Component
Betanin
Red-violet betacyanin; betanidin 5-O-beta-glucoside. Distinct from betaine.
22 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
What it acts on
Betanin stimulated or inhibited MPO chlorination at neutral pH depending on concentration; at pH 5 only inhibition was observed.
Experimental context and source evidence
- dose
- Micromolar substrates; concentration-dependent chlorination assays
- duration
- Rapid kinetic measurements at 25 degrees C; pH 7.0 and pH 5.0
- evidence_access
- Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
- evidence_scope
- literature_reviewed; source-derived curation, not universally established human effects
- experimental_model
- Purified human myeloperoxidase; cell-free chemistry
- limitations
- MPO substrates can stimulate or inhibit chlorination depending on conditions; not a universal MPO inhibitor.
- nutrient_topic
- Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
- organism
- Purified human myeloperoxidase; cell-free chemistry
- plain_language
- Betanin stimulated or inhibited MPO chlorination at neutral pH depending on concentration; at pH 5 only inhibition was observed.
- primary_references
- Mechanism of interaction of betanin and indicaxanthin with human myeloperoxidase and hypochlorous acid. (2005). https://pubmed.ncbi.nlm.nih.gov/15913556/ DOI: 10.1016/j.bbrc.2005.05.031
- route
- In vitro reagent addition
- tissue
- MPO redox cycle and HOCl solution
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 137–145
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Purified human myeloperoxidase; cell-free chemistry · source_derived_draft · unverified_draft
## betalains-betanin-chlorination Betanin stimulated or inhibited MPO chlorination at neutral pH depending on concentration; at pH 5 only inhibition was observed. Model/species: Purified human myeloperoxidase; cell-free chemistry Tissue: MPO redox cycle and HOCl solution Exposure: Micromolar substrates; concentration-dependent chlorination assays Route: In vitro reagent addition Duration: Rapid kinetic measurements at 25 degrees C; pH 7.0 and pH 5.0 Limits: MPO substrates can stimulate or inhibit chlorination depending on conditions; not a universal MPO inhibitor. Primary reference: Mechanism of interaction of betanin and indicaxanthin with human myeloperoxidase and hypochlorous acid. (2005). https://pubmed.ncbi.nlm.nih.gov/15913556/ DOI: 10.1016/j.bbrc.2005.05.031
Complete structured claim and evidenceBetanin reacted directly with hypochlorous acid in the kinetic assay.
Experimental context and source evidence
- dose
- Micromolar substrates; concentration-dependent chlorination assays
- duration
- Rapid kinetic measurements at 25 degrees C; pH 7.0 and pH 5.0
- evidence_access
- Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
- evidence_scope
- literature_reviewed; source-derived curation, not universally established human effects
- experimental_model
- Purified human myeloperoxidase; cell-free chemistry
- limitations
- MPO substrates can stimulate or inhibit chlorination depending on conditions; not a universal MPO inhibitor.
- nutrient_topic
- Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
- organism
- Purified human myeloperoxidase; cell-free chemistry
- plain_language
- Betanin reacted directly with hypochlorous acid in the kinetic assay.
- primary_references
- Mechanism of interaction of betanin and indicaxanthin with human myeloperoxidase and hypochlorous acid. (2005). https://pubmed.ncbi.nlm.nih.gov/15913556/ DOI: 10.1016/j.bbrc.2005.05.031
- route
- In vitro reagent addition
- tissue
- MPO redox cycle and HOCl solution
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 127–135
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Purified human myeloperoxidase; cell-free chemistry · source_derived_draft · unverified_draft
## betalains-betanin-hocl Betanin reacted directly with hypochlorous acid in the kinetic assay. Model/species: Purified human myeloperoxidase; cell-free chemistry Tissue: MPO redox cycle and HOCl solution Exposure: Micromolar substrates; concentration-dependent chlorination assays Route: In vitro reagent addition Duration: Rapid kinetic measurements at 25 degrees C; pH 7.0 and pH 5.0 Limits: MPO substrates can stimulate or inhibit chlorination depending on conditions; not a universal MPO inhibitor. Primary reference: Mechanism of interaction of betanin and indicaxanthin with human myeloperoxidase and hypochlorous acid. (2005). https://pubmed.ncbi.nlm.nih.gov/15913556/ DOI: 10.1016/j.bbrc.2005.05.031
Complete structured claim and evidenceBetanin is the 5-O-beta-glucoside of betanidin.
Experimental context and source evidence
- dose
- Assay-specific submicromolar to micromolar concentrations; oral arm 300 mL beet juice with 120 mg betanin
- duration
- Kinetic assays; urine collected 2-4 h after ingestion
- evidence_access
- Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
- evidence_scope
- literature_reviewed; source-derived curation, not universally established human effects
- experimental_model
- Cell-free biochemical systems and four human volunteers
- limitations
- Chemical activity does not establish clinical efficacy or a dietary iron interaction. Identity only; not a demonstrated human conversion rate.
