Component

Inner mitochondrial membrane potential

Electrical potential across the inner mitochondrial membrane.

5 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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 it acts on

  1. Dissipating membrane potential reduced Mg uptake in the human MRS2 mitochondrial assay.

    Inner mitochondrial membrane potential → Mitochondrial magnesium uptake source_derived_draftungraded
    Experimental context and source evidence
    evidence-system
    FCCP or valinomycin exposure of isolated mitochondria
    experimental_model
    FCCP or valinomycin exposure of isolated mitochondria
    limitations
    Pharmacological potential collapse can affect other mitochondrial properties; does not imply direct ATP hydrolysis by MRS2.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Human
    plain_language
    The inner membrane electrical gradient helps drive magnesium into mitochondria.
    primary_references
    [human-mrs2-2023-permeation] Molecular basis of Mg2+ permeation through the human mitochondrial Mrs2 channel (2023). https://www.nature.com/articles/s41467-023-40516-2 DOI: 10.1038/s41467-023-40516-2
    tissue
    HEK293F-derived mitochondria
    tissue_or_cell_type
    HEK293F-derived mitochondria

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1235–1246

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · FCCP or valinomycin exposure of isolated mitochondria · source_derived_draft · unverified_draft

    ### mitochondrial-potential-supports-mrs2-uptake Dissipating membrane potential reduced Mg uptake in the human MRS2 mitochondrial assay. Condition category: normal nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The inner membrane electrical gradient helps drive magnesium into mitochondria. organism: Human tissue_or_cell_type: HEK293F-derived mitochondria experimental_model: FCCP or valinomycin exposure of isolated mitochondria limitations: Pharmacological potential collapse can affect other mitochondrial properties; does not imply direct ATP hydrolysis by MRS2. evidence-system: FCCP or valinomycin exposure of isolated mitochondria tissue: HEK293F-derived mitochondria [human-mrs2-2023-permeation] Molecular basis of Mg2+ permeation through the human mitochondrial Mrs2 channel (2023). https://www.nature.com/articles/s41467-023-40516-2 DOI: 10.1038/s41467-023-40516-2
    Complete structured claim and evidence

  2. Depolarization or mitochondrial disruption inhibited ThTP synthesis in rat brain mitochondrial preparations.

    Inner mitochondrial membrane potential → Thiamine triphosphate synthesis source_derived_draftungraded
    Experimental context and source evidence
    evidence-scope
    Brain mitochondria
    evidence_locator
    Results: ThTP synthesis in isolated mitochondria and energy coupling
    evidence_spans
    [{"source_document": "artifacts/thiamine_transport_sources/gangolf-2010-thtp-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1672}]
    experimental_model
    Isolated rat brain mitochondria; ThDP/Pi incubation, respiratory substrates and inhibitors.
    limitations
    Proton-motive-force dependence is supported; the proposed ATP-synthase identity was not definitively established.
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Rattus norvegicus
    plain_language
    Intact, energized mitochondria were required for this B1-phosphate reaction.
    primary_references
    [gangolf-2010-thtp] Thiamine Triphosphate Synthesis in Rat Brain Occurs in Mitochondria and Is Coupled to the Respiratory Chain (2010). https://pmc.ncbi.nlm.nih.gov/articles/PMC2804207/ DOI: 10.1074/jbc.M109.054379
    tissue_or_cell_type
    Brain mitochondria

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 617–629

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated rat brain mitochondria; ThDP/Pi incubation, respiratory substrates and inhibitors. · source_derived_draft · unverified_draft

    ### b1-brain-thtp-proton-motive-dependence Depolarization or mitochondrial disruption inhibited ThTP synthesis in rat brain mitochondrial preparations. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Intact, energized mitochondria were required for this B1-phosphate reaction. organism: Rattus norvegicus tissue_or_cell_type: Brain mitochondria experimental_model: Isolated rat brain mitochondria; ThDP/Pi incubation, respiratory substrates and inhibitors. limitations: Proton-motive-force dependence is supported; the proposed ATP-synthase identity was not definitively established. evidence_spans: [{"source_document": "artifacts/thiamine_transport_sources/gangolf-2010-thtp-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1672}] evidence_locator: Results: ThTP synthesis in isolated mitochondria and energy coupling evidence-scope: Brain mitochondria [gangolf-2010-thtp] Thiamine Triphosphate Synthesis in Rat Brain Occurs in Mitochondria and Is Coupled to the Respiratory Chain (2010). https://pmc.ncbi.nlm.nih.gov/articles/PMC2804207/ DOI: 10.1074/jbc.M109.054379
    Complete structured claim and evidence

