Nutrient chapter

Tartrazine

Synthetic azo colorant, E102 / FD&C Yellow No. 5; sodium salt CAS 1934-21-0. Not an essential nutrient or established therapeutic agent. Distinct from Sunset Yellow FCF / E110 and from its own reduction and oxidation products. Results from dye mixtures are not attributed to tartrazine alone.

42 recorded mechanisms · 0 availability situations · 1 preserved sources. Draft and verified records are labeled separately.

Read recorded mechanisms Open recursive mind map

The mechanisms

What the sources say this nutrient does, one relationship at a time. Plain wording comes first; the technical statement follows.

Purified E. coli K12 azoreductase I used tartrazine as a substrate.
Escherichia coli K12 azoreductase I preparation → Tartrazine source_derived_draftungraded
Experimental context and source evidence
dose
Tartrazine among tested substrates; exact substrate/cofactor concentrations unavailable in abstract
duration
Assay interval unavailable in primary abstract
evidence_access
Primary PubMed abstract; unrecovered method details explicitly retained.
evidence_scope
literature_reviewed; source-specific experimental curation
experimental_model
Purified Escherichia coli K12 azoreductases I and II
limitations
Both NADH and NADPH served as electron donors in enzyme characterization. This does not prove that niacin intake controls dye metabolism in humans. Protein genes and tartrazine-specific kinetic constants are unresolved.
nutrient_topic
Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine
organism
Purified Escherichia coli K12 azoreductases I and II
plain_language
Purified E. coli K12 azoreductase I used tartrazine as a substrate.
primary_references
Purification of two azoreductases from Escherichia coli K12. (1993). https://pubmed.ncbi.nlm.nih.gov/8112774/
route
In vitro enzyme/substrate incubation
tissue
Cell-free azo-reduction assays
Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 17–26
Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Purified Escherichia coli K12 azoreductases I and II · source_derived_draft · unverified_draft
## tartrazine-azoreductase-i Purified E. coli K12 azoreductase I used tartrazine as a substrate. Model/species: Purified Escherichia coli K12 azoreductases I and II Tissue: Cell-free azo-reduction assays Exposure: Tartrazine among tested substrates; exact substrate/cofactor concentrations unavailable in abstract Route: In vitro enzyme/substrate incubation Duration: Assay interval unavailable in primary abstract Limits: Both NADH and NADPH served as electron donors in enzyme characterization. This does not prove that niacin intake controls dye metabolism in humans. Protein genes and tartrazine-specific kinetic constants are unresolved. Primary reference: Purification of two azoreductases from Escherichia coli K12. (1993). https://pubmed.ncbi.nlm.nih.gov/8112774/ Access: Primary PubMed abstract; unrecovered method details explicitly retained.
Complete structured claim and evidence
Purified E. coli K12 azoreductase II used tartrazine less efficiently than azoreductase I.
Escherichia coli K12 azoreductase II preparation → Tartrazine source_derived_draftungraded
Experimental context and source evidence
dose
Tartrazine among tested substrates; exact substrate/cofactor concentrations unavailable in abstract
duration
Assay interval unavailable in primary abstract
evidence_access
Primary PubMed abstract; unrecovered method details explicitly retained.
evidence_scope
literature_reviewed; source-specific experimental curation
experimental_model
Purified Escherichia coli K12 azoreductases I and II
limitations
Both NADH and NADPH served as electron donors in enzyme characterization. This does not prove that niacin intake controls dye metabolism in humans. Protein genes and tartrazine-specific kinetic constants are unresolved.
nutrient_topic
Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine
organism
Purified Escherichia coli K12 azoreductases I and II
plain_language
Purified E. coli K12 azoreductase II used tartrazine less efficiently than azoreductase I.
primary_references
Purification of two azoreductases from Escherichia coli K12. (1993). https://pubmed.ncbi.nlm.nih.gov/8112774/
route
In vitro enzyme/substrate incubation
tissue
Cell-free azo-reduction assays
Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 28–37
Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Purified Escherichia coli K12 azoreductases I and II · source_derived_draft · unverified_draft
## tartrazine-azoreductase-ii Purified E. coli K12 azoreductase II used tartrazine less efficiently than azoreductase I. Model/species: Purified Escherichia coli K12 azoreductases I and II Tissue: Cell-free azo-reduction assays Exposure: Tartrazine among tested substrates; exact substrate/cofactor concentrations unavailable in abstract Route: In vitro enzyme/substrate incubation Duration: Assay interval unavailable in primary abstract Limits: Both NADH and NADPH served as electron donors in enzyme characterization. This does not prove that niacin intake controls dye metabolism in humans. Protein genes and tartrazine-specific kinetic constants are unresolved. Primary reference: Purification of two azoreductases from Escherichia coli K12. (1993). https://pubmed.ncbi.nlm.nih.gov/8112774/ Access: Primary PubMed abstract; unrecovered method details explicitly retained.
Complete structured claim and evidence
NADH functioned as an electron donor for the purified azoreductases characterized with an azo-dye substrate panel including tartrazine.
NADH → Escherichia coli K12 azoreductase I preparation source_derived_draftungraded
Experimental context and source evidence
dose
Tartrazine among tested substrates; exact substrate/cofactor concentrations unavailable in abstract
duration
Assay interval unavailable in primary abstract
evidence_access
Primary PubMed abstract; unrecovered method details explicitly retained.
evidence_scope
literature_reviewed; source-specific experimental curation
experimental_model
Purified Escherichia coli K12 azoreductases I and II
limitations
Both NADH and NADPH served as electron donors in enzyme characterization. This does not prove that niacin intake controls dye metabolism in humans. Protein genes and tartrazine-specific kinetic constants are unresolved.
nutrient_topic
Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine
organism
Purified Escherichia coli K12 azoreductases I and II
plain_language
NADH functioned as an electron donor for the purified azoreductases characterized with an azo-dye substrate panel including tartrazine.
primary_references
Purification of two azoreductases from Escherichia coli K12. (1993). https://pubmed.ncbi.nlm.nih.gov/8112774/
route
In vitro enzyme/substrate incubation
tissue
Cell-free azo-reduction assays
Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 39–48
Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Purified Escherichia coli K12 azoreductases I and II · source_derived_draft · unverified_draft
## tartrazine-nadh-donor NADH functioned as an electron donor for the purified azoreductases characterized with an azo-dye substrate panel including tartrazine. Model/species: Purified Escherichia coli K12 azoreductases I and II Tissue: Cell-free azo-reduction assays Exposure: Tartrazine among tested substrates; exact substrate/cofactor concentrations unavailable in abstract Route: In vitro enzyme/substrate incubation Duration: Assay interval unavailable in primary abstract Limits: Both NADH and NADPH served as electron donors in enzyme characterization. This does not prove that niacin intake controls dye metabolism in humans. Protein genes and tartrazine-specific kinetic constants are unresolved. Primary reference: Purification of two azoreductases from Escherichia coli K12. (1993). https://pubmed.ncbi.nlm.nih.gov/8112774/ Access: Primary PubMed abstract; unrecovered method details explicitly retained.
Complete structured claim and evidence
NADPH also functioned as an electron donor for the purified E. coli azoreductase preparations.
NADPH → Escherichia coli K12 azoreductase I preparation source_derived_draftungraded
Experimental context and source evidence
dose
Tartrazine among tested substrates; exact substrate/cofactor concentrations unavailable in abstract
duration
Assay interval unavailable in primary abstract
evidence_access
Primary PubMed abstract; unrecovered method details explicitly retained.
evidence_scope
literature_reviewed; source-specific experimental curation
experimental_model
Purified Escherichia coli K12 azoreductases I and II
limitations
Both NADH and NADPH served as electron donors in enzyme characterization. This does not prove that niacin intake controls dye metabolism in humans. Protein genes and tartrazine-specific kinetic constants are unresolved.
nutrient_topic
Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine
organism
Purified Escherichia coli K12 azoreductases I and II
plain_language
NADPH also functioned as an electron donor for the purified E. coli azoreductase preparations.
primary_references
Purification of two azoreductases from Escherichia coli K12. (1993). https://pubmed.ncbi.nlm.nih.gov/8112774/
route
In vitro enzyme/substrate incubation
tissue
Cell-free azo-reduction assays
Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 50–59
Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Purified Escherichia coli K12 azoreductases I and II · source_derived_draft · unverified_draft
## tartrazine-nadph-donor NADPH also functioned as an electron donor for the purified E. coli azoreductase preparations. Model/species: Purified Escherichia coli K12 azoreductases I and II Tissue: Cell-free azo-reduction assays Exposure: Tartrazine among tested substrates; exact substrate/cofactor concentrations unavailable in abstract Route: In vitro enzyme/substrate incubation Duration: Assay interval unavailable in primary abstract Limits: Both NADH and NADPH served as electron donors in enzyme characterization. This does not prove that niacin intake controls dye metabolism in humans. Protein genes and tartrazine-specific kinetic constants are unresolved. Primary reference: Purification of two azoreductases from Escherichia coli K12. (1993). https://pubmed.ncbi.nlm.nih.gov/8112774/ Access: Primary PubMed abstract; unrecovered method details explicitly retained.
Complete structured claim and evidence
Human-gut E. coli isolate AZO-Ec decolorized tartrazine under the aerobic culture conditions.
Tartrazine → Tartrazine decolorization by human-gut E. coli isolate AZO-Ec source_derived_draftungraded
Experimental context and source evidence
dose
Tartrazine 10, 20 and 30 micromolar; selected strains
duration
30 min comparison, time courses up to 5 h
evidence_access
Primary full-text methods/results and metadata.
evidence_scope
literature_reviewed; source-specific experimental curation
experimental_model
Bacterial isolates from healthy adult human stool: E. coli AZO-Ec and E. faecalis AZO-Ef
limitations
Decolorization is an activity readout, not a complete product mass balance or a clinical microbiome intervention. Strain, pH and oxygen dependence preclude assigning one universal rate.
nutrient_topic
Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine
organism