- nutrient_topic
- Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
- organism
- Cell-free biochemical systems and four human volunteers
- plain_language
- Betanin is the 5-O-beta-glucoside of betanidin.
- primary_references
- Betalains--a new class of dietary cationized antioxidants. (2001). https://pubmed.ncbi.nlm.nih.gov/11714300/ DOI: 10.1021/jf010456f
- route
- In vitro addition; separate oral juice arm
- tissue
- Lipid emulsions, membranes, LDL; urine arm separate
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 17–25
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Cell-free biochemical systems and four human volunteers · source_derived_draft · unverified_draft
## betalains-betanin-identity Betanin is the 5-O-beta-glucoside of betanidin. Model/species: Cell-free biochemical systems and four human volunteers Tissue: Lipid emulsions, membranes, LDL; urine arm separate Exposure: Assay-specific submicromolar to micromolar concentrations; oral arm 300 mL beet juice with 120 mg betanin Route: In vitro addition; separate oral juice arm Duration: Kinetic assays; urine collected 2-4 h after ingestion Limits: Chemical activity does not establish clinical efficacy or a dietary iron interaction. Identity only; not a demonstrated human conversion rate. Primary reference: Betalains--a new class of dietary cationized antioxidants. (2001). https://pubmed.ncbi.nlm.nih.gov/11714300/ DOI: 10.1021/jf010456f
Complete structured claim and evidenceAdded betanin inhibited iron-redox-driven lipid peroxidation in cell-free lipid preparations.
Experimental context and source evidence
- dose
- Assay-specific submicromolar to micromolar concentrations; oral arm 300 mL beet juice with 120 mg betanin
- duration
- Kinetic assays; urine collected 2-4 h after ingestion
- evidence_access
- Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
- evidence_scope
- literature_reviewed; source-derived curation, not universally established human effects
- experimental_model
- Cell-free biochemical systems and four human volunteers
- limitations
- Chemical activity does not establish clinical efficacy or a dietary iron interaction.
- nutrient_topic
- Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
- organism
- Cell-free biochemical systems and four human volunteers
- plain_language
- Added betanin inhibited iron-redox-driven lipid peroxidation in cell-free lipid preparations.
- primary_references
- Betalains--a new class of dietary cationized antioxidants. (2001). https://pubmed.ncbi.nlm.nih.gov/11714300/ DOI: 10.1021/jf010456f
- route
- In vitro addition; separate oral juice arm
- tissue
- Lipid emulsions, membranes, LDL; urine arm separate
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 27–35
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Cell-free biochemical systems and four human volunteers · source_derived_draft · unverified_draft
## betalains-betanin-iron-oxidation Added betanin inhibited iron-redox-driven lipid peroxidation in cell-free lipid preparations. Model/species: Cell-free biochemical systems and four human volunteers Tissue: Lipid emulsions, membranes, LDL; urine arm separate Exposure: Assay-specific submicromolar to micromolar concentrations; oral arm 300 mL beet juice with 120 mg betanin Route: In vitro addition; separate oral juice arm Duration: Kinetic assays; urine collected 2-4 h after ingestion Limits: Chemical activity does not establish clinical efficacy or a dietary iron interaction. Primary reference: Betalains--a new class of dietary cationized antioxidants. (2001). https://pubmed.ncbi.nlm.nih.gov/11714300/ DOI: 10.1021/jf010456f
Complete structured claim and evidenceAdding betanin to human plasma produced pigment-enriched LDL after particle isolation.
Experimental context and source evidence
- dose
- 25-100 micromolar pigment added to plasma; copper-triggered LDL oxidation
- duration
- Kinetic oxidation assay; incubation duration not specified in accessed abstract
- evidence_access
- Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
- evidence_scope
- literature_reviewed; source-derived curation, not universally established human effects
- experimental_model
- Human pooled plasma from 10 healthy donors; isolated LDL
- limitations
- Plasma spiking exceeds typical dietary parent-pigment exposure; vitamin synergy refers only to this assay.
- nutrient_topic
- Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
- organism
- Human pooled plasma from 10 healthy donors; isolated LDL
- plain_language
- Adding betanin to human plasma produced pigment-enriched LDL after particle isolation.
