Component

Decavanadate(V)

Context-specific entity; species, compartment and exposure are stated on each claim.

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.

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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. Vanadate-treated rat cardiomyocytes showed sustained elevation of cytosolic calcium after 24 hours near the viability-loss concentrations.

    Decavanadate(V) → Cytosolic calcium in vanadate-exposed rat cardiomyocytes source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Fura-2 imaging in neonatal rat cardiomyocytes.
    limitations
    Association does not identify whether SERCA, other transporters or secondary cell injury caused the calcium rise.
    nutrient_topic
    Vanadium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Vanadium
    plain_language
    Ion regulation changed alongside mitochondrial injury.
    primary_references
    Vanadate induces necrotic death in neonatal rat cardiomyocytes through mitochondrial membrane depolarization. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18251508/ · DOI 10.1021/tx700204r

    Vanadium: speciation, phosphate-sensitive enzymes and cross-nutrient mechanisms (2026-09-19) · lines 302–308

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Fura-2 imaging in neonatal rat cardiomyocytes. · source_derived_draft · unverified_draft

    ## vanadium-cardiac-calcium Ion regulation changed alongside mitochondrial injury. Vanadate-treated rat cardiomyocytes showed sustained elevation of cytosolic calcium after 24 hours near the viability-loss concentrations. Model: Fura-2 imaging in neonatal rat cardiomyocytes. Limitations: Association does not identify whether SERCA, other transporters or secondary cell injury caused the calcium rise. Evidence access: Primary abstract Vanadate induces necrotic death in neonatal rat cardiomyocytes through mitochondrial membrane depolarization. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18251508/ · DOI 10.1021/tx700204r
    Complete structured claim and evidence

  2. Decavanadate and mixed metavanadate solutions depolarized mitochondria in neonatal rat cardiomyocytes within six hours; half-maximal depolarization occurred near 6.5 micromolar total vanadium.

    Decavanadate(V) → Mitochondrial depolarization in vanadate-exposed neonatal rat cardiomyocytes source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Neonatal rat cardiomyocytes; fluorescent membrane-potential probes.
    limitations
    Total vanadium differs from decamer concentration: 6.5 micromolar total V equals 0.65 micromolar V10. No human threshold is established.
    nutrient_topic
    Vanadium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Vanadium
    plain_language
    Mitochondrial electrical failure preceded later cell death.
    primary_references
    Vanadate induces necrotic death in neonatal rat cardiomyocytes through mitochondrial membrane depolarization. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18251508/ · DOI 10.1021/tx700204r

    Vanadium: speciation, phosphate-sensitive enzymes and cross-nutrient mechanisms (2026-09-19) · lines 286–292

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Neonatal rat cardiomyocytes; fluorescent membrane-potential probes. · source_derived_draft · unverified_draft

    ## vanadium-cardiac-depolarization Mitochondrial electrical failure preceded later cell death. Decavanadate and mixed metavanadate solutions depolarized mitochondria in neonatal rat cardiomyocytes within six hours; half-maximal depolarization occurred near 6.5 micromolar total vanadium. Model: Neonatal rat cardiomyocytes; fluorescent membrane-potential probes. Limitations: Total vanadium differs from decamer concentration: 6.5 micromolar total V equals 0.65 micromolar V10. No human threshold is established. Evidence access: Primary abstract Vanadate induces necrotic death in neonatal rat cardiomyocytes through mitochondrial membrane depolarization. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18251508/ · DOI 10.1021/tx700204r
    Complete structured claim and evidence

  3. After 24 hours, both solutions caused necrotic cell death without significant caspase-3 activation; approximately 10 micromolar total V produced 50% viability loss.

