Component

Intracellular calcium-store release

Measured mobilization of calcium from intracellular stores; model belongs to each claim.

4 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 acts on it

  1. Significant inhibition of caffeine-evoked calcium release required 20 µM boric acid in LNCaP cells and 150 µM in non-tumor PWR1E cells.

    Boric acid / orthoboric acid / B(OH)3 → Intracellular calcium-store release source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/boron-research/19554099.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "17bd65bde36f54d1bb0688118212419b31643b9fc61323d12ef1ad6a78a173bb", "start_char": 0, "end_char": 1809, "text_sha256": "17bd65bde36f54d1bb0688118212419b31643b9fc61323d12ef1ad6a78a173bb"}
    experimental_model
    Calcium imaging and flow cytometry in three human prostate cell lines
    exposure
    Boric acid 1–150 µM depending on agonist and cell line; DU-145 storage assay 50 µM for 1 hour
    limitations
    RyR-sensitive flux is not proof of direct binding to a particular RyR isoform. Cell-line exposure responses do not establish dietary prevention of prostate cancer.
    nutrient_topic
    Boron research collection; topical membership is not evidence of a direct dietary effect. · Boron
    organism
    Human DU-145, LNCaP and PWR1E cells
    plain_language
    Different prostate cell types needed different concentrations for the measured response.
    primary_references
    [boron-p19554099] Receptor activated Ca(2+) release is inhibited by boric acid in prostate cancer cells. (2009). https://pubmed.ncbi.nlm.nih.gov/19554099/ DOI: 10.1371/journal.pone.0006009
    tissue_or_cell_type
    Cancer and non-tumor prostate cell cultures

    Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 352–363

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Calcium imaging and flow cytometry in three human prostate cell lines · source_derived_draft · unverified_draft

    ### boron-cell-type-calcium-threshold Significant inhibition of caffeine-evoked calcium release required 20 µM boric acid in LNCaP cells and 150 µM in non-tumor PWR1E cells. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: Different prostate cell types needed different concentrations for the measured response. organism: Human DU-145, LNCaP and PWR1E cells tissue_or_cell_type: Cancer and non-tumor prostate cell cultures experimental_model: Calcium imaging and flow cytometry in three human prostate cell lines limitations: RyR-sensitive flux is not proof of direct binding to a particular RyR isoform. Cell-line exposure responses do not establish dietary prevention of prostate cancer. exposure: Boric acid 1–150 µM depending on agonist and cell line; DU-145 storage assay 50 µM for 1 hour evidence_span: {"source_cache": "artifacts/boron-research/19554099.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "17bd65bde36f54d1bb0688118212419b31643b9fc61323d12ef1ad6a78a173bb", "start_char": 0, "end_char": 1809, "text_sha256": "17bd65bde36f54d1bb0688118212419b31643b9fc61323d12ef1ad6a78a173bb"} [boron-p19554099] Receptor activated Ca(2+) release is inhibited by boric acid in prostate cancer cells. (2009). https://pubmed.ncbi.nlm.nih.gov/19554099/ DOI: 10.1371/journal.pone.0006009
    Complete structured claim and evidence

  2. Boric acid partly inhibited NAD+-evoked calcium transients at 250 µM and completely at 1,000 µM in DU-145 cells; NADP+-evoked and mechanical responses were inhibited at 1,000 µM.

    Boric acid / orthoboric acid / B(OH)3 → Intracellular calcium-store release source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/boron-research/18516691.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5fc4f02e11634c2a2d111a99ee4c6175fe8839a8f28152b656b3c29be6745206", "start_char": 0, "end_char": 1733, "text_sha256": "5fc4f02e11634c2a2d111a99ee4c6175fe8839a8f28152b656b3c29be6745206"}
    experimental_model
    Human prostate cancer cell culture and mass spectrometry
    exposure
    Boric acid 100–1,000 µM; methylboronic acid comparator
    limitations
    These are cell-culture exposures, including concentrations far above usual circulating levels. Adduct detection and calcium responses do not prove cancer prevention or direct channel binding.
    nutrient_topic
    Boron research collection; topical membership is not evidence of a direct dietary effect. · Boron
    organism
    Human DU-145 cells; cell-free complex analysis
    plain_language
    At the tested concentrations, boric acid reduced several ways these cancer cells released stored calcium.
    primary_references
    [boron-p18516691] Boric acid inhibits stored Ca2+ release in DU-145 prostate cancer cells. (2009). https://pubmed.ncbi.nlm.nih.gov/18516691/ DOI: 10.1007/s10565-008-9085-7
    tissue_or_cell_type
    Prostate cancer cells

    Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 274–285

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human prostate cancer cell culture and mass spectrometry · source_derived_draft · unverified_draft

    ### boron-nad-calcium-response Boric acid partly inhibited NAD+-evoked calcium transients at 250 µM and completely at 1,000 µM in DU-145 cells; NADP+-evoked and mechanical responses were inhibited at 1,000 µM. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: At the tested concentrations, boric acid reduced several ways these cancer cells released stored calcium. organism: Human DU-145 cells; cell-free complex analysis tissue_or_cell_type: Prostate cancer cells experimental_model: Human prostate cancer cell culture and mass spectrometry limitations: These are cell-culture exposures, including concentrations far above usual circulating levels. Adduct detection and calcium responses do not prove cancer prevention or direct channel binding. exposure: Boric acid 100–1,000 µM; methylboronic acid comparator evidence_span: {"source_cache": "artifacts/boron-research/18516691.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5fc4f02e11634c2a2d111a99ee4c6175fe8839a8f28152b656b3c29be6745206", "start_char": 0, "end_char": 1733, "text_sha256": "5fc4f02e11634c2a2d111a99ee4c6175fe8839a8f28152b656b3c29be6745206"} [boron-p18516691] Boric acid inhibits stored Ca2+ release in DU-145 prostate cancer cells. (2009). https://pubmed.ncbi.nlm.nih.gov/18516691/ DOI: 10.1007/s10565-008-9085-7
    Complete structured claim and evidence

  3. Boric acid reduced calcium release evoked by ryanodine-receptor agonists in DU-145 cells; cADPR inhibition was detected at 50 µM and responses to other agonists at different concentrations.

    Boric acid / orthoboric acid / B(OH)3 → Intracellular calcium-store release source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/boron-research/19554099.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "17bd65bde36f54d1bb0688118212419b31643b9fc61323d12ef1ad6a78a173bb", "start_char": 0, "end_char": 1809, "text_sha256": "17bd65bde36f54d1bb0688118212419b31643b9fc61323d12ef1ad6a78a173bb"}
    experimental_model
    Calcium imaging and flow cytometry in three human prostate cell lines
    exposure
    Boric acid 1–150 µM depending on agonist and cell line; DU-145 storage assay 50 µM for 1 hour
    limitations
    RyR-sensitive flux is not proof of direct binding to a particular RyR isoform. Cell-line exposure responses do not establish dietary prevention of prostate cancer.
    nutrient_topic
    Boron research collection; topical membership is not evidence of a direct dietary effect. · Boron
    organism
    Human DU-145, LNCaP and PWR1E cells
    plain_language
    Boric acid changed release from a particular calcium store in these cells.
    primary_references
    [boron-p19554099] Receptor activated Ca(2+) release is inhibited by boric acid in prostate cancer cells. (2009). https://pubmed.ncbi.nlm.nih.gov/19554099/ DOI: 10.1371/journal.pone.0006009
    tissue_or_cell_type
    Cancer and non-tumor prostate cell cultures

    Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 326–337

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Calcium imaging and flow cytometry in three human prostate cell lines · source_derived_draft · unverified_draft