Bacterial isolates from healthy adult human stool: E. coli AZO-Ec and E. faecalis AZO-Ef
plain_language
Human-gut E. coli isolate AZO-Ec decolorized tartrazine under the aerobic culture conditions.
primary_references
Azoreductase activity of dye-decolorizing bacteria isolated from the human gut microbiota. (2019). https://pubmed.ncbi.nlm.nih.gov/30940826/ DOI: 10.1038/s41598-019-41894-8
route
In vitro culture exposure
tissue
Aerobic bacterial culture
Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 61–70
Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Bacterial isolates from healthy adult human stool: E. coli AZO-Ec and E. faecalis AZO-Ef · source_derived_draft · unverified_draft
## tartrazine-ecoli-reduction Human-gut E. coli isolate AZO-Ec decolorized tartrazine under the aerobic culture conditions. Model/species: Bacterial isolates from healthy adult human stool: E. coli AZO-Ec and E. faecalis AZO-Ef Tissue: Aerobic bacterial culture Exposure: Tartrazine 10, 20 and 30 micromolar; selected strains Route: In vitro culture exposure Duration: 30 min comparison, time courses up to 5 h Limits: Decolorization is an activity readout, not a complete product mass balance or a clinical microbiome intervention. Strain, pH and oxygen dependence preclude assigning one universal rate. Primary reference: Azoreductase activity of dye-decolorizing bacteria isolated from the human gut microbiota. (2019). https://pubmed.ncbi.nlm.nih.gov/30940826/ DOI: 10.1038/s41598-019-41894-8 Access: Primary full-text methods/results and metadata.
Complete structured claim and evidence
Human-gut E. faecalis isolate AZO-Ef decolorized tartrazine in the substrate-panel experiment.
Tartrazine → Tartrazine decolorization by human-gut E. faecalis isolate AZO-Ef source_derived_draftungraded
Experimental context and source evidence
dose
Tartrazine 10, 20 and 30 micromolar; selected strains
duration
30 min comparison, time courses up to 5 h
evidence_access
Primary full-text methods/results and metadata.
evidence_scope
literature_reviewed; source-specific experimental curation
experimental_model
Bacterial isolates from healthy adult human stool: E. coli AZO-Ec and E. faecalis AZO-Ef
limitations
Decolorization is an activity readout, not a complete product mass balance or a clinical microbiome intervention. Strain, pH and oxygen dependence preclude assigning one universal rate.
nutrient_topic
Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine
organism
Bacterial isolates from healthy adult human stool: E. coli AZO-Ec and E. faecalis AZO-Ef
plain_language
Human-gut E. faecalis isolate AZO-Ef decolorized tartrazine in the substrate-panel experiment.
primary_references
Azoreductase activity of dye-decolorizing bacteria isolated from the human gut microbiota. (2019). https://pubmed.ncbi.nlm.nih.gov/30940826/ DOI: 10.1038/s41598-019-41894-8
route
In vitro culture exposure
tissue
Aerobic bacterial culture
Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 72–81
Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Bacterial isolates from healthy adult human stool: E. coli AZO-Ec and E. faecalis AZO-Ef · source_derived_draft · unverified_draft
## tartrazine-enterococcus-reduction Human-gut E. faecalis isolate AZO-Ef decolorized tartrazine in the substrate-panel experiment. Model/species: Bacterial isolates from healthy adult human stool: E. coli AZO-Ec and E. faecalis AZO-Ef Tissue: Aerobic bacterial culture Exposure: Tartrazine 10, 20 and 30 micromolar; selected strains Route: In vitro culture exposure Duration: 30 min comparison, time courses up to 5 h Limits: Decolorization is an activity readout, not a complete product mass balance or a clinical microbiome intervention. Strain, pH and oxygen dependence preclude assigning one universal rate. Primary reference: Azoreductase activity of dye-decolorizing bacteria isolated from the human gut microbiota. (2019). https://pubmed.ncbi.nlm.nih.gov/30940826/ DOI: 10.1038/s41598-019-41894-8 Access: Primary full-text methods/results and metadata.
Complete structured claim and evidence
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
The reduced tartrazine pyrazole product SCAP was chemically identified.
Tartrazine → SCAP: reduced pyrazole metabolite of tartrazine 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
The reduced tartrazine pyrazole product SCAP was chemically identified.
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 94–103
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-scap-product The reduced tartrazine pyrazole product SCAP was chemically identified. 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
SCAP oxidation on exposure to air produced the characterized purple derivative purpurazoic acid.
SCAP: reduced pyrazole metabolite of tartrazine → Purpurazoic acid / PPA 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
SCAP oxidation on exposure to air produced the characterized purple derivative purpurazoic acid.
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 105–114
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-ppa-oxidation SCAP oxidation on exposure to air produced the characterized purple derivative purpurazoic acid. 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
SCAP reduced HEK293-cell viability with a reported IC50 of 89 micromolar.
SCAP: reduced pyrazole metabolite of tartrazine → Viability of human HEK293 cells source_derived_draftungraded
Experimental context and source evidence
dose
SCAP and PPA concentration series; IC50 values 89 and 78 micromolar respectively
duration
Viability exposure duration 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
Human HEK293 cells exposed to chemically characterized metabolites
limitations
These concentrations concern isolated metabolites, not parent tartrazine, and do not establish human dietary toxicity or cancer risk.
nutrient_topic
Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine
organism
Human HEK293 cells exposed to chemically characterized metabolites
plain_language
SCAP reduced HEK293-cell viability with a reported IC50 of 89 micromolar.
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 metabolite addition
tissue
Cell viability assay
Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 116–125
Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Human HEK293 cells exposed to chemically characterized metabolites · source_derived_draft · unverified_draft
## tartrazine-scap-viability SCAP reduced HEK293-cell viability with a reported IC50 of 89 micromolar. Model/species: Human HEK293 cells exposed to chemically characterized metabolites Tissue: Cell viability assay Exposure: SCAP and PPA concentration series; IC50 values 89 and 78 micromolar respectively Route: In vitro metabolite addition Duration: Viability exposure duration not specified in accessed abstract Limits: These concentrations concern isolated metabolites, not parent tartrazine, and do not establish human dietary toxicity or cancer risk. 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
Purpurazoic acid reduced HEK293-cell viability with a reported IC50 of 78 micromolar.
Purpurazoic acid / PPA → Viability of human HEK293 cells source_derived_draftungraded
Experimental context and source evidence
dose
SCAP and PPA concentration series; IC50 values 89 and 78 micromolar respectively
duration
Viability exposure duration 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
Human HEK293 cells exposed to chemically characterized metabolites
limitations
These concentrations concern isolated metabolites, not parent tartrazine, and do not establish human dietary toxicity or cancer risk.
nutrient_topic
Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine
organism
Human HEK293 cells exposed to chemically characterized metabolites
plain_language
Purpurazoic acid reduced HEK293-cell viability with a reported IC50 of 78 micromolar.
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 metabolite addition
tissue
Cell viability assay
Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 127–136
Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Human HEK293 cells exposed to chemically characterized metabolites · source_derived_draft · unverified_draft
## tartrazine-ppa-viability Purpurazoic acid reduced HEK293-cell viability with a reported IC50 of 78 micromolar. Model/species: Human HEK293 cells exposed to chemically characterized metabolites Tissue: Cell viability assay Exposure: SCAP and PPA concentration series; IC50 values 89 and 78 micromolar respectively Route: In vitro metabolite addition Duration: Viability exposure duration not specified in accessed abstract Limits: These concentrations concern isolated metabolites, not parent tartrazine, and do not establish human dietary toxicity or cancer risk. 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
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
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
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
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
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
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
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
Tartrazine inhibited human BCRP-mediated probe transport in the membrane-vesicle screen.
Tartrazine → Human ABCG2 / breast cancer resistance protein source_derived_draftungraded
Experimental context and source evidence
dose
Food-additive screen at 50 micromolar; concentration-response experiments
duration
Exact incubation interval not recovered from accessed primary material
evidence_access
Primary PubMed abstract and publisher supplementary screening table; assay detail gaps retained.
evidence_scope
literature_reviewed; source-specific experimental curation
experimental_model
Human ABCG2 / BCRP transporter in membrane-vesicle assay
limitations
Primary abstract and publisher supplementary screening table inspected; no unverified IC50 assigned. Vesicle inhibition does not establish increased drug absorption, vitamin depletion or inhibition of every ABC transporter.
nutrient_topic
Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine
organism
Human ABCG2 / BCRP transporter in membrane-vesicle assay
plain_language
Tartrazine inhibited human BCRP-mediated probe transport in the membrane-vesicle screen.
primary_references
Interaction of Food Additives with Intestinal Efflux Transporters. (2017). https://pubmed.ncbi.nlm.nih.gov/28921988/ DOI: 10.1021/acs.molpharmaceut.7b00563
route
In vitro exposure to membrane vesicles
tissue
Probe-substrate efflux
Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 215–224
Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Human ABCG2 / BCRP transporter in membrane-vesicle assay · source_derived_draft · unverified_draft
## tartrazine-bcrp-inhibition Tartrazine inhibited human BCRP-mediated probe transport in the membrane-vesicle screen. Model/species: Human ABCG2 / BCRP transporter in membrane-vesicle assay Tissue: Probe-substrate efflux Exposure: Food-additive screen at 50 micromolar; concentration-response experiments Route: In vitro exposure to membrane vesicles Duration: Exact incubation interval not recovered from accessed primary material Limits: Primary abstract and publisher supplementary screening table inspected; no unverified IC50 assigned. Vesicle inhibition does not establish increased drug absorption, vitamin depletion or inhibition of every ABC transporter. Primary reference: Interaction of Food Additives with Intestinal Efflux Transporters. (2017). https://pubmed.ncbi.nlm.nih.gov/28921988/ DOI: 10.1021/acs.molpharmaceut.7b00563 Access: Primary PubMed abstract and publisher supplementary screening table; assay detail gaps retained.
Complete structured claim and evidence