- primary_references
- Increased resistance to oxidation of betalain-enriched human low density lipoproteins. (2003). https://pubmed.ncbi.nlm.nih.gov/12868496/ DOI: 10.1080/1071576031000097490
- route
- Ex vivo spiking, not oral dosing
- tissue
- Plasma and LDL
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 47–55
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Human pooled plasma from 10 healthy donors; isolated LDL · source_derived_draft · unverified_draft
## betalains-betanin-ldl-binding Adding betanin to human plasma produced pigment-enriched LDL after particle isolation. Model/species: Human pooled plasma from 10 healthy donors; isolated LDL Tissue: Plasma and LDL Exposure: 25-100 micromolar pigment added to plasma; copper-triggered LDL oxidation Route: Ex vivo spiking, not oral dosing Duration: Kinetic oxidation assay; incubation duration not specified in accessed abstract Limits: Plasma spiking exceeds typical dietary parent-pigment exposure; vitamin synergy refers only to this assay. Primary reference: Increased resistance to oxidation of betalain-enriched human low density lipoproteins. (2003). https://pubmed.ncbi.nlm.nih.gov/12868496/ DOI: 10.1080/1071576031000097490
Complete structured claim and evidenceLDL enriched with betanin showed a longer lag before copper-induced oxidation.
Experimental context and source evidence
- dose
- 25-100 micromolar pigment added to plasma; copper-triggered LDL oxidation
- duration
- Kinetic oxidation assay; incubation duration not specified in accessed abstract
- evidence_access
- Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
- evidence_scope
- literature_reviewed; source-derived curation, not universally established human effects
- experimental_model
- Human pooled plasma from 10 healthy donors; isolated LDL
- limitations
- Plasma spiking exceeds typical dietary parent-pigment exposure; vitamin synergy refers only to this assay.
- nutrient_topic
- Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
- organism
- Human pooled plasma from 10 healthy donors; isolated LDL
- plain_language
- LDL enriched with betanin showed a longer lag before copper-induced oxidation.
- primary_references
- Increased resistance to oxidation of betalain-enriched human low density lipoproteins. (2003). https://pubmed.ncbi.nlm.nih.gov/12868496/ DOI: 10.1080/1071576031000097490
- route
- Ex vivo spiking, not oral dosing
- tissue
- Plasma and LDL
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 57–65
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Human pooled plasma from 10 healthy donors; isolated LDL · source_derived_draft · unverified_draft
## betalains-betanin-ldl-oxidation LDL enriched with betanin showed a longer lag before copper-induced oxidation. Model/species: Human pooled plasma from 10 healthy donors; isolated LDL Tissue: Plasma and LDL Exposure: 25-100 micromolar pigment added to plasma; copper-triggered LDL oxidation Route: Ex vivo spiking, not oral dosing Duration: Kinetic oxidation assay; incubation duration not specified in accessed abstract Limits: Plasma spiking exceeds typical dietary parent-pigment exposure; vitamin synergy refers only to this assay. Primary reference: Increased resistance to oxidation of betalain-enriched human low density lipoproteins. (2003). https://pubmed.ncbi.nlm.nih.gov/12868496/ DOI: 10.1080/1071576031000097490
Complete structured claim and evidenceBetanin lowered NOX2 mRNA in the stimulated murine macrophage comparison.
Experimental context and source evidence
- dose
- Individual pigments 1-100 micromolar; LPS inflammatory stimulation or hydrogen peroxide oxidative challenge
- duration
- Not specified in accessed primary abstract
- evidence_access
- Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
- evidence_scope
- literature_reviewed; source-derived curation, not universally established human effects
- experimental_model
- Mouse RAW 264.7 macrophages
- limitations
- Mouse-cell results are separate from human intestinal assays. Pro-oxidant effects under peroxide challenge do not imply every dietary exposure is harmful. Transcript measurement; not direct enzyme inhibition.
- nutrient_topic
- Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
- organism
- Mouse RAW 264.7 macrophages
- plain_language
- Betanin lowered NOX2 mRNA in the stimulated murine macrophage comparison.
- primary_references
- Differential Effects of Betacyanin and Betaxanthin Pigments on Oxidative Stress and Inflammatory Response in Murine Macrophages. (2023). https://pubmed.ncbi.nlm.nih.gov/37203590/ DOI: 10.1002/mnfr.202200583
- route
- In vitro exposure
- tissue
- Macrophages
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 397–405
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Mouse RAW 264.7 macrophages · source_derived_draft · unverified_draft
## betalains-betanin-mouse-nox2 Betanin lowered NOX2 mRNA in the stimulated murine macrophage comparison. Model/species: Mouse RAW 264.7 macrophages Tissue: Macrophages Exposure: Individual pigments 1-100 micromolar; LPS inflammatory stimulation or hydrogen peroxide oxidative challenge Route: In vitro exposure Duration: Not specified in accessed primary abstract Limits: Mouse-cell results are separate from human intestinal assays. Pro-oxidant effects under peroxide challenge do not imply every dietary exposure is harmful. Transcript measurement; not direct enzyme inhibition. Primary reference: Differential Effects of Betacyanin and Betaxanthin Pigments on Oxidative Stress and Inflammatory Response in Murine Macrophages. (2023). https://pubmed.ncbi.nlm.nih.gov/37203590/ DOI: 10.1002/mnfr.202200583
Complete structured claim and evidenceBetanin donated one electron to MPO compound I, producing compound II.