What acts on it

  1. DIM limited the loss of mitochondrial membrane potential and excessive ROS generation in the atrophy models.

    3,3'-Diindolylmethane / DIM → Inner mitochondrial membrane potential source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/dim-research/42308990.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4bd26fd33c370df293346c5680820459a885a7545286d92c9e1c27220d41f2cb", "start_char": 0, "end_char": 2803, "text_sha256": "4bd26fd33c370df293346c5680820459a885a7545286d92c9e1c27220d41f2cb"}
    experimental_model
    Dexamethasone atrophy and aging-model experiments
    exposure
    DIM in experimental atrophy/aging models
    limitations
    2026 preclinical study, not a human sarcopenia trial. Mouse STIM1 stays distinct from the human selenium-linked STIM1 record.
    nutrient_topic
    Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. · 3,3'-Diindolylmethane / DIM
    organism
    Mouse muscle, mouse C2C12 myotubes and C. elegans
    plain_language
    Mitochondrial measurements improved in this preclinical setting.
    primary_references
    [dim-p42308990] 3,3'-Diindolylmethane ameliorates muscle atrophy by modulating mitochondrial function and calcium homeostasis. (2026). https://pubmed.ncbi.nlm.nih.gov/42308990/ DOI: 10.1016/j.phymed.2026.158409
    tissue_or_cell_type
    Mitochondrial function and store-operated calcium entry

    Diindolylmethane (DIM): formation, receptor signaling, metabolism and drug interactions (2026-09-17) · lines 1468–1479

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dexamethasone atrophy and aging-model experiments · source_derived_draft · unverified_draft

    ### dim-muscle-mito DIM limited the loss of mitochondrial membrane potential and excessive ROS generation in the atrophy models. Condition category: normal nutrient_topic: Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Mitochondrial measurements improved in this preclinical setting. organism: Mouse muscle, mouse C2C12 myotubes and C. elegans tissue_or_cell_type: Mitochondrial function and store-operated calcium entry experimental_model: Dexamethasone atrophy and aging-model experiments limitations: 2026 preclinical study, not a human sarcopenia trial. Mouse STIM1 stays distinct from the human selenium-linked STIM1 record. exposure: DIM in experimental atrophy/aging models evidence_span: {"source_cache": "artifacts/dim-research/42308990.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4bd26fd33c370df293346c5680820459a885a7545286d92c9e1c27220d41f2cb", "start_char": 0, "end_char": 2803, "text_sha256": "4bd26fd33c370df293346c5680820459a885a7545286d92c9e1c27220d41f2cb"} [dim-p42308990] 3,3'-Diindolylmethane ameliorates muscle atrophy by modulating mitochondrial function and calcium homeostasis. (2026). https://pubmed.ncbi.nlm.nih.gov/42308990/ DOI: 10.1016/j.phymed.2026.158409
    Complete structured claim and evidence

  2. Lariciresinol lowered mitochondrial membrane potential in hepatoma cells, measured by JC-1 staining, alongside apoptosis-associated protein changes on western blot.

    Lariciresinol, enantiomer unresolved → Inner mitochondrial membrane potential source_derived_draftungraded
    Experimental context and source evidence
    duration
    Not stated here
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    Human HepG2 hepatoma cells
    exposure
    Lariciresinol, dose-dependent
    limitations
    The enantiomer is not stated, and the abstract does not give the concentration range or the inhibitory concentration.
    organism
    Human HepG2 hepatoma cells
    plain_language
    Lariciresinol lowered mitochondrial membrane potential in hepatoma cells, measured by JC-1 staining, alongside apoptosis-associated protein changes on western blot.
    primary_references
    Lariciresinol induces apoptosis in HepG2 cells via mitochondrial-mediated apoptosis pathway. (2018). https://pubmed.ncbi.nlm.nih.gov/29247613/ DOI: 10.1016/j.ejphar.2017.12.015
    route
    In vitro
    tissue
    Mitochondrial membrane potential and apoptosis-associated proteins