Tartrazine did not stimulate P-glycoprotein-specific ATPase activity in the membrane assay.
Tartrazine → ATPase activity of recombinant human ABCB1 / P-glycoprotein source_derived_draftungraded
Experimental context and source evidence
dose
Tartrazine 0.41-900 micromolar; verapamil and orthovanadate controls
duration
Manufacturer ATPase assay interval not stated in accessed methods
evidence_access
Primary full-text methods/results and metadata.
evidence_scope
literature_reviewed; source-specific experimental curation
experimental_model
Recombinant human P-glycoprotein in membrane preparations
limitations
A negative ATPase-stimulation result is bounded by the assay and does not establish universal lack of transport interactions.
nutrient_topic
Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine
organism
Recombinant human P-glycoprotein in membrane preparations
plain_language
Tartrazine did not stimulate P-glycoprotein-specific ATPase activity in the membrane assay.
primary_references
Food dyes as P-glycoprotein modulators. (2020). https://pubmed.ncbi.nlm.nih.gov/33011351/ DOI: 10.1016/j.fct.2020.111785
route
In vitro membrane assay
tissue
ATPase stimulation assay
Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 226–235
Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Recombinant human P-glycoprotein in membrane preparations · source_derived_draft · unverified_draft
## tartrazine-pgp-atpase-null Tartrazine did not stimulate P-glycoprotein-specific ATPase activity in the membrane assay. Model/species: Recombinant human P-glycoprotein in membrane preparations Tissue: ATPase stimulation assay Exposure: Tartrazine 0.41-900 micromolar; verapamil and orthovanadate controls Route: In vitro membrane assay Duration: Manufacturer ATPase assay interval not stated in accessed methods Limits: A negative ATPase-stimulation result is bounded by the assay and does not establish universal lack of transport interactions. Primary reference: Food dyes as P-glycoprotein modulators. (2020). https://pubmed.ncbi.nlm.nih.gov/33011351/ DOI: 10.1016/j.fct.2020.111785 Access: Primary full-text methods/results and metadata.
Complete structured claim and evidence
Tartrazine did not inhibit human P-glycoprotein-mediated rhodamine-123 efflux in the cell assay.
Tartrazine → Human P-glycoprotein / ABCB1 / MDR1 source_derived_draftungraded
Experimental context and source evidence
dose
Tartrazine 0.1-1000 micromolar, rhodamine-123 5 micromolar; GF120918 positive control
duration
1 h at 37 C
evidence_access
Primary full-text methods/results and metadata.
evidence_scope
literature_reviewed; source-specific experimental curation
experimental_model
LLC-MDR1-WT cells expressing recombinant human ABCB1
limitations
Human transporter in a heterologous cell system. Negative P-gp inhibition is not inconsistent with a BCRP effect in a different assay.
nutrient_topic
Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine
organism
LLC-MDR1-WT cells expressing recombinant human ABCB1
plain_language
Tartrazine did not inhibit human P-glycoprotein-mediated rhodamine-123 efflux in the cell assay.
primary_references
Food dyes as P-glycoprotein modulators. (2020). https://pubmed.ncbi.nlm.nih.gov/33011351/ DOI: 10.1016/j.fct.2020.111785
route
In vitro co-incubation
tissue
Rhodamine-123 efflux assay
Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 237–246
Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · LLC-MDR1-WT cells expressing recombinant human ABCB1 · source_derived_draft · unverified_draft
## tartrazine-pgp-efflux-null Tartrazine did not inhibit human P-glycoprotein-mediated rhodamine-123 efflux in the cell assay. Model/species: LLC-MDR1-WT cells expressing recombinant human ABCB1 Tissue: Rhodamine-123 efflux assay Exposure: Tartrazine 0.1-1000 micromolar, rhodamine-123 5 micromolar; GF120918 positive control Route: In vitro co-incubation Duration: 1 h at 37 C Limits: Human transporter in a heterologous cell system. Negative P-gp inhibition is not inconsistent with a BCRP effect in a different assay. Primary reference: Food dyes as P-glycoprotein modulators. (2020). https://pubmed.ncbi.nlm.nih.gov/33011351/ DOI: 10.1016/j.fct.2020.111785 Access: Primary full-text methods/results and metadata.
Complete structured claim and evidence
Apically applied tartrazine did not change sulfasalazine permeability through Caco-2 monolayers.
Tartrazine → Sulfasalazine permeability through human Caco-2 monolayers source_derived_draftungraded
Experimental context and source evidence
dose
Tartrazine 200 micromolar apically with sulfasalazine 500 micromolar; Ko-143 comparator
duration
Samples at 20, 40, 60, 90 and 120 min
evidence_access
Primary full-text methods/results and metadata.
evidence_scope
literature_reviewed; source-specific experimental curation
experimental_model
Human Caco-2 intestinal monolayers
limitations
Cell-monolayer null result is not a clinical drug-interaction trial; transporter accessibility can differ from inside-out vesicles. Bilateral addition also had a limited effect, at most twofold.
nutrient_topic
Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine
organism
Human Caco-2 intestinal monolayers
plain_language
Apically applied tartrazine did not change sulfasalazine permeability through Caco-2 monolayers.
primary_references
Food Additives Inhibit Intestinal Drug Transporters but Have Limited Effect on In Vitro Drug Permeability. (2025). https://pubmed.ncbi.nlm.nih.gov/40773056/ DOI: 10.1021/acs.molpharmaceut.5c00705
route
In vitro apical addition
tissue
Transepithelial drug transport
Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 248–257
Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Human Caco-2 intestinal monolayers · source_derived_draft · unverified_draft
## tartrazine-sulfasalazine-null Apically applied tartrazine did not change sulfasalazine permeability through Caco-2 monolayers. Model/species: Human Caco-2 intestinal monolayers Tissue: Transepithelial drug transport Exposure: Tartrazine 200 micromolar apically with sulfasalazine 500 micromolar; Ko-143 comparator Route: In vitro apical addition Duration: Samples at 20, 40, 60, 90 and 120 min Limits: Cell-monolayer null result is not a clinical drug-interaction trial; transporter accessibility can differ from inside-out vesicles. Bilateral addition also had a limited effect, at most twofold. Primary reference: Food Additives Inhibit Intestinal Drug Transporters but Have Limited Effect on In Vitro Drug Permeability. (2025). https://pubmed.ncbi.nlm.nih.gov/40773056/ DOI: 10.1021/acs.molpharmaceut.5c00705 Access: Primary full-text methods/results and metadata.
Complete structured claim and evidence
Tartrazine inhibited dopamine sulfation in human liver cytosol.
Tartrazine → Dopamine sulfation by human liver cytosol source_derived_draftungraded
Experimental context and source evidence
dose
Tartrazine in an additive-inhibition panel; concentration and substrate amounts not in abstract
duration
Assay 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
Human liver cytosolic preparations
limitations
A functional sulfation assay does not demonstrate direct SULT1A3 binding or altered human brain dopamine. Ethinyloestradiol findings for other additives are not transferred to tartrazine.
nutrient_topic
Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine
organism
Human liver cytosolic preparations
plain_language
Tartrazine inhibited dopamine sulfation in human liver cytosol.
primary_references
Common food additives are potent inhibitors of human liver 17 alpha-ethinyloestradiol and dopamine sulphotransferases. (1993). https://pubmed.ncbi.nlm.nih.gov/8250957/ DOI: 10.1016/0006-2952(93)90575-h
route
In vitro cytosolic enzyme assay
tissue
Dopamine sulfation
Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 259–268
Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Human liver cytosolic preparations · source_derived_draft · unverified_draft
## tartrazine-dopamine-sulfation Tartrazine inhibited dopamine sulfation in human liver cytosol. Model/species: Human liver cytosolic preparations Tissue: Dopamine sulfation Exposure: Tartrazine in an additive-inhibition panel; concentration and substrate amounts not in abstract Route: In vitro cytosolic enzyme assay Duration: Assay interval not specified in accessed abstract Limits: A functional sulfation assay does not demonstrate direct SULT1A3 binding or altered human brain dopamine. Ethinyloestradiol findings for other additives are not transferred to tartrazine. Primary reference: Common food additives are potent inhibitors of human liver 17 alpha-ethinyloestradiol and dopamine sulphotransferases. (1993). https://pubmed.ncbi.nlm.nih.gov/8250957/ DOI: 10.1016/0006-2952(93)90575-h Access: Primary PubMed abstract; unrecovered method details explicitly retained.
Complete structured claim and evidence
Tartrazine activated the human ER-alpha reporter in MCF-7 cells, with a reported EC50 of 160 nM.
Tartrazine → Human ER-alpha-dependent reporter transcription in MCF-7 cells source_derived_draftungraded
Experimental context and source evidence
dose
Tartrazine concentration response; reported EC50 160 nM
duration
Reporter exposure 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
Human ESR1-positive MCF-7 breast cancer cells
limitations
Reporter activation is not direct receptor-binding proof or demonstrated estrogenic disease in humans; the proposed link to primary biliary disease remains a hypothesis.
nutrient_topic
Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine
organism
Human ESR1-positive MCF-7 breast cancer cells
plain_language
Tartrazine activated the human ER-alpha reporter in MCF-7 cells, with a reported EC50 of 160 nM.
primary_references
Tartrazine and sunset yellow are xenoestrogens in a new screening assay to identify modulators of human oestrogen receptor transcriptional activity. (2012). https://pubmed.ncbi.nlm.nih.gov/22562034/ DOI: 10.1016/j.tox.2012.04.014
route
In vitro cell exposure
tissue
Estrogen-response-element reporter
Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 270–279
Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Human ESR1-positive MCF-7 breast cancer cells · source_derived_draft · unverified_draft
## tartrazine-estrogen-reporter Tartrazine activated the human ER-alpha reporter in MCF-7 cells, with a reported EC50 of 160 nM. Model/species: Human ESR1-positive MCF-7 breast cancer cells Tissue: Estrogen-response-element reporter Exposure: Tartrazine concentration response; reported EC50 160 nM Route: In vitro cell exposure Duration: Reporter exposure interval not specified in accessed abstract Limits: Reporter activation is not direct receptor-binding proof or demonstrated estrogenic disease in humans; the proposed link to primary biliary disease remains a hypothesis. Primary reference: Tartrazine and sunset yellow are xenoestrogens in a new screening assay to identify modulators of human oestrogen receptor transcriptional activity. (2012). https://pubmed.ncbi.nlm.nih.gov/22562034/ DOI: 10.1016/j.tox.2012.04.014 Access: Primary PubMed abstract; unrecovered method details explicitly retained.
Complete structured claim and evidence