Experimental context and source evidence
- dose
- Micromolar substrates; concentration-dependent chlorination assays
- duration
- Rapid kinetic measurements at 25 degrees C; pH 7.0 and pH 5.0
- evidence_access
- Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
- evidence_scope
- literature_reviewed; source-derived curation, not universally established human effects
- experimental_model
- Purified human myeloperoxidase; cell-free chemistry
- limitations
- MPO substrates can stimulate or inhibit chlorination depending on conditions; not a universal MPO inhibitor. Negative direction denotes consumption of compound I, not overall inhibition of MPO.
- nutrient_topic
- Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
- organism
- Purified human myeloperoxidase; cell-free chemistry
- plain_language
- Betanin donated one electron to MPO compound I, producing compound II.
- primary_references
- Mechanism of interaction of betanin and indicaxanthin with human myeloperoxidase and hypochlorous acid. (2005). https://pubmed.ncbi.nlm.nih.gov/15913556/ DOI: 10.1016/j.bbrc.2005.05.031
- route
- In vitro reagent addition
- tissue
- MPO redox cycle and HOCl solution
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 107–115
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Purified human myeloperoxidase; cell-free chemistry · source_derived_draft · unverified_draft
## betalains-betanin-mpo-i Betanin donated one electron to MPO compound I, producing compound II. Model/species: Purified human myeloperoxidase; cell-free chemistry Tissue: MPO redox cycle and HOCl solution Exposure: Micromolar substrates; concentration-dependent chlorination assays Route: In vitro reagent addition Duration: Rapid kinetic measurements at 25 degrees C; pH 7.0 and pH 5.0 Limits: MPO substrates can stimulate or inhibit chlorination depending on conditions; not a universal MPO inhibitor. Negative direction denotes consumption of compound I, not overall inhibition of MPO. Primary reference: Mechanism of interaction of betanin and indicaxanthin with human myeloperoxidase and hypochlorous acid. (2005). https://pubmed.ncbi.nlm.nih.gov/15913556/ DOI: 10.1016/j.bbrc.2005.05.031
Complete structured claim and evidenceBetanin reduced MPO compound II to the native ferric enzyme.
Experimental context and source evidence
- dose
- Micromolar substrates; concentration-dependent chlorination assays
- duration
- Rapid kinetic measurements at 25 degrees C; pH 7.0 and pH 5.0
- evidence_access
- Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
- evidence_scope
- literature_reviewed; source-derived curation, not universally established human effects
- experimental_model
- Purified human myeloperoxidase; cell-free chemistry
- limitations
- MPO substrates can stimulate or inhibit chlorination depending on conditions; not a universal MPO inhibitor. Negative direction denotes consumption of compound II; this step can restore chlorination activity.
- nutrient_topic
- Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
- organism
- Purified human myeloperoxidase; cell-free chemistry
- plain_language
- Betanin reduced MPO compound II to the native ferric enzyme.
- primary_references
- Mechanism of interaction of betanin and indicaxanthin with human myeloperoxidase and hypochlorous acid. (2005). https://pubmed.ncbi.nlm.nih.gov/15913556/ DOI: 10.1016/j.bbrc.2005.05.031
- route
- In vitro reagent addition
- tissue
- MPO redox cycle and HOCl solution
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 117–125
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Purified human myeloperoxidase; cell-free chemistry · source_derived_draft · unverified_draft
## betalains-betanin-mpo-ii Betanin reduced MPO compound II to the native ferric enzyme. Model/species: Purified human myeloperoxidase; cell-free chemistry Tissue: MPO redox cycle and HOCl solution Exposure: Micromolar substrates; concentration-dependent chlorination assays Route: In vitro reagent addition Duration: Rapid kinetic measurements at 25 degrees C; pH 7.0 and pH 5.0 Limits: MPO substrates can stimulate or inhibit chlorination depending on conditions; not a universal MPO inhibitor. Negative direction denotes consumption of compound II; this step can restore chlorination activity. Primary reference: Mechanism of interaction of betanin and indicaxanthin with human myeloperoxidase and hypochlorous acid. (2005). https://pubmed.ncbi.nlm.nih.gov/15913556/ DOI: 10.1016/j.bbrc.2005.05.031
Complete structured claim and evidenceBetanin showed low apparent permeability across Caco-2 monolayers; the reported three-pigment range was 4.2-8.9 x 10^-7 cm/s.
Experimental context and source evidence
- dose
- Betalains 5-80 micromolar
- duration
- Not specified in accessed primary abstract
- evidence_access
- Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
- evidence_scope
- literature_reviewed; source-derived curation, not universally established human effects
- experimental_model
- Human Caco-2 intestinal epithelial cell model
- limitations
- Low apparent permeability in cultured cells is not a measured human oral bioavailability fraction; findings depend on pigment and assay. The range spans the three compounds; it is not an assigned compound-specific coefficient.