    Lariciresinol: five molecules under one name, and the mechanisms each one carries (2026-09-22) · lines 209–218

    Original AI-assisted curation of twelve primary studies, every abstract read and all DOIs cross-checked against live PubMed metadata. Mechanism edges only, with no conclusion or claim of benefit recorded. Three author clusters account for eight of the twelve and carry shared laboratory keys. Study-specific concentrations, negative findings and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft

    ## lariciresinol-lowers-mitochondrial-membrane-potential Lariciresinol lowered mitochondrial membrane potential in hepatoma cells, measured by JC-1 staining, alongside apoptosis-associated protein changes on western blot. Model/species: Human HepG2 hepatoma cells Tissue/system: Mitochondrial membrane potential and apoptosis-associated proteins Exposure: Lariciresinol, dose-dependent Route: In vitro Duration: Not stated here Limits: The enantiomer is not stated, and the abstract does not give the concentration range or the inhibitory concentration. Primary reference: Lariciresinol induces apoptosis in HepG2 cells via mitochondrial-mediated apoptosis pathway. (2018). https://pubmed.ncbi.nlm.nih.gov/29247613/ DOI: 10.1016/j.ejphar.2017.12.015 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Sulfite reduced glutamate-driven mitochondrial membrane potential and ATP synthesis, while malate- and succinate-supported membrane potential was not affected.

    Sulfite / SO3(2-) → Mitochondrial ATP production source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/molybdenum-research/15273247.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d2f73a9ca41e4d51b85d3a66ada08511055ce6ff7462beb0e7eaf21aadf37279", "start_char": 0, "end_char": 1606, "text_sha256": "d2f73a9ca41e4d51b85d3a66ada08511055ce6ff7462beb0e7eaf21aadf37279"}
    experimental_model
    Rat brain mitochondria/extracts, purified enzyme and Neuro-2a/PC12 cells
    exposure
    Micromolar sulfite exposure
    limitations
    Experimental substrate dependence; not a measurement of these effects in people with ordinary low molybdenum intake.
    nutrient_topic
    Molybdenum research collection; topical membership is not evidence of a direct dietary effect. · Molybdenum
    organism
    Rattus norvegicus tissue; rodent cell lines
    plain_language
    The effect depended on which fuel route supplied the mitochondria.
    primary_references
    [mo-p15273247] A mechanism of sulfite neurotoxicity: direct inhibition of glutamate dehydrogenase. (2004). https://pubmed.ncbi.nlm.nih.gov/15273247/ DOI: 10.1074/jbc.m402759200
    tissue_or_cell_type
    Mitochondrial glutamate oxidation
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 1379–1390

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat brain mitochondria/extracts, purified enzyme and Neuro-2a/PC12 cells · source_derived_draft · unverified_draft

    ### mo-sulfite-atp Sulfite reduced glutamate-driven mitochondrial membrane potential and ATP synthesis, while malate- and succinate-supported membrane potential was not affected. Condition category: machinery_impairment nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: The effect depended on which fuel route supplied the mitochondria. organism: Rattus norvegicus tissue; rodent cell lines tissue_or_cell_type: Mitochondrial glutamate oxidation experimental_model: Rat brain mitochondria/extracts, purified enzyme and Neuro-2a/PC12 cells limitations: Experimental substrate dependence; not a measurement of these effects in people with ordinary low molybdenum intake. exposure: Micromolar sulfite exposure evidence_span: {"source_cache": "artifacts/molybdenum-research/15273247.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d2f73a9ca41e4d51b85d3a66ada08511055ce6ff7462beb0e7eaf21aadf37279", "start_char": 0, "end_char": 1606, "text_sha256": "d2f73a9ca41e4d51b85d3a66ada08511055ce6ff7462beb0e7eaf21aadf37279"} [mo-p15273247] A mechanism of sulfite neurotoxicity: direct inhibition of glutamate dehydrogenase. (2004). https://pubmed.ncbi.nlm.nih.gov/15273247/ DOI: 10.1074/jbc.m402759200
    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