The selected food-color-reactive children had lower serum zinc after the tartrazine challenge.
Tartrazine → Serum zinc in selected food-color-reactive children source_derived_draftungraded
Experimental context and source evidence
dose
Single 50 mg tartrazine beverage challenge
duration
120 min monitoring
evidence_access
Primary full-text methods/results and metadata.
evidence_scope
literature_reviewed; source-specific experimental curation
experimental_model
Selected children with parent-reported food-color reactions; tartrazine group n=23, matched tartrazine control subgroup n=5
limitations
No placebo challenge group in this 1997 experiment; selected population and small control subgroup. The source reports significant changes, but provides no zinc balance or intracellular threshold. Association does not prove chelation, ADHD causation, or benefit from zinc supplementation.
nutrient_topic
Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine
organism
Selected children with parent-reported food-color reactions; tartrazine group n=23, matched tartrazine control subgroup n=5
plain_language
The selected food-color-reactive children had lower serum zinc after the tartrazine challenge.
primary_references
Assessment of Chemical Factors in Relation to Child Hyperactivity (1997). https://doi.org/10.1080/13590849762466 DOI: 10.1080/13590849762466
route
Oral beverage
tissue
Serum and urine zinc
Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 281–290
Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Selected children with parent-reported food-color reactions; tartrazine group n=23, matched tartrazine control subgroup n=5 · source_derived_draft · unverified_draft
## tartrazine-zinc-serum The selected food-color-reactive children had lower serum zinc after the tartrazine challenge. Model/species: Selected children with parent-reported food-color reactions; tartrazine group n=23, matched tartrazine control subgroup n=5 Tissue: Serum and urine zinc Exposure: Single 50 mg tartrazine beverage challenge Route: Oral beverage Duration: 120 min monitoring Limits: No placebo challenge group in this 1997 experiment; selected population and small control subgroup. The source reports significant changes, but provides no zinc balance or intracellular threshold. Association does not prove chelation, ADHD causation, or benefit from zinc supplementation. Primary reference: Assessment of Chemical Factors in Relation to Child Hyperactivity (1997). https://doi.org/10.1080/13590849762466 DOI: 10.1080/13590849762466 Access: Primary full-text methods/results and metadata.
Complete structured claim and evidence
The selected food-color-reactive children had higher urinary zinc output after the tartrazine challenge.
Tartrazine → Urinary zinc in selected food-color-reactive children source_derived_draftungraded
Experimental context and source evidence
dose
Single 50 mg tartrazine beverage challenge
duration
120 min monitoring
evidence_access
Primary full-text methods/results and metadata.
evidence_scope
literature_reviewed; source-specific experimental curation
experimental_model
Selected children with parent-reported food-color reactions; tartrazine group n=23, matched tartrazine control subgroup n=5
limitations
No placebo challenge group in this 1997 experiment; selected population and small control subgroup. The source reports significant changes, but provides no zinc balance or intracellular threshold. Association does not prove chelation, ADHD causation, or benefit from zinc supplementation.
nutrient_topic
Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine
organism
Selected children with parent-reported food-color reactions; tartrazine group n=23, matched tartrazine control subgroup n=5
plain_language
The selected food-color-reactive children had higher urinary zinc output after the tartrazine challenge.
primary_references
Assessment of Chemical Factors in Relation to Child Hyperactivity (1997). https://doi.org/10.1080/13590849762466 DOI: 10.1080/13590849762466
route
Oral beverage
tissue
Serum and urine zinc
Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 292–301
Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Selected children with parent-reported food-color reactions; tartrazine group n=23, matched tartrazine control subgroup n=5 · source_derived_draft · unverified_draft
## tartrazine-zinc-urine The selected food-color-reactive children had higher urinary zinc output after the tartrazine challenge. Model/species: Selected children with parent-reported food-color reactions; tartrazine group n=23, matched tartrazine control subgroup n=5 Tissue: Serum and urine zinc Exposure: Single 50 mg tartrazine beverage challenge Route: Oral beverage Duration: 120 min monitoring Limits: No placebo challenge group in this 1997 experiment; selected population and small control subgroup. The source reports significant changes, but provides no zinc balance or intracellular threshold. Association does not prove chelation, ADHD causation, or benefit from zinc supplementation. Primary reference: Assessment of Chemical Factors in Relation to Child Hyperactivity (1997). https://doi.org/10.1080/13590849762466 DOI: 10.1080/13590849762466 Access: Primary full-text methods/results and metadata.
Complete structured claim and evidence
The small matched control subgroup showed no significant zinc change after tartrazine.
Tartrazine → Serum and urinary zinc response in control children source_derived_draftungraded
Experimental context and source evidence
dose
Single 50 mg tartrazine beverage challenge
duration
120 min monitoring
evidence_access
Primary full-text methods/results and metadata.
evidence_scope
literature_reviewed; source-specific experimental curation
experimental_model
Selected children with parent-reported food-color reactions; tartrazine group n=23, matched tartrazine control subgroup n=5
limitations
No placebo challenge group in this 1997 experiment; selected population and small control subgroup. The source reports significant changes, but provides no zinc balance or intracellular threshold. Association does not prove chelation, ADHD causation, or benefit from zinc supplementation.
nutrient_topic
Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine
organism
Selected children with parent-reported food-color reactions; tartrazine group n=23, matched tartrazine control subgroup n=5
plain_language
The small matched control subgroup showed no significant zinc change after tartrazine.
primary_references
Assessment of Chemical Factors in Relation to Child Hyperactivity (1997). https://doi.org/10.1080/13590849762466 DOI: 10.1080/13590849762466
route
Oral beverage
tissue
Serum and urine zinc
Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 303–312
Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Selected children with parent-reported food-color reactions; tartrazine group n=23, matched tartrazine control subgroup n=5 · source_derived_draft · unverified_draft
## tartrazine-zinc-control-null The small matched control subgroup showed no significant zinc change after tartrazine. Model/species: Selected children with parent-reported food-color reactions; tartrazine group n=23, matched tartrazine control subgroup n=5 Tissue: Serum and urine zinc Exposure: Single 50 mg tartrazine beverage challenge Route: Oral beverage Duration: 120 min monitoring Limits: No placebo challenge group in this 1997 experiment; selected population and small control subgroup. The source reports significant changes, but provides no zinc balance or intracellular threshold. Association does not prove chelation, ADHD causation, or benefit from zinc supplementation. Primary reference: Assessment of Chemical Factors in Relation to Child Hyperactivity (1997). https://doi.org/10.1080/13590849762466 DOI: 10.1080/13590849762466 Access: Primary full-text methods/results and metadata.
Complete structured claim and evidence
The blinded challenge identified dose-related irritability, restlessness or sleep disturbance in a subset of the selected children.
Tartrazine → Parent-rated behavior after blinded tartrazine challenge in selected children source_derived_draftungraded
Experimental context and source evidence
dose
Placebo or tartrazine 1, 2, 5, 10, 20 or 50 mg each challenge morning
duration
21-day repeated-measures study; ratings for each 24 h
evidence_access
Primary PubMed abstract; unrecovered method details explicitly retained.
evidence_scope
literature_reviewed; source-specific experimental curation
experimental_model
Selected children aged 2-14 years: 34 suspected/uncertain reactors and 20 controls
limitations
Recruitment enriched for suspected reactions; parent ratings and individual-response classification do not prove universal effects or a mechanism mediated by zinc.
nutrient_topic
Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine
organism
Selected children aged 2-14 years: 34 suspected/uncertain reactors and 20 controls
plain_language
The blinded challenge identified dose-related irritability, restlessness or sleep disturbance in a subset of the selected children.
primary_references
Synthetic food coloring and behavior: a dose response effect in a double-blind, placebo-controlled, repeated-measures study. (1994). https://pubmed.ncbi.nlm.nih.gov/7965420/ DOI: 10.1016/s0022-3476(94)70059-1
route
Oral administration
tissue
Blinded parent-rated behavior
Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 314–323
Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Selected children aged 2-14 years: 34 suspected/uncertain reactors and 20 controls · source_derived_draft · unverified_draft
## tartrazine-behavior-challenge The blinded challenge identified dose-related irritability, restlessness or sleep disturbance in a subset of the selected children. Model/species: Selected children aged 2-14 years: 34 suspected/uncertain reactors and 20 controls Tissue: Blinded parent-rated behavior Exposure: Placebo or tartrazine 1, 2, 5, 10, 20 or 50 mg each challenge morning Route: Oral administration Duration: 21-day repeated-measures study; ratings for each 24 h Limits: Recruitment enriched for suspected reactions; parent ratings and individual-response classification do not prove universal effects or a mechanism mediated by zinc. Primary reference: Synthetic food coloring and behavior: a dose response effect in a double-blind, placebo-controlled, repeated-measures study. (1994). https://pubmed.ncbi.nlm.nih.gov/7965420/ DOI: 10.1016/s0022-3476(94)70059-1 Access: Primary PubMed abstract; unrecovered method details explicitly retained.
Complete structured claim and evidence
Four of 156 aspirin-intolerant asthmatics had a double-blind-confirmed tartrazine response with more than a 25% FEV1 fall and symptoms.
Tartrazine → Airway response to tartrazine in aspirin-intolerant asthmatics source_derived_draftungraded
Experimental context and source evidence
dose
Increasing tartrazine doses up to 25 mg; positive open challenges repeated double blind