- nutrient_topic
- Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
- organism
- Human Caco-2 intestinal epithelial cell model
- plain_language
- Betanin showed low apparent permeability across Caco-2 monolayers; the reported three-pigment range was 4.2-8.9 x 10^-7 cm/s.
- primary_references
- Uptake and Immunomodulatory Properties of Betanin, Vulgaxanthin I and Indicaxanthin towards Caco-2 Intestinal Cells. (2022). https://pubmed.ncbi.nlm.nih.gov/36009345/ DOI: 10.3390/antiox11081627
- route
- In vitro exposure
- tissue
- Intestinal cells and monolayer transport
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 367–375
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Human Caco-2 intestinal epithelial cell model · source_derived_draft · unverified_draft
## betalains-betanin-transport Betanin showed low apparent permeability across Caco-2 monolayers; the reported three-pigment range was 4.2-8.9 x 10^-7 cm/s. Model/species: Human Caco-2 intestinal epithelial cell model Tissue: Intestinal cells and monolayer transport Exposure: Betalains 5-80 micromolar Route: In vitro exposure Duration: Not specified in accessed primary abstract Limits: Low apparent permeability in cultured cells is not a measured human oral bioavailability fraction; findings depend on pigment and assay. The range spans the three compounds; it is not an assigned compound-specific coefficient. Primary reference: Uptake and Immunomodulatory Properties of Betanin, Vulgaxanthin I and Indicaxanthin towards Caco-2 Intestinal Cells. (2022). https://pubmed.ncbi.nlm.nih.gov/36009345/ DOI: 10.3390/antiox11081627
Complete structured claim and evidenceBetanin did not produce the early vitamin E preservation observed with indicaxanthin in this LDL experiment.
Experimental context and source evidence
- dose
- 25-100 micromolar pigment added to plasma; copper-triggered LDL oxidation
- duration
- Kinetic oxidation assay; incubation duration not specified in accessed abstract
- evidence_access
- Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
- evidence_scope
- literature_reviewed; source-derived curation, not universally established human effects
- experimental_model
- Human pooled plasma from 10 healthy donors; isolated LDL
- limitations
- Plasma spiking exceeds typical dietary parent-pigment exposure; vitamin synergy refers only to this assay.
- nutrient_topic
- Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
- organism
- Human pooled plasma from 10 healthy donors; isolated LDL
- plain_language
- Betanin did not produce the early vitamin E preservation observed with indicaxanthin in this LDL experiment.
- primary_references
- Increased resistance to oxidation of betalain-enriched human low density lipoproteins. (2003). https://pubmed.ncbi.nlm.nih.gov/12868496/ DOI: 10.1080/1071576031000097490
- route
- Ex vivo spiking, not oral dosing
- tissue
- Plasma and LDL
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 97–105
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Human pooled plasma from 10 healthy donors; isolated LDL · source_derived_draft · unverified_draft
## betalains-betanin-vitamin-e-null Betanin did not produce the early vitamin E preservation observed with indicaxanthin in this LDL experiment. Model/species: Human pooled plasma from 10 healthy donors; isolated LDL Tissue: Plasma and LDL Exposure: 25-100 micromolar pigment added to plasma; copper-triggered LDL oxidation Route: Ex vivo spiking, not oral dosing Duration: Kinetic oxidation assay; incubation duration not specified in accessed abstract Limits: Plasma spiking exceeds typical dietary parent-pigment exposure; vitamin synergy refers only to this assay. Primary reference: Increased resistance to oxidation of betalain-enriched human low density lipoproteins. (2003). https://pubmed.ncbi.nlm.nih.gov/12868496/ DOI: 10.1080/1071576031000097490
Complete structured claim and evidenceBetanin increased heme oxygenase-1 in the Caco-2 comparison; the two tested betaxanthins did not share this response.
Experimental context and source evidence
- dose
- Betalains 5-80 micromolar
- duration
- Not specified in accessed primary abstract
- evidence_access
- Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
- evidence_scope
- literature_reviewed; source-derived curation, not universally established human effects
- experimental_model
- Human Caco-2 intestinal epithelial cell model
- limitations
- Low apparent permeability in cultured cells is not a measured human oral bioavailability fraction; findings depend on pigment and assay. Expression response in this cell model; not direct HMOX1 activation or a demonstrated increase in heme turnover.
- nutrient_topic
- Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
- organism
- Human Caco-2 intestinal epithelial cell model
- plain_language
- Betanin increased heme oxygenase-1 in the Caco-2 comparison; the two tested betaxanthins did not share this response.
