Component

Mitochondrial complex-I function and ATP in rat striatal neurons

Species, preparation, dose and limitations are retained on linked claims.

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. Annonacin inhibited mitochondrial complex-I-linked energy production, producing a concentration-dependent ATP fall, tau redistribution and death in cultured rat striatal neurons.

    Experimental context and source evidence
    dose
    Annonacin concentration series
    duration
    48 hours
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    evidence_scope
    literature_reviewed; model-specific source-derived curation
    experimental_model
    Primary rat striatal neurons
    limitations
    Purified-cell exposure establishes a hazard mechanism, not the dose delivered to human neurons by a particular graviola food.
    nutrient_topic
    Graviola (Annona muricata) chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Graviola / Annona muricata
    organism
    Primary rat striatal neurons
    plain_language
    Annonacin inhibited mitochondrial complex-I-linked energy production, producing a concentration-dependent ATP fall, tau redistribution and death in cultured rat striatal neurons.
    primary_references
    Annonacin, a natural mitochondrial complex I inhibitor, causes tau pathology in cultured neurons. (2007). https://pubmed.ncbi.nlm.nih.gov/17634376/ DOI: 10.1523/JNEUROSCI.1644-07.2007
    route
    In vitro
    tissue
    ATP, mitochondrial transport, tau localization and cell death

    Graviola (Annona muricata): mechanism of action and interactions (2026-09-20) · lines 44–53

    Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · Primary rat striatal neurons · source_derived_draft · unverified_draft

    ## graviola-complex1-atp Annonacin inhibited mitochondrial complex-I-linked energy production, producing a concentration-dependent ATP fall, tau redistribution and death in cultured rat striatal neurons. Model/species: Primary rat striatal neurons Tissue/system: ATP, mitochondrial transport, tau localization and cell death Exposure: Annonacin concentration series Route: In vitro Duration: 48 hours Limits: Purified-cell exposure establishes a hazard mechanism, not the dose delivered to human neurons by a particular graviola food. Primary reference: Annonacin, a natural mitochondrial complex I inhibitor, causes tau pathology in cultured neurons. (2007). https://pubmed.ncbi.nlm.nih.gov/17634376/ DOI: 10.1523/JNEUROSCI.1644-07.2007 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    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.

    Evidence, AI assistance and curation standards