duration
Acute challenge; exact observation window not specified in abstract
evidence_access
Primary PubMed abstract; unrecovered method details explicitly retained.
evidence_scope
literature_reviewed; source-specific experimental curation
experimental_model
156 patients with confirmed aspirin-induced asthma in a multicenter study
limitations
Four confirmed reactions do not establish universal aspirin-tartrazine cross-reactivity or a shared IgE/COX mechanism. Results are specific to the recruited population.
nutrient_topic
Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine
organism
156 patients with confirmed aspirin-induced asthma in a multicenter study
plain_language
Four of 156 aspirin-intolerant asthmatics had a double-blind-confirmed tartrazine response with more than a 25% FEV1 fall and symptoms.
primary_references
Intolerance to tartrazine in aspirin-induced asthma: results of a multicenter study. (1988). https://pubmed.ncbi.nlm.nih.gov/3387687/ DOI: 10.1159/000195391
route
Oral tartrazine; aspirin intolerance was a selection criterion, not co-administration
tissue
Oral challenge, spirometry and symptoms
Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 325–334
Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · 156 patients with confirmed aspirin-induced asthma in a multicenter study · source_derived_draft · unverified_draft
## tartrazine-aspirin-asthma Four of 156 aspirin-intolerant asthmatics had a double-blind-confirmed tartrazine response with more than a 25% FEV1 fall and symptoms. Model/species: 156 patients with confirmed aspirin-induced asthma in a multicenter study Tissue: Oral challenge, spirometry and symptoms Exposure: Increasing tartrazine doses up to 25 mg; positive open challenges repeated double blind Route: Oral tartrazine; aspirin intolerance was a selection criterion, not co-administration Duration: Acute challenge; exact observation window not specified in abstract Limits: Four confirmed reactions do not establish universal aspirin-tartrazine cross-reactivity or a shared IgE/COX mechanism. Results are specific to the recruited population. Primary reference: Intolerance to tartrazine in aspirin-induced asthma: results of a multicenter study. (1988). https://pubmed.ncbi.nlm.nih.gov/3387687/ DOI: 10.1159/000195391 Access: Primary PubMed abstract; unrecovered method details explicitly retained.
Complete structured claim and evidence
The 26-adult crossover study found no significant cutaneous, respiratory or cardiovascular difference between tartrazine and placebo.
Tartrazine → Cutaneous, respiratory and cardiovascular responses in atopic adults source_derived_draftungraded
Experimental context and source evidence
dose
Tartrazine 35 mg versus placebo
duration
Acute challenge; exact observation period not in abstract
evidence_access
Primary PubMed abstract; unrecovered method details explicitly retained.
evidence_scope
literature_reviewed; source-specific experimental curation
experimental_model
26 atopic adults with rhinitis, asthma, urticaria or NSAID-related reactions
limitations
Small study with no significant group response does not rule out rare individual intolerance.
nutrient_topic
Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine
organism
26 atopic adults with rhinitis, asthma, urticaria or NSAID-related reactions
plain_language
The 26-adult crossover study found no significant cutaneous, respiratory or cardiovascular difference between tartrazine and placebo.
primary_references
Safety of ingestion of yellow tartrazine by double-blind placebo controlled challenge in 26 atopic adults. (2010). https://pubmed.ncbi.nlm.nih.gov/20106580/ DOI: 10.1016/j.aller.2009.09.009
route
Oral administration
tissue
Double-blind placebo-controlled crossover challenge
Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 336–345
Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · 26 atopic adults with rhinitis, asthma, urticaria or NSAID-related reactions · source_derived_draft · unverified_draft
## tartrazine-atopic-null The 26-adult crossover study found no significant cutaneous, respiratory or cardiovascular difference between tartrazine and placebo. Model/species: 26 atopic adults with rhinitis, asthma, urticaria or NSAID-related reactions Tissue: Double-blind placebo-controlled crossover challenge Exposure: Tartrazine 35 mg versus placebo Route: Oral administration Duration: Acute challenge; exact observation period not in abstract Limits: Small study with no significant group response does not rule out rare individual intolerance. Primary reference: Safety of ingestion of yellow tartrazine by double-blind placebo controlled challenge in 26 atopic adults. (2010). https://pubmed.ncbi.nlm.nih.gov/20106580/ DOI: 10.1016/j.aller.2009.09.009 Access: Primary PubMed abstract; unrecovered method details explicitly retained.
Complete structured claim and evidence
Tartrazine did not increase gut micronucleus frequency under the tested acute mouse protocol.
Tartrazine → Mouse gut micronucleus frequency source_derived_draftungraded
Experimental context and source evidence
dose
Tartrazine doses up to 2000 mg/kg body weight
duration
Doses 24 h apart
evidence_access
Primary PubMed abstract; unrecovered method details explicitly retained.
evidence_scope
literature_reviewed; source-specific experimental curation
experimental_model
Mice in the in vivo gut micronucleus assay
limitations
No micronucleus increase under this protocol does not exclude transient DNA damage, other endpoints, or chronic effects. Co-studied dyes and their metabolites are not pooled as tartrazine-specific results.
nutrient_topic
Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine
organism
Mice in the in vivo gut micronucleus assay
plain_language
Tartrazine did not increase gut micronucleus frequency under the tested acute mouse protocol.
primary_references
Lack of genotoxic effect of food dyes amaranth, sunset yellow and tartrazine and their metabolites in the gut micronucleus assay in mice. (2009). https://pubmed.ncbi.nlm.nih.gov/19095036/ DOI: 10.1016/j.fct.2008.11.034
route
Oral gavage twice
tissue
Intestinal genotoxicity endpoint
Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 347–356
Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Mice in the in vivo gut micronucleus assay · source_derived_draft · unverified_draft
## tartrazine-gut-micronucleus-null Tartrazine did not increase gut micronucleus frequency under the tested acute mouse protocol. Model/species: Mice in the in vivo gut micronucleus assay Tissue: Intestinal genotoxicity endpoint Exposure: Tartrazine doses up to 2000 mg/kg body weight Route: Oral gavage twice Duration: Doses 24 h apart Limits: No micronucleus increase under this protocol does not exclude transient DNA damage, other endpoints, or chronic effects. Co-studied dyes and their metabolites are not pooled as tartrazine-specific results. Primary reference: Lack of genotoxic effect of food dyes amaranth, sunset yellow and tartrazine and their metabolites in the gut micronucleus assay in mice. (2009). https://pubmed.ncbi.nlm.nih.gov/19095036/ DOI: 10.1016/j.fct.2008.11.034 Access: Primary PubMed abstract; unrecovered method details explicitly retained.
Complete structured claim and evidence
High-dose oral tartrazine lowered measured brain ascorbic acid in the rat experiment.
Tartrazine → Rat brain ascorbic acid content source_derived_draftungraded
Experimental context and source evidence
dose
Tartrazine 700 mg/kg body weight for 2 weeks
duration
2 treatment weeks; endpoint tissue analysis
evidence_access
Primary full-text methods/results and metadata.
evidence_scope
literature_reviewed; source-specific experimental curation
experimental_model
Male Wistar rats; six per group
limitations
Very high animal exposure. Results section reports lower ascorbic acid with no significant GSH or MDA change from tartrazine alone; broader abstract/discussion wording should not replace these results.
nutrient_topic
Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine
organism
Male Wistar rats; six per group
plain_language
High-dose oral tartrazine lowered measured brain ascorbic acid in the rat experiment.
primary_references
High-Dose Aspirin Reverses Tartrazine-Induced Cell Growth Dysregulation Independent of p53 Signaling and Antioxidant Mechanisms in Rat Brain. (2019). https://pubmed.ncbi.nlm.nih.gov/31032366/ DOI: 10.1155/2019/9096404
route
Oral tartrazine
tissue
Brain tissue biochemical and histological endpoints
Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 358–367
Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Male Wistar rats; six per group · source_derived_draft · unverified_draft
## tartrazine-brain-ascorbate High-dose oral tartrazine lowered measured brain ascorbic acid in the rat experiment. Model/species: Male Wistar rats; six per group Tissue: Brain tissue biochemical and histological endpoints Exposure: Tartrazine 700 mg/kg body weight for 2 weeks Route: Oral tartrazine Duration: 2 treatment weeks; endpoint tissue analysis Limits: Very high animal exposure. Results section reports lower ascorbic acid with no significant GSH or MDA change from tartrazine alone; broader abstract/discussion wording should not replace these results. Primary reference: High-Dose Aspirin Reverses Tartrazine-Induced Cell Growth Dysregulation Independent of p53 Signaling and Antioxidant Mechanisms in Rat Brain. (2019). https://pubmed.ncbi.nlm.nih.gov/31032366/ DOI: 10.1155/2019/9096404 Access: Primary full-text methods/results and metadata.
Complete structured claim and evidence
Tartrazine alone did not significantly change brain reduced glutathione relative to control rats.
Tartrazine → Rat brain reduced glutathione content source_derived_draftungraded
Experimental context and source evidence
dose
Tartrazine 700 mg/kg body weight for 2 weeks
duration
2 treatment weeks; endpoint tissue analysis
evidence_access
Primary full-text methods/results and metadata.
evidence_scope
literature_reviewed; source-specific experimental curation
experimental_model
Male Wistar rats; six per group
limitations
Very high animal exposure. Results section reports lower ascorbic acid with no significant GSH or MDA change from tartrazine alone; broader abstract/discussion wording should not replace these results.
nutrient_topic
Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine
organism
Male Wistar rats; six per group
plain_language
Tartrazine alone did not significantly change brain reduced glutathione relative to control rats.
primary_references
High-Dose Aspirin Reverses Tartrazine-Induced Cell Growth Dysregulation Independent of p53 Signaling and Antioxidant Mechanisms in Rat Brain. (2019). https://pubmed.ncbi.nlm.nih.gov/31032366/ DOI: 10.1155/2019/9096404
route
Oral tartrazine
tissue
Brain tissue biochemical and histological endpoints
Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 369–378
Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Male Wistar rats; six per group · source_derived_draft · unverified_draft