    Decavanadate(V) → Necrotic death in vanadate-exposed rat cardiomyocytes source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Neonatal rat ventricular cells; MTT and propidium iodide assays.
    limitations
    No clinical cardiac-risk estimate can be derived from the culture concentration.
    nutrient_topic
    Vanadium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Vanadium
    plain_language
    The injury phenotype was necrotic in this experiment.
    primary_references
    Vanadate induces necrotic death in neonatal rat cardiomyocytes through mitochondrial membrane depolarization. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18251508/ · DOI 10.1021/tx700204r

    Vanadium: speciation, phosphate-sensitive enzymes and cross-nutrient mechanisms (2026-09-19) · lines 294–300

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Neonatal rat ventricular cells; MTT and propidium iodide assays. · source_derived_draft · unverified_draft

    ## vanadium-cardiac-necrosis The injury phenotype was necrotic in this experiment. After 24 hours, both solutions caused necrotic cell death without significant caspase-3 activation; approximately 10 micromolar total V produced 50% viability loss. Model: Neonatal rat ventricular cells; MTT and propidium iodide assays. Limitations: No clinical cardiac-risk estimate can be derived from the culture concentration. Evidence access: Primary abstract Vanadate induces necrotic death in neonatal rat cardiomyocytes through mitochondrial membrane depolarization. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18251508/ · DOI 10.1021/tx700204r
    Complete structured claim and evidence

  4. Decavanadate inhibited isolated Sparus aurata heart mitochondrial oxygen consumption more potently than monomeric vanadate in the reported assay.

    Decavanadate(V) → Respiration of isolated Sparus aurata heart mitochondria source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Fish cardiac mitochondria; IC50 400 nM V10 versus 23 micromolar V1 as reported.
    limitations
    Species and concentration basis matter; compare ten V atoms per decamer before inferring a per-atom potency ratio.
    nutrient_topic
    Vanadium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Vanadium
    plain_language
    Oligomeric form changed potency in an isolated organelle.
    primary_references
    Mitochondria as a target for decavanadate toxicity in Sparus aurata heart. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17420061/ · DOI 10.1016/j.aquatox.2007.03.005

    Vanadium: speciation, phosphate-sensitive enzymes and cross-nutrient mechanisms (2026-09-19) · lines 310–316

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Fish cardiac mitochondria; IC50 400 nM V10 versus 23 micromolar V1 as reported. · source_derived_draft · unverified_draft

    ## vanadium-fish-decamer-potency Oligomeric form changed potency in an isolated organelle. Decavanadate inhibited isolated Sparus aurata heart mitochondrial oxygen consumption more potently than monomeric vanadate in the reported assay. Model: Fish cardiac mitochondria; IC50 400 nM V10 versus 23 micromolar V1 as reported. Limitations: Species and concentration basis matter; compare ten V atoms per decamer before inferring a per-atom potency ratio. Evidence access: Primary abstract Mitochondria as a target for decavanadate toxicity in Sparus aurata heart. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17420061/ · DOI 10.1016/j.aquatox.2007.03.005
    Complete structured claim and evidence

  5. Up to 5 micromolar V10 did not inhibit measured F0F1-ATPase activity, NADH levels or complexes I/II, while complex-III redox steady state changed.

    Decavanadate(V) → Complex III redox state in fish cardiac mitochondria source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Isolated fish cardiac mitochondrial assays.
    limitations
    Complex-III redox change does not itself establish a direct molecular binding target.
    nutrient_topic
    Vanadium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Vanadium
    plain_language
    Respiratory inhibition did not mean every mitochondrial enzyme was inhibited.
    primary_references
    Mitochondria as a target for decavanadate toxicity in Sparus aurata heart. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17420061/ · DOI 10.1016/j.aquatox.2007.03.005

    Vanadium: speciation, phosphate-sensitive enzymes and cross-nutrient mechanisms (2026-09-19) · lines 318–324

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Isolated fish cardiac mitochondrial assays. · source_derived_draft · unverified_draft

    ## vanadium-fish-target-specificity Respiratory inhibition did not mean every mitochondrial enzyme was inhibited. Up to 5 micromolar V10 did not inhibit measured F0F1-ATPase activity, NADH levels or complexes I/II, while complex-III redox steady state changed. Model: Isolated fish cardiac mitochondrial assays. Limitations: Complex-III redox change does not itself establish a direct molecular binding target. Evidence access: Primary abstract Mitochondria as a target for decavanadate toxicity in Sparus aurata heart. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17420061/ · DOI 10.1016/j.aquatox.2007.03.005
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

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