Component

Cytosolic free calcium in rat AR42J pancreatic cells

Experimental model, exposure and limitations remain on each linked record.

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. Added sulfanilic acid caused a progressive cytosolic calcium rise in AR42J cells.

    Experimental context and source evidence
    dose
    Sulfanilic acid 1 micromolar-1 mM; mitochondrial depolarization reported at 1 mM
    duration
    Acute calcium time course; other assay intervals not specified in abstract
    evidence_access
    Primary PubMed abstract; unrecovered method details explicitly retained.
    evidence_scope
    literature_reviewed; source-specific experimental curation
    experimental_model
    Rat pancreatic AR42J cell line
    limitations
    The metabolite was administered directly. No measured oral tartrazine-to-pancreas exposure or pancreatitis outcome is established. Oxidant production was reported to be calcium-independent.
    nutrient_topic
    Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine
    organism
    Rat pancreatic AR42J cell line
    plain_language
    Added sulfanilic acid caused a progressive cytosolic calcium rise in AR42J cells.
    primary_references
    Sulfanilic acid increases intracellular free-calcium concentration, induces reactive oxygen species production and impairs trypsin secretion in pancreatic AR42J cells. (2018). https://pubmed.ncbi.nlm.nih.gov/29986830/ DOI: 10.1016/j.fct.2018.07.001
    route
    In vitro metabolite exposure
    tissue
    Calcium, redox, mitochondrial and secretory assays

    Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 138–147

    Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Rat pancreatic AR42J cell line · source_derived_draft · unverified_draft

    ## tartrazine-metabolite-calcium Added sulfanilic acid caused a progressive cytosolic calcium rise in AR42J cells. Model/species: Rat pancreatic AR42J cell line Tissue: Calcium, redox, mitochondrial and secretory assays Exposure: Sulfanilic acid 1 micromolar-1 mM; mitochondrial depolarization reported at 1 mM Route: In vitro metabolite exposure Duration: Acute calcium time course; other assay intervals not specified in abstract Limits: The metabolite was administered directly. No measured oral tartrazine-to-pancreas exposure or pancreatitis outcome is established. Oxidant production was reported to be calcium-independent. Primary reference: Sulfanilic acid increases intracellular free-calcium concentration, induces reactive oxygen species production and impairs trypsin secretion in pancreatic AR42J cells. (2018). https://pubmed.ncbi.nlm.nih.gov/29986830/ DOI: 10.1016/j.fct.2018.07.001 Access: Primary PubMed abstract; unrecovered method details explicitly retained.
    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