- primary_references
- Uptake and Immunomodulatory Properties of Betanin, Vulgaxanthin I and Indicaxanthin towards Caco-2 Intestinal Cells. (2022). https://pubmed.ncbi.nlm.nih.gov/36009345/ DOI: 10.3390/antiox11081627
- route
- In vitro exposure
- tissue
- Intestinal cells and monolayer transport
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 357–365
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Human Caco-2 intestinal epithelial cell model · source_derived_draft · unverified_draft
## betalains-caco2-hmox1 Betanin increased heme oxygenase-1 in the Caco-2 comparison; the two tested betaxanthins did not share this response. Model/species: Human Caco-2 intestinal epithelial cell model Tissue: Intestinal cells and monolayer transport Exposure: Betalains 5-80 micromolar Route: In vitro exposure Duration: Not specified in accessed primary abstract Limits: Low apparent permeability in cultured cells is not a measured human oral bioavailability fraction; findings depend on pigment and assay. Expression response in this cell model; not direct HMOX1 activation or a demonstrated increase in heme turnover. Primary reference: Uptake and Immunomodulatory Properties of Betanin, Vulgaxanthin I and Indicaxanthin towards Caco-2 Intestinal Cells. (2022). https://pubmed.ncbi.nlm.nih.gov/36009345/ DOI: 10.3390/antiox11081627
Complete structured claim and evidenceBetanin increased GSTP transcript and protein abundance in THLE-2 cells.
Experimental context and source evidence
- dose
- Betanin 2, 10 and 20 micromolar
- duration
- Not specified in accessed primary abstract
- evidence_access
- Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
- evidence_scope
- literature_reviewed; source-derived curation, not universally established human effects
- experimental_model
- Human THLE-2 non-tumour liver and HepG2 hepatoma cell lines
- limitations
- Responses differed by cell line. Nuclear translocation is not proof of universal transcriptional activation; kinase association does not prove direct binding. Glutathione is the shared GST substrate; this study does not show betanin raises glutathione synthesis or reverses deficiency.
- nutrient_topic
- Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
- organism
- Human THLE-2 non-tumour liver and HepG2 hepatoma cell lines
- plain_language
- Betanin increased GSTP transcript and protein abundance in THLE-2 cells.
- primary_references
- Betanin, a beetroot component, induces nuclear factor erythroid-2-related factor 2-mediated expression of detoxifying/antioxidant enzymes in human liver cell lines. (2013). https://pubmed.ncbi.nlm.nih.gov/23769299/ DOI: 10.1017/S0007114513001645
- route
- In vitro incubation
- tissue
- Liver-derived cells; cytosol and nucleus
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 237–245
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Human THLE-2 non-tumour liver and HepG2 hepatoma cell lines · source_derived_draft · unverified_draft
## betalains-gstp-expression Betanin increased GSTP transcript and protein abundance in THLE-2 cells. Model/species: Human THLE-2 non-tumour liver and HepG2 hepatoma cell lines Tissue: Liver-derived cells; cytosol and nucleus Exposure: Betanin 2, 10 and 20 micromolar Route: In vitro incubation Duration: Not specified in accessed primary abstract Limits: Responses differed by cell line. Nuclear translocation is not proof of universal transcriptional activation; kinase association does not prove direct binding. Glutathione is the shared GST substrate; this study does not show betanin raises glutathione synthesis or reverses deficiency. Primary reference: Betanin, a beetroot component, induces nuclear factor erythroid-2-related factor 2-mediated expression of detoxifying/antioxidant enzymes in human liver cell lines. (2013). https://pubmed.ncbi.nlm.nih.gov/23769299/ DOI: 10.1017/S0007114513001645
Complete structured claim and evidenceBetanin did not alter GSTP1 methylation in HepG2 cells.
Experimental context and source evidence
- dose
- Betanin 2, 10 and 20 micromolar
- duration
- Not specified in accessed primary abstract
- evidence_access
- Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
- evidence_scope
- literature_reviewed; source-derived curation, not universally established human effects
- experimental_model
- Human THLE-2 non-tumour liver and HepG2 hepatoma cell lines
- limitations
- Responses differed by cell line. Nuclear translocation is not proof of universal transcriptional activation; kinase association does not prove direct binding.
- nutrient_topic
- Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
- organism
- Human THLE-2 non-tumour liver and HepG2 hepatoma cell lines
- plain_language
- Betanin did not alter GSTP1 methylation in HepG2 cells.
- primary_references
- Betanin, a beetroot component, induces nuclear factor erythroid-2-related factor 2-mediated expression of detoxifying/antioxidant enzymes in human liver cell lines. (2013). https://pubmed.ncbi.nlm.nih.gov/23769299/ DOI: 10.1017/S0007114513001645
- route
- In vitro incubation
- tissue
- Liver-derived cells; cytosol and nucleus
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 247–255
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Human THLE-2 non-tumour liver and HepG2 hepatoma cell lines · source_derived_draft · unverified_draft
## betalains-hepg2-methylation-null Betanin did not alter GSTP1 methylation in HepG2 cells. Model/species: Human THLE-2 non-tumour liver and HepG2 hepatoma cell lines Tissue: Liver-derived cells; cytosol and nucleus Exposure: Betanin 2, 10 and 20 micromolar Route: In vitro incubation Duration: Not specified in accessed primary abstract Limits: Responses differed by cell line. Nuclear translocation is not proof of universal transcriptional activation; kinase association does not prove direct binding. Primary reference: Betanin, a beetroot component, induces nuclear factor erythroid-2-related factor 2-mediated expression of detoxifying/antioxidant enzymes in human liver cell lines. (2013). https://pubmed.ncbi.nlm.nih.gov/23769299/ DOI: 10.1017/S0007114513001645
Complete structured claim and evidenceBetanin reduced lipid hydroperoxide formation during MPO/nitrite-mediated oxidation of human LDL.