## tartrazine-brain-gsh-null Tartrazine alone did not significantly change brain reduced glutathione relative to control rats. Model/species: Male Wistar rats; six per group Tissue: Brain tissue biochemical and histological endpoints Exposure: Tartrazine 700 mg/kg body weight for 2 weeks Route: Oral tartrazine Duration: 2 treatment weeks; endpoint tissue analysis Limits: Very high animal exposure. Results section reports lower ascorbic acid with no significant GSH or MDA change from tartrazine alone; broader abstract/discussion wording should not replace these results. Primary reference: High-Dose Aspirin Reverses Tartrazine-Induced Cell Growth Dysregulation Independent of p53 Signaling and Antioxidant Mechanisms in Rat Brain. (2019). https://pubmed.ncbi.nlm.nih.gov/31032366/ DOI: 10.1155/2019/9096404 Access: Primary full-text methods/results and metadata.
Complete structured claim and evidence
Tartrazine alone did not significantly change the brain MDA assay endpoint in this two-week rat study.
Tartrazine → Rat brain malondialdehyde assay signal source_derived_draftungraded
Experimental context and source evidence
dose
Tartrazine 700 mg/kg body weight for 2 weeks
duration
2 treatment weeks; endpoint tissue analysis
evidence_access
Primary full-text methods/results and metadata.
evidence_scope
literature_reviewed; source-specific experimental curation
experimental_model
Male Wistar rats; six per group
limitations
Very high animal exposure. Results section reports lower ascorbic acid with no significant GSH or MDA change from tartrazine alone; broader abstract/discussion wording should not replace these results.
nutrient_topic
Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine
organism
Male Wistar rats; six per group
plain_language
Tartrazine alone did not significantly change the brain MDA assay endpoint in this two-week rat study.
primary_references
High-Dose Aspirin Reverses Tartrazine-Induced Cell Growth Dysregulation Independent of p53 Signaling and Antioxidant Mechanisms in Rat Brain. (2019). https://pubmed.ncbi.nlm.nih.gov/31032366/ DOI: 10.1155/2019/9096404
route
Oral tartrazine
tissue
Brain tissue biochemical and histological endpoints
Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 380–389
Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Male Wistar rats; six per group · source_derived_draft · unverified_draft
## tartrazine-brain-mda-null Tartrazine alone did not significantly change the brain MDA assay endpoint in this two-week rat study. Model/species: Male Wistar rats; six per group Tissue: Brain tissue biochemical and histological endpoints Exposure: Tartrazine 700 mg/kg body weight for 2 weeks Route: Oral tartrazine Duration: 2 treatment weeks; endpoint tissue analysis Limits: Very high animal exposure. Results section reports lower ascorbic acid with no significant GSH or MDA change from tartrazine alone; broader abstract/discussion wording should not replace these results. Primary reference: High-Dose Aspirin Reverses Tartrazine-Induced Cell Growth Dysregulation Independent of p53 Signaling and Antioxidant Mechanisms in Rat Brain. (2019). https://pubmed.ncbi.nlm.nih.gov/31032366/ DOI: 10.1155/2019/9096404 Access: Primary full-text methods/results and metadata.
Complete structured claim and evidence
Aspirin pretreatment and co-exposure attenuated the brain histological injury observed with high-dose tartrazine.
Aspirin / acetylsalicylic acid → Brain histopathology in high-dose tartrazine-exposed rats source_derived_draftungraded
Experimental context and source evidence
dose
Aspirin 150 mg/kg body weight for 3 weeks, starting one week before tartrazine 700 mg/kg for 2 weeks
duration
3 weeks total; 2 weeks co-exposure
evidence_access
Primary full-text methods/results and metadata.
evidence_scope
literature_reviewed; source-specific experimental curation
experimental_model
Male Wistar rats; six per group
limitations
High-dose preclinical experiment, not an aspirin treatment recommendation. The routes differ and the study does not establish antioxidant or p53 mediation.
nutrient_topic
Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine
organism
Male Wistar rats; six per group
plain_language
Aspirin pretreatment and co-exposure attenuated the brain histological injury observed with high-dose tartrazine.
primary_references
High-Dose Aspirin Reverses Tartrazine-Induced Cell Growth Dysregulation Independent of p53 Signaling and Antioxidant Mechanisms in Rat Brain. (2019). https://pubmed.ncbi.nlm.nih.gov/31032366/ DOI: 10.1155/2019/9096404
route
Intraperitoneal aspirin plus oral tartrazine
tissue
Brain histopathology
Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 391–400
Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Male Wistar rats; six per group · source_derived_draft · unverified_draft
## tartrazine-aspirin-histology Aspirin pretreatment and co-exposure attenuated the brain histological injury observed with high-dose tartrazine. Model/species: Male Wistar rats; six per group Tissue: Brain histopathology Exposure: Aspirin 150 mg/kg body weight for 3 weeks, starting one week before tartrazine 700 mg/kg for 2 weeks Route: Intraperitoneal aspirin plus oral tartrazine Duration: 3 weeks total; 2 weeks co-exposure Limits: High-dose preclinical experiment, not an aspirin treatment recommendation. The routes differ and the study does not establish antioxidant or p53 mediation. Primary reference: High-Dose Aspirin Reverses Tartrazine-Induced Cell Growth Dysregulation Independent of p53 Signaling and Antioxidant Mechanisms in Rat Brain. (2019). https://pubmed.ncbi.nlm.nih.gov/31032366/ DOI: 10.1155/2019/9096404 Access: Primary full-text methods/results and metadata.
Complete structured claim and evidence
Tartrazine formed assemblies with the synthetic antimicrobial peptide DHVAR4.
Tartrazine → DHVAR4 antimicrobial peptide source_derived_draftungraded
Experimental context and source evidence
dose
DHVAR4 plus tartrazine; concentrations and ratios not specified in accessed abstract
duration
Assay intervals 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
Synthetic histatin-derived DHVAR4 peptide, model lipid bilayers and tested bacterial cultures
limitations
No clinical antimicrobial efficacy or effect on all natural histatins is established. Species-specific bactericidal thresholds and mammalian exposure require the full protocol.
nutrient_topic
Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine
organism
Synthetic histatin-derived DHVAR4 peptide, model lipid bilayers and tested bacterial cultures
plain_language
Tartrazine formed assemblies with the synthetic antimicrobial peptide DHVAR4.
primary_references
Anionic food color tartrazine enhances antibacterial efficacy of histatin-derived peptide DHVAR4 by fine-tuning its membrane activity. (2020). https://pubmed.ncbi.nlm.nih.gov/32115014/ DOI: 10.1017/S0033583520000013
route
In vitro mixing and membrane/bacterial assays
tissue
Peptide-dye association and membrane activity
Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 402–411
Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Synthetic histatin-derived DHVAR4 peptide, model lipid bilayers and tested bacterial cultures · source_derived_draft · unverified_draft
## tartrazine-peptide-association Tartrazine formed assemblies with the synthetic antimicrobial peptide DHVAR4. Model/species: Synthetic histatin-derived DHVAR4 peptide, model lipid bilayers and tested bacterial cultures Tissue: Peptide-dye association and membrane activity Exposure: DHVAR4 plus tartrazine; concentrations and ratios not specified in accessed abstract Route: In vitro mixing and membrane/bacterial assays Duration: Assay intervals not specified in accessed abstract Limits: No clinical antimicrobial efficacy or effect on all natural histatins is established. Species-specific bactericidal thresholds and mammalian exposure require the full protocol. Primary reference: Anionic food color tartrazine enhances antibacterial efficacy of histatin-derived peptide DHVAR4 by fine-tuning its membrane activity. (2020). https://pubmed.ncbi.nlm.nih.gov/32115014/ DOI: 10.1017/S0033583520000013 Access: Primary PubMed abstract; unrecovered method details explicitly retained.
Complete structured claim and evidence
Tartrazine favored the membrane-associated helical conformation of DHVAR4.
Tartrazine → Membrane-associated helical conformation of DHVAR4 source_derived_draftungraded
Experimental context and source evidence
dose
DHVAR4 plus tartrazine; concentrations and ratios not specified in accessed abstract
duration
Assay intervals 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
Synthetic histatin-derived DHVAR4 peptide, model lipid bilayers and tested bacterial cultures
limitations
No clinical antimicrobial efficacy or effect on all natural histatins is established. Species-specific bactericidal thresholds and mammalian exposure require the full protocol.
nutrient_topic
Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine
organism
Synthetic histatin-derived DHVAR4 peptide, model lipid bilayers and tested bacterial cultures
plain_language
Tartrazine favored the membrane-associated helical conformation of DHVAR4.
primary_references
Anionic food color tartrazine enhances antibacterial efficacy of histatin-derived peptide DHVAR4 by fine-tuning its membrane activity. (2020). https://pubmed.ncbi.nlm.nih.gov/32115014/ DOI: 10.1017/S0033583520000013
route
In vitro mixing and membrane/bacterial assays
tissue
Peptide-dye association and membrane activity
Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 413–422
Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Synthetic histatin-derived DHVAR4 peptide, model lipid bilayers and tested bacterial cultures · source_derived_draft · unverified_draft
## tartrazine-peptide-helix Tartrazine favored the membrane-associated helical conformation of DHVAR4. Model/species: Synthetic histatin-derived DHVAR4 peptide, model lipid bilayers and tested bacterial cultures Tissue: Peptide-dye association and membrane activity Exposure: DHVAR4 plus tartrazine; concentrations and ratios not specified in accessed abstract Route: In vitro mixing and membrane/bacterial assays Duration: Assay intervals not specified in accessed abstract Limits: No clinical antimicrobial efficacy or effect on all natural histatins is established. Species-specific bactericidal thresholds and mammalian exposure require the full protocol. Primary reference: Anionic food color tartrazine enhances antibacterial efficacy of histatin-derived peptide DHVAR4 by fine-tuning its membrane activity. (2020). https://pubmed.ncbi.nlm.nih.gov/32115014/ DOI: 10.1017/S0033583520000013 Access: Primary PubMed abstract; unrecovered method details explicitly retained.
Complete structured claim and evidence
Tartrazine increased DHVAR4 antibacterial activity in the tested cultures.
Tartrazine → DHVAR4 antibacterial activity against tested Gram-positive and Gram-negative bacteria source_derived_draftungraded
Experimental context and source evidence
dose
DHVAR4 plus tartrazine; concentrations and ratios not specified in accessed abstract
duration
Assay intervals 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
Synthetic histatin-derived DHVAR4 peptide, model lipid bilayers and tested bacterial cultures
limitations
No clinical antimicrobial efficacy or effect on all natural histatins is established. Species-specific bactericidal thresholds and mammalian exposure require the full protocol.
nutrient_topic
Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine
organism
Synthetic histatin-derived DHVAR4 peptide, model lipid bilayers and tested bacterial cultures
plain_language
Tartrazine increased DHVAR4 antibacterial activity in the tested cultures.
primary_references
Anionic food color tartrazine enhances antibacterial efficacy of histatin-derived peptide DHVAR4 by fine-tuning its membrane activity. (2020). https://pubmed.ncbi.nlm.nih.gov/32115014/ DOI: 10.1017/S0033583520000013
route
In vitro mixing and membrane/bacterial assays
tissue
Peptide-dye association and membrane activity
Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 424–433
Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Synthetic histatin-derived DHVAR4 peptide, model lipid bilayers and tested bacterial cultures · source_derived_draft · unverified_draft
## tartrazine-peptide-antibacterial Tartrazine increased DHVAR4 antibacterial activity in the tested cultures. Model/species: Synthetic histatin-derived DHVAR4 peptide, model lipid bilayers and tested bacterial cultures Tissue: Peptide-dye association and membrane activity Exposure: DHVAR4 plus tartrazine; concentrations and ratios not specified in accessed abstract Route: In vitro mixing and membrane/bacterial assays Duration: Assay intervals not specified in accessed abstract Limits: No clinical antimicrobial efficacy or effect on all natural histatins is established. Species-specific bactericidal thresholds and mammalian exposure require the full protocol. Primary reference: Anionic food color tartrazine enhances antibacterial efficacy of histatin-derived peptide DHVAR4 by fine-tuning its membrane activity. (2020). https://pubmed.ncbi.nlm.nih.gov/32115014/ DOI: 10.1017/S0033583520000013 Access: Primary PubMed abstract; unrecovered method details explicitly retained.
Complete structured claim and evidence
Dissolved tartrazine reduced optical scattering by bringing the aqueous refractive index closer to that of high-index components.
Tartrazine → Refractive-index matching by aqueous tartrazine in optical phantoms source_derived_draftungraded
Experimental context and source evidence
dose
Tartrazine solution 0.6 M in representative optical phantom experiment
duration
Optical measurements; no oral exposure
evidence_access
Primary full-text methods/results and metadata.
evidence_scope
literature_reviewed; source-specific experimental curation
experimental_model
Aqueous silica scattering phantoms and ex vivo tissue experiments
limitations
Strong absorption alters refractive index and reduces scattering in a red spectral window; this is a physical mechanism, not receptor pharmacology or a dietary health effect.
nutrient_topic
Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine
organism
Aqueous silica scattering phantoms and ex vivo tissue experiments
plain_language
Dissolved tartrazine reduced optical scattering by bringing the aqueous refractive index closer to that of high-index components.
primary_references
Achieving optical transparency in live animals with absorbing molecules. (2024). https://pubmed.ncbi.nlm.nih.gov/39236186/ DOI: 10.1126/science.adm6869
route
Physical addition of dye to aqueous scattering medium
tissue
Optical refractive-index matching
Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 435–444
Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Aqueous silica scattering phantoms and ex vivo tissue experiments · source_derived_draft · unverified_draft
## tartrazine-optical-index Dissolved tartrazine reduced optical scattering by bringing the aqueous refractive index closer to that of high-index components. Model/species: Aqueous silica scattering phantoms and ex vivo tissue experiments Tissue: Optical refractive-index matching Exposure: Tartrazine solution 0.6 M in representative optical phantom experiment Route: Physical addition of dye to aqueous scattering medium Duration: Optical measurements; no oral exposure Limits: Strong absorption alters refractive index and reduces scattering in a red spectral window; this is a physical mechanism, not receptor pharmacology or a dietary health effect. Primary reference: Achieving optical transparency in live animals with absorbing molecules. (2024). https://pubmed.ncbi.nlm.nih.gov/39236186/ DOI: 10.1126/science.adm6869 Access: Primary full-text methods/results and metadata.
Complete structured claim and evidence
Topical tartrazine produced reversible optical clearing in live-mouse imaging experiments.
Tartrazine → Reversible optical transparency of topically treated mouse tissue source_derived_draftungraded
Experimental context and source evidence
dose
Tartrazine sodium salt 18-30% w/w in agarose gel
duration
Visible clearing at approximately 5 min; reversible with water rinsing
evidence_access
Primary full-text methods/results and metadata.
evidence_scope
literature_reviewed; source-specific experimental curation
experimental_model
Live anesthetized mice from several strains in imaging experiments
limitations
Concentrated experimental topical exposure; human efficacy and long-term safety are not established. Does not imply that consuming food dye makes tissue transparent.
nutrient_topic
Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine
organism
Live anesthetized mice from several strains in imaging experiments
plain_language
Topical tartrazine produced reversible optical clearing in live-mouse imaging experiments.
primary_references
Achieving optical transparency in live animals with absorbing molecules. (2024). https://pubmed.ncbi.nlm.nih.gov/39236186/ DOI: 10.1126/science.adm6869
route
Topical application to depilated skin
tissue
Scalp, abdominal skin and hindlimb imaging
Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 446–455
Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Live anesthetized mice from several strains in imaging experiments · source_derived_draft · unverified_draft
## tartrazine-mouse-optical-clearing Topical tartrazine produced reversible optical clearing in live-mouse imaging experiments. Model/species: Live anesthetized mice from several strains in imaging experiments Tissue: Scalp, abdominal skin and hindlimb imaging Exposure: Tartrazine sodium salt 18-30% w/w in agarose gel Route: Topical application to depilated skin Duration: Visible clearing at approximately 5 min; reversible with water rinsing Limits: Concentrated experimental topical exposure; human efficacy and long-term safety are not established. Does not imply that consuming food dye makes tissue transparent. Primary reference: Achieving optical transparency in live animals with absorbing molecules. (2024). https://pubmed.ncbi.nlm.nih.gov/39236186/ DOI: 10.1126/science.adm6869 Access: Primary full-text methods/results and metadata.
Complete structured claim and evidence
Tartrazine inhibited compound-48/80- and antigen-triggered histamine release from rat peritoneal mast cells.
Tartrazine → Histamine release from rat peritoneal mast cells source_derived_draftungraded
Experimental context and source evidence
dose
Tartrazine 10 micromolar-10 mM with compound 48/80 or egg-albumin challenge
duration
Acute release assay; antigen inhibition strongest with simultaneous addition
evidence_access
Primary PubMed abstract; unrecovered method details explicitly retained.
evidence_scope
literature_reviewed; source-specific experimental curation
experimental_model
Purified rat peritoneal mast cells
limitations
Secretagogue and timing alter the response. This is not a demonstration of spontaneous histamine release or a human allergic mechanism.
nutrient_topic
Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine
organism
Purified rat peritoneal mast cells
plain_language
Tartrazine inhibited compound-48/80- and antigen-triggered histamine release from rat peritoneal mast cells.
primary_references
The effect of tartrazine on histamine release from rat peritoneal mast cells. (1984). https://pubmed.ncbi.nlm.nih.gov/6204951/ DOI: 10.1016/0192-0561(84)90021-3
route
In vitro co-exposure
tissue
Secretagogue-induced histamine release
Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 457–466
Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Purified rat peritoneal mast cells · source_derived_draft · unverified_draft
## tartrazine-mast-cell-inhibition Tartrazine inhibited compound-48/80- and antigen-triggered histamine release from rat peritoneal mast cells. Model/species: Purified rat peritoneal mast cells Tissue: Secretagogue-induced histamine release Exposure: Tartrazine 10 micromolar-10 mM with compound 48/80 or egg-albumin challenge Route: In vitro co-exposure Duration: Acute release assay; antigen inhibition strongest with simultaneous addition Limits: Secretagogue and timing alter the response. This is not a demonstration of spontaneous histamine release or a human allergic mechanism. Primary reference: The effect of tartrazine on histamine release from rat peritoneal mast cells. (1984). https://pubmed.ncbi.nlm.nih.gov/6204951/ DOI: 10.1016/0192-0561(84)90021-3 Access: Primary PubMed abstract; unrecovered method details explicitly retained.
Complete structured claim and evidence
Tartrazine at 0.1-1 mM augmented A23187-triggered histamine release in the rat mast-cell assay.
Tartrazine → Histamine release from rat peritoneal mast cells source_derived_draftungraded
Experimental context and source evidence
dose
Tartrazine 0.1-1 mM with calcium ionophore A23187
duration
Maximum augmentation with 0-5 min preincubation
evidence_access
Primary PubMed abstract; unrecovered method details explicitly retained.
evidence_scope
literature_reviewed; source-specific experimental curation
experimental_model
Purified rat peritoneal mast cells
limitations
The ionophore interaction cannot be generalized to every mast-cell stimulus; higher concentrations had a small inhibitory effect.
nutrient_topic
Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine
organism
Purified rat peritoneal mast cells
plain_language
Tartrazine at 0.1-1 mM augmented A23187-triggered histamine release in the rat mast-cell assay.
primary_references
The effect of tartrazine on histamine release from rat peritoneal mast cells. (1984). https://pubmed.ncbi.nlm.nih.gov/6204951/ DOI: 10.1016/0192-0561(84)90021-3
route
In vitro preincubation and challenge
tissue
Calcium-ionophore-triggered histamine release
Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 468–477
Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Purified rat peritoneal mast cells · source_derived_draft · unverified_draft
## tartrazine-mast-cell-augmentation Tartrazine at 0.1-1 mM augmented A23187-triggered histamine release in the rat mast-cell assay. Model/species: Purified rat peritoneal mast cells Tissue: Calcium-ionophore-triggered histamine release Exposure: Tartrazine 0.1-1 mM with calcium ionophore A23187 Route: In vitro preincubation and challenge Duration: Maximum augmentation with 0-5 min preincubation Limits: The ionophore interaction cannot be generalized to every mast-cell stimulus; higher concentrations had a small inhibitory effect. Primary reference: The effect of tartrazine on histamine release from rat peritoneal mast cells. (1984). https://pubmed.ncbi.nlm.nih.gov/6204951/ DOI: 10.1016/0192-0561(84)90021-3 Access: Primary PubMed abstract; unrecovered method details explicitly retained.
Complete structured claim and evidence

