Component

Sulfanilic acid

4-Aminobenzenesulfonic acid; tartrazine azo-reduction product, not intact tartrazine.

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

    Sulfanilic acid → Cytosolic free calcium in rat AR42J pancreatic cells source_derived_draftungraded
    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

  2. Sulfanilic acid lowered the GSH/GSSG ratio in AR42J cells.

    Sulfanilic acid → GSH/GSSG ratio in rat AR42J pancreatic cells source_derived_draftungraded
    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
    Sulfanilic acid lowered the GSH/GSSG ratio 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 160–169

    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-gsh Sulfanilic acid lowered the GSH/GSSG ratio 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

  3. Sulfanilic acid at 1 mM depolarized the mitochondrial membrane potential in AR42J cells.

    Sulfanilic acid → Mitochondrial membrane potential in rat AR42J cells source_derived_draftungraded
    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
    Sulfanilic acid at 1 mM depolarized the mitochondrial membrane potential 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 171–180

    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-mitochondria Sulfanilic acid at 1 mM depolarized the mitochondrial membrane potential 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

  4. Sulfanilic acid increased oxidant-sensitive signal in AR42J cells; the reported effect did not require the calcium rise.

    Sulfanilic acid → Oxidant-sensitive signal in rat AR42J pancreatic cells source_derived_draftungraded
    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
    Sulfanilic acid increased oxidant-sensitive signal in AR42J cells; the reported effect did not require the calcium rise.
    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 149–158

    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-ros Sulfanilic acid increased oxidant-sensitive signal in AR42J cells; the reported effect did not require the calcium rise. 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

  5. Sulfanilic acid pretreatment impaired CCK-8-evoked trypsin secretion from AR42J cells.

    Sulfanilic acid → CCK-8-stimulated trypsin secretion by rat AR42J cells source_derived_draftungraded
    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
    Sulfanilic acid pretreatment impaired CCK-8-evoked trypsin secretion from 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 193–202

    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-secretion Sulfanilic acid pretreatment impaired CCK-8-evoked trypsin secretion from 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

  6. Sulfanilic acid decreased SOD2 expression in the AR42J experiment.

    Sulfanilic acid → Rat mitochondrial superoxide dismutase / Sod2 source_derived_draftungraded
    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
    Sulfanilic acid decreased SOD2 expression in the AR42J experiment.
    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 182–191

    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-sod2 Sulfanilic acid decreased SOD2 expression in the AR42J experiment. 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

What acts on it

  1. Tartrazine azo reduction yields sulfanilic acid as one of the cleavage products.

    Tartrazine → Sulfanilic acid source_derived_draftungraded
    Experimental context and source evidence
    dose
    Tartrazine/isolated metabolites; preparative concentrations not recovered from primary abstract
    duration
    Reaction intervals not recovered from accessed abstract
    evidence_access
    Primary PubMed abstract; unrecovered method details explicitly retained.
    evidence_scope
    literature_reviewed; source-specific experimental curation
    experimental_model
    Human-stool bacterial isolates and analytical chemistry of tartrazine products
    limitations
    SCAP and PPA identities were experimentally characterized. The additional yellow derivative remains proposed and is not imported as an established metabolite. Human circulating exposure was not measured.
    nutrient_topic
    Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine
    organism
    Human-stool bacterial isolates and analytical chemistry of tartrazine products
    plain_language
    Tartrazine azo reduction yields sulfanilic acid as one of the cleavage products.
    primary_references
    Preparation, analysis and toxicity characterisation of the redox metabolites of the azo food dye tartrazine. (2023). https://pubmed.ncbi.nlm.nih.gov/37980979/ DOI: 10.1016/j.fct.2023.114193
    route
    In vitro biotransformation and chemical characterization
    tissue
    Azo reduction followed by oxidation on exposure to air

    Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 83–92

    Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Human-stool bacterial isolates and analytical chemistry of tartrazine products · source_derived_draft · unverified_draft

    ## tartrazine-sulfanilic-product Tartrazine azo reduction yields sulfanilic acid as one of the cleavage products. Model/species: Human-stool bacterial isolates and analytical chemistry of tartrazine products Tissue: Azo reduction followed by oxidation on exposure to air Exposure: Tartrazine/isolated metabolites; preparative concentrations not recovered from primary abstract Route: In vitro biotransformation and chemical characterization Duration: Reaction intervals not recovered from accessed abstract Limits: SCAP and PPA identities were experimentally characterized. The additional yellow derivative remains proposed and is not imported as an established metabolite. Human circulating exposure was not measured. Primary reference: Preparation, analysis and toxicity characterisation of the redox metabolites of the azo food dye tartrazine. (2023). https://pubmed.ncbi.nlm.nih.gov/37980979/ DOI: 10.1016/j.fct.2023.114193 Access: Primary PubMed abstract; unrecovered method details explicitly retained.
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Melatonin pretreatment reduced sulfanilic-acid-associated impairment of trypsin secretion.

    Melatonin → CCK-8-stimulated trypsin secretion by rat AR42J cells source_derived_draftungraded
    Experimental context and source evidence
    dose
    Sulfanilic acid exposure; melatonin pretreatment 100 micromolar; exact CCK-8 series not in abstract
    duration
    Pretreatment interval not specified in accessed abstract
    evidence_access
    Primary PubMed abstract; unrecovered method details explicitly retained.
    evidence_scope
    literature_reviewed; source-specific experimental curation
    experimental_model
    Rat AR42J pancreatic cells
    limitations
    Pharmacological antioxidant rescue does not establish a clinical melatonin regimen or a specific melatonin receptor mechanism.
    nutrient_topic
    Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine
    organism
    Rat AR42J pancreatic cells
    plain_language
    Melatonin pretreatment reduced sulfanilic-acid-associated impairment of trypsin secretion.
    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 pretreatment and secretagogue challenge
    tissue
    CCK-8-stimulated secretion

    Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 204–213

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

    ## tartrazine-melatonin-rescue Melatonin pretreatment reduced sulfanilic-acid-associated impairment of trypsin secretion. Model/species: Rat AR42J pancreatic cells Tissue: CCK-8-stimulated secretion Exposure: Sulfanilic acid exposure; melatonin pretreatment 100 micromolar; exact CCK-8 series not in abstract Route: In vitro pretreatment and secretagogue challenge Duration: Pretreatment interval not specified in accessed abstract Limits: Pharmacological antioxidant rescue does not establish a clinical melatonin regimen or a specific melatonin receptor mechanism. 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