Experimental context and source evidence
- dose
- Experimental betanin addition; concentration not specified in accessed abstract
- duration
- Oxidation time courses; duration not specified in accessed abstract
- evidence_access
- Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
- evidence_scope
- literature_reviewed; source-derived curation, not universally established human effects
- experimental_model
- Isolated human LDL and MPO/nitrite biochemical system
- limitations
- Oxidation products were not chemically identified; clinical LDL lowering was not tested.
- nutrient_topic
- Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
- organism
- Isolated human LDL and MPO/nitrite biochemical system
- plain_language
- Betanin reduced lipid hydroperoxide formation during MPO/nitrite-mediated oxidation of human LDL.
- primary_references
- Betanin inhibits the myeloperoxidase/nitrite-induced oxidation of human low-density lipoproteins. (2007). https://pubmed.ncbi.nlm.nih.gov/17364963/ DOI: 10.1080/10715760601038783
- route
- In vitro addition
- tissue
- LDL lipid compartment
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 187–195
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Isolated human LDL and MPO/nitrite biochemical system · source_derived_draft · unverified_draft
## betalains-mpo-ldl Betanin reduced lipid hydroperoxide formation during MPO/nitrite-mediated oxidation of human LDL. Model/species: Isolated human LDL and MPO/nitrite biochemical system Tissue: LDL lipid compartment Exposure: Experimental betanin addition; concentration not specified in accessed abstract Route: In vitro addition Duration: Oxidation time courses; duration not specified in accessed abstract Limits: Oxidation products were not chemically identified; clinical LDL lowering was not tested. Primary reference: Betanin inhibits the myeloperoxidase/nitrite-induced oxidation of human low-density lipoproteins. (2007). https://pubmed.ncbi.nlm.nih.gov/17364963/ DOI: 10.1080/10715760601038783
Complete structured claim and evidenceBetanin increased NQO1 transcript and protein abundance in THLE-2 cells.
Experimental context and source evidence
- dose
- Betanin 2, 10 and 20 micromolar
- duration
- Not specified in accessed primary abstract
- evidence_access
- Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
- evidence_scope
- literature_reviewed; source-derived curation, not universally established human effects
- experimental_model
- Human THLE-2 non-tumour liver and HepG2 hepatoma cell lines
- limitations
- Responses differed by cell line. Nuclear translocation is not proof of universal transcriptional activation; kinase association does not prove direct binding.
- nutrient_topic
- Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
- organism
- Human THLE-2 non-tumour liver and HepG2 hepatoma cell lines
- plain_language
- Betanin increased NQO1 transcript and protein abundance in THLE-2 cells.
- primary_references
- Betanin, a beetroot component, induces nuclear factor erythroid-2-related factor 2-mediated expression of detoxifying/antioxidant enzymes in human liver cell lines. (2013). https://pubmed.ncbi.nlm.nih.gov/23769299/ DOI: 10.1017/S0007114513001645
- route
- In vitro incubation
- tissue
- Liver-derived cells; cytosol and nucleus
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 227–235
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Human THLE-2 non-tumour liver and HepG2 hepatoma cell lines · source_derived_draft · unverified_draft
## betalains-nqo1-expression Betanin increased NQO1 transcript and protein abundance in THLE-2 cells. Model/species: Human THLE-2 non-tumour liver and HepG2 hepatoma cell lines Tissue: Liver-derived cells; cytosol and nucleus Exposure: Betanin 2, 10 and 20 micromolar Route: In vitro incubation Duration: Not specified in accessed primary abstract Limits: Responses differed by cell line. Nuclear translocation is not proof of universal transcriptional activation; kinase association does not prove direct binding. Primary reference: Betanin, a beetroot component, induces nuclear factor erythroid-2-related factor 2-mediated expression of detoxifying/antioxidant enzymes in human liver cell lines. (2013). https://pubmed.ncbi.nlm.nih.gov/23769299/ DOI: 10.1017/S0007114513001645
Complete structured claim and evidenceBetanin increased Nrf2 binding to antioxidant response elements in THLE-2 cells; this response was absent in HepG2 cells.