    ### boron-ryr-sensitive-calcium Boric acid reduced calcium release evoked by ryanodine-receptor agonists in DU-145 cells; cADPR inhibition was detected at 50 µM and responses to other agonists at different concentrations. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: Boric acid changed release from a particular calcium store in these cells. organism: Human DU-145, LNCaP and PWR1E cells tissue_or_cell_type: Cancer and non-tumor prostate cell cultures experimental_model: Calcium imaging and flow cytometry in three human prostate cell lines limitations: RyR-sensitive flux is not proof of direct binding to a particular RyR isoform. Cell-line exposure responses do not establish dietary prevention of prostate cancer. exposure: Boric acid 1–150 µM depending on agonist and cell line; DU-145 storage assay 50 µM for 1 hour evidence_span: {"source_cache": "artifacts/boron-research/19554099.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "17bd65bde36f54d1bb0688118212419b31643b9fc61323d12ef1ad6a78a173bb", "start_char": 0, "end_char": 1809, "text_sha256": "17bd65bde36f54d1bb0688118212419b31643b9fc61323d12ef1ad6a78a173bb"} [boron-p19554099] Receptor activated Ca(2+) release is inhibited by boric acid in prostate cancer cells. (2009). https://pubmed.ncbi.nlm.nih.gov/19554099/ DOI: 10.1371/journal.pone.0006009
    Complete structured claim and evidence

  4. Extracellular cyclic ADP-ribose generated by human CD38-expressing COS1 cells was detected by calcium release from sea-urchin egg microsomes.

    Cyclic ADP-ribose → Intracellular calcium-store release source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    true
    evidence_span
    {"source_cache": "artifacts/niacin-consumption-sources/cd381993.abstract.txt", "locator": "Indexed abstract", "start_char": 0, "end_char": 540, "file_sha256": "e8ba405a5300f922bcf34c358d95735b86637331f4cf15a009ac5bf8df93f1e5", "text_sha256": "e8ba405a5300f922bcf34c358d95735b86637331f4cf15a009ac5bf8df93f1e5"}
    experimental_model
    Human CD38 expression in monkey COS1 cells with sea-urchin microsome bioassay
    exposure
    CD38 cDNA transfection; NAD+ extracellular substrate
    limitations
    This mixed-species bioassay does not demonstrate intracellular trafficking of extracellular cADPR or calcium regulation after oral niacin.
    nutrient_topic
    Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
    organism
    Human protein; African green monkey cells; sea urchin microsomes
    plain_language
    A CD38-generated messenger mobilized calcium in an egg-microsome bioassay.
    primary_references
    [b3-cons-cd381993] Human lymphocyte antigen CD38 catalyzes the production of cyclic ADP-ribose. (1993). https://pubmed.ncbi.nlm.nih.gov/8253202/ DOI: 10.1016/0014-5793(93)80735-d
    tissue_or_cell_type
    COS1 kidney-cell culture; sea-urchin egg microsomes

    Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 607–619

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human CD38 expression in monkey COS1 cells with sea-urchin microsome bioassay · source_derived_draft · unverified_draft

    ### b3-cons-cadpr-store-calcium Extracellular cyclic ADP-ribose generated by human CD38-expressing COS1 cells was detected by calcium release from sea-urchin egg microsomes. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A CD38-generated messenger mobilized calcium in an egg-microsome bioassay. organism: Human protein; African green monkey cells; sea urchin microsomes tissue_or_cell_type: COS1 kidney-cell culture; sea-urchin egg microsomes experimental_model: Human CD38 expression in monkey COS1 cells with sea-urchin microsome bioassay limitations: This mixed-species bioassay does not demonstrate intracellular trafficking of extracellular cADPR or calcium regulation after oral niacin. exposure: CD38 cDNA transfection; NAD+ extracellular substrate cross_nutrient: true evidence_span: {"source_cache": "artifacts/niacin-consumption-sources/cd381993.abstract.txt", "locator": "Indexed abstract", "start_char": 0, "end_char": 540, "file_sha256": "e8ba405a5300f922bcf34c358d95735b86637331f4cf15a009ac5bf8df93f1e5", "text_sha256": "e8ba405a5300f922bcf34c358d95735b86637331f4cf15a009ac5bf8df93f1e5"} [b3-cons-cd381993] Human lymphocyte antigen CD38 catalyzes the production of cyclic ADP-ribose. (1993). https://pubmed.ncbi.nlm.nih.gov/8253202/ DOI: 10.1016/0014-5793(93)80735-d
    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.

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