Availability and dependencies

Each situation shows the normal role first, then what the sources report under a specific condition. A shortfall in the diet, a fault in the machinery, and a low blood reading are kept separate because they are not the same thing.

The sources

Every document behind this chapter is preserved word for word. Open one to read it in full with its recorded conflicts marked in place.

Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20)Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · unverified_draftRead preserved source

Recorded disagreements

Where two sources say different things, both are kept and the difference is explained. You can discuss a disagreement or propose a mechanism that might account for it.

Open questions in this collection

Questions the curators could not answer from the sources in front of them, kept here with the reason each one is still open. These are gaps in this collection, not findings or proof that no one has studied them.

Chapters are assembled from supplied drafts and curated literature summaries. Statements remain unverified against the primary studies, and the ledger is not medical advice.

Evidence, AI assistance and curation standards

Tartrazine

The mechanisms

Purified E. coli K12 azoreductase I used tartrazine as a substrate.

Purified E. coli K12 azoreductase II used tartrazine less efficiently than azoreductase I.

NADH functioned as an electron donor for the purified azoreductases characterized with an azo-dye substrate panel including tartrazine.

NADPH also functioned as an electron donor for the purified E. coli azoreductase preparations.

Human-gut E. coli isolate AZO-Ec decolorized tartrazine under the aerobic culture conditions.

Human-gut E. faecalis isolate AZO-Ef decolorized tartrazine in the substrate-panel experiment.

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

The reduced tartrazine pyrazole product SCAP was chemically identified.

SCAP oxidation on exposure to air produced the characterized purple derivative purpurazoic acid.

SCAP reduced HEK293-cell viability with a reported IC50 of 89 micromolar.

Purpurazoic acid reduced HEK293-cell viability with a reported IC50 of 78 micromolar.

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

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

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

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

Sulfanilic acid decreased SOD2 expression in the AR42J experiment.

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

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

Tartrazine inhibited human BCRP-mediated probe transport in the membrane-vesicle screen.

Tartrazine did not stimulate P-glycoprotein-specific ATPase activity in the membrane assay.

Tartrazine did not inhibit human P-glycoprotein-mediated rhodamine-123 efflux in the cell assay.

Apically applied tartrazine did not change sulfasalazine permeability through Caco-2 monolayers.

Tartrazine inhibited dopamine sulfation in human liver cytosol.

Tartrazine activated the human ER-alpha reporter in MCF-7 cells, with a reported EC50 of 160 nM.

The selected food-color-reactive children had lower serum zinc after the tartrazine challenge.

The selected food-color-reactive children had higher urinary zinc output after the tartrazine challenge.

The small matched control subgroup showed no significant zinc change after tartrazine.

The blinded challenge identified dose-related irritability, restlessness or sleep disturbance in a subset of the selected children.

Four of 156 aspirin-intolerant asthmatics had a double-blind-confirmed tartrazine response with more than a 25% FEV1 fall and symptoms.

The 26-adult crossover study found no significant cutaneous, respiratory or cardiovascular difference between tartrazine and placebo.

Tartrazine did not increase gut micronucleus frequency under the tested acute mouse protocol.

High-dose oral tartrazine lowered measured brain ascorbic acid in the rat experiment.

Tartrazine alone did not significantly change brain reduced glutathione relative to control rats.

Tartrazine alone did not significantly change the brain MDA assay endpoint in this two-week rat study.

Aspirin pretreatment and co-exposure attenuated the brain histological injury observed with high-dose tartrazine.

Tartrazine formed assemblies with the synthetic antimicrobial peptide DHVAR4.

Tartrazine favored the membrane-associated helical conformation of DHVAR4.

Tartrazine increased DHVAR4 antibacterial activity in the tested cultures.

Dissolved tartrazine reduced optical scattering by bringing the aqueous refractive index closer to that of high-index components.

Topical tartrazine produced reversible optical clearing in live-mouse imaging experiments.

Tartrazine inhibited compound-48/80- and antigen-triggered histamine release from rat peritoneal mast cells.

Tartrazine at 0.1-1 mM augmented A23187-triggered histamine release in the rat mast-cell assay.

Availability and dependencies

The sources

Recorded disagreements

Open questions in this collection