Component

Garlic-dependent sulfide production by isolated human erythrocytes

Garlic-dependent sulfide production by isolated human erythrocytes. 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. Glucose sustained sulfide production during repeated garlic-juice exposures in isolated human erythrocytes.

    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_condition
    Garlic juice without glucose present · Garlic juice tested in the 2007 erythrocyte and vessel study Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_condition
    Garlic juice without glucose present · D-glucose Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_contrast
    {"intervention": "Garlic juice with glucose", "comparator": "Garlic juice without glucose", "endpoint": "Glucose sustained sulfide production during repeated garlic-juice exposures in isolated human erythrocytes.", "effect_direction": "increase", "combination": "joint", "conditions": [{"entity_slug": "glucose", "state": "present"}, {"entity_slug": "garlic-juice-benavides-2007", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Isolated human RBCs, oxygen-controlled/anoxic assay, repeated garlic additions with or without 10 mM glucose.
    interpretation_status
    Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
    limitations
    Ex vivo resource dependence; not a glucose-intake recommendation or selective G6PD/B2 experiment.
    plain_language
    Glucose sustained sulfide production during repeated garlic-juice exposures in isolated human erythrocytes.
    primary_references
    Hydrogen sulfide mediates the vasoactivity of garlic. | 2007 | DOI 10.1073/pnas.0705710104 | PMID 17951430 | https://pubmed.ncbi.nlm.nih.gov/17951430/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC2084282/ | https://doi.org/10.1073/pnas.0705710104
    source_locator
    Reviewed reference lines 79-79; exact primary location described in quoted passage where extracted.

    Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 79–79

    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 · Isolated human RBCs, oxygen-controlled/anoxic assay, repeated garlic additions with or without 10 mM glucose. · Recorded from source · Recorded from source

    **Glucose and erythrocyte redox state.** In isolated human erythrocytes, glucose sustained sulfide production during repeated garlic-juice exposures. Without glucose, production capacity declined and the GSH/GSSG balance shifted despite conserved total glutathione equivalents. This is a resource-dependent ex vivo observation. NADPH production through the pentose-phosphate pathway was a proposed explanation, not a selective G6PD perturbation or proof of a B2-dependent clinical response. [Benavides 2007](https://pmc.ncbi.nlm.nih.gov/articles/PMC2084282/)
    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.