 · Mouse single-gene knockout compared with its wild-type littermate background. · source_derived_draft · unverified_draft

    **Sensory activation.** Experiments identified allicin-dependent activation of TRPA1 and TRPV1. In the later mouse study, allicin stimulated dorsal-root-ganglion neurons and pain-related behavior. Removing either Trpa1 or Trpv1 reduced, but did not abolish, the behavioral response. The channels provide overlapping sensory routes rather than one exclusive receptor. Irritation, chemical burns, and allergic dermatitis are different outcomes. [Macpherson 2005](https://pubmed.ncbi.nlm.nih.gov/15916949/) [Salazar 2008](https://pmc.ncbi.nlm.nih.gov/articles/PMC4370189/)
    Complete structured claim and evidence
  2. Loss of mouse-trpv1 reduced but did not abolish allicin-evoked pain-related behavior.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    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_condition
    Wild-type with the same allicin exposure deleted · Mouse transient receptor potential vanilloid 1 / Trpv1 Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_condition
    Wild-type with the same allicin exposure present · Allicin Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_contrast
    {"intervention": "mouse-trpv1 deletion with allicin", "comparator": "Wild-type with the same allicin exposure", "endpoint": "Loss of mouse-trpv1 reduced but did not abolish allicin-evoked pain-related behavior.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "mouse-trpv1", "state": "deleted"}, {"entity_slug": "allicin", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Mouse single-gene knockout compared with its wild-type littermate background.
    interpretation_status
    Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
    limitations
    No double-knockout inference; behavioral assay, not proof of human allergy or burns.
    plain_language
    Loss of mouse-trpv1 reduced but did not abolish allicin-evoked pain-related behavior.
    primary_references
    A single N-terminal cysteine in TRPV1 determines activation by pungent compounds from onion and garlic. | 2008 | DOI 10.1038/nn2056 | PMID 18297068 | https://pubmed.ncbi.nlm.nih.gov/18297068/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC4370189/ | https://doi.org/10.1038/nn2056
    source_locator
    Reviewed reference lines 71-71; exact primary location described in quoted passage where extracted.
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 71–71

    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 · Mouse single-gene knockout compared with its wild-type littermate background. · source_derived_draft · unverified_draft

    **Sensory activation.** Experiments identified allicin-dependent activation of TRPA1 and TRPV1. In the later mouse study, allicin stimulated dorsal-root-ganglion neurons and pain-related behavior. Removing either Trpa1 or Trpv1 reduced, but did not abolish, the behavioral response. The channels provide overlapping sensory routes rather than one exclusive receptor. Irritation, chemical burns, and allergic dermatitis are different outcomes. [Macpherson 2005](https://pubmed.ncbi.nlm.nih.gov/15916949/) [Salazar 2008](https://pmc.ncbi.nlm.nih.gov/articles/PMC4370189/)
    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.