Experimental context and source evidence
- dose
- Betanin 2, 10 and 20 micromolar
- duration
- Not specified in accessed primary abstract
- evidence_access
- Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
- evidence_scope
- literature_reviewed; source-derived curation, not universally established human effects
- experimental_model
- Human THLE-2 non-tumour liver and HepG2 hepatoma cell lines
- limitations
- Responses differed by cell line. Nuclear translocation is not proof of universal transcriptional activation; kinase association does not prove direct binding. Same-study cell-context difference, not a scientific contradiction.
- nutrient_topic
- Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
- organism
- Human THLE-2 non-tumour liver and HepG2 hepatoma cell lines
- plain_language
- Betanin increased Nrf2 binding to antioxidant response elements in THLE-2 cells; this response was absent in HepG2 cells.
- primary_references
- Betanin, a beetroot component, induces nuclear factor erythroid-2-related factor 2-mediated expression of detoxifying/antioxidant enzymes in human liver cell lines. (2013). https://pubmed.ncbi.nlm.nih.gov/23769299/ DOI: 10.1017/S0007114513001645
- route
- In vitro incubation
- tissue
- Liver-derived cells; cytosol and nucleus
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 217–225
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Human THLE-2 non-tumour liver and HepG2 hepatoma cell lines · source_derived_draft · unverified_draft
## betalains-nrf2-are Betanin increased Nrf2 binding to antioxidant response elements in THLE-2 cells; this response was absent in HepG2 cells. Model/species: Human THLE-2 non-tumour liver and HepG2 hepatoma cell lines Tissue: Liver-derived cells; cytosol and nucleus Exposure: Betanin 2, 10 and 20 micromolar Route: In vitro incubation Duration: Not specified in accessed primary abstract Limits: Responses differed by cell line. Nuclear translocation is not proof of universal transcriptional activation; kinase association does not prove direct binding. Same-study cell-context difference, not a scientific contradiction. Primary reference: Betanin, a beetroot component, induces nuclear factor erythroid-2-related factor 2-mediated expression of detoxifying/antioxidant enzymes in human liver cell lines. (2013). https://pubmed.ncbi.nlm.nih.gov/23769299/ DOI: 10.1017/S0007114513001645
Complete structured claim and evidenceBetanin promoted nuclear redistribution of Nrf2 in both THLE-2 and HepG2 cells.
Experimental context and source evidence
- dose
- Betanin 2, 10 and 20 micromolar
- duration
- Not specified in accessed primary abstract
- evidence_access
- Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
- evidence_scope
- literature_reviewed; source-derived curation, not universally established human effects
- experimental_model
- Human THLE-2 non-tumour liver and HepG2 hepatoma cell lines
- limitations
- Responses differed by cell line. Nuclear translocation is not proof of universal transcriptional activation; kinase association does not prove direct binding.
- nutrient_topic
- Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
- organism
- Human THLE-2 non-tumour liver and HepG2 hepatoma cell lines
- plain_language
- Betanin promoted nuclear redistribution of Nrf2 in both THLE-2 and HepG2 cells.
- primary_references
- Betanin, a beetroot component, induces nuclear factor erythroid-2-related factor 2-mediated expression of detoxifying/antioxidant enzymes in human liver cell lines. (2013). https://pubmed.ncbi.nlm.nih.gov/23769299/ DOI: 10.1017/S0007114513001645
- route
- In vitro incubation
- tissue
- Liver-derived cells; cytosol and nucleus
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 207–215
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Human THLE-2 non-tumour liver and HepG2 hepatoma cell lines · source_derived_draft · unverified_draft
## betalains-nrf2-translocation Betanin promoted nuclear redistribution of Nrf2 in both THLE-2 and HepG2 cells. Model/species: Human THLE-2 non-tumour liver and HepG2 hepatoma cell lines Tissue: Liver-derived cells; cytosol and nucleus Exposure: Betanin 2, 10 and 20 micromolar Route: In vitro incubation Duration: Not specified in accessed primary abstract Limits: Responses differed by cell line. Nuclear translocation is not proof of universal transcriptional activation; kinase association does not prove direct binding. Primary reference: Betanin, a beetroot component, induces nuclear factor erythroid-2-related factor 2-mediated expression of detoxifying/antioxidant enzymes in human liver cell lines. (2013). https://pubmed.ncbi.nlm.nih.gov/23769299/ DOI: 10.1017/S0007114513001645
Complete structured claim and evidence
Where it participates (unsigned role)
Betanin was undetectable at all sampled plasma time points after beetroot juice or whole beetroot in this crossover study.
Experimental context and source evidence
- dose
- 250 mL beetroot juice or 300 g whole beetroot versus placebo
- duration
- Baseline and 1, 2, 3, 5 and 8 h
- evidence_access
- Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
- evidence_scope
- literature_reviewed; source-derived curation, not universally established human effects
- experimental_model
- Ten healthy men in a randomized crossover study
- limitations
- An undetectable parent compound is not proof of zero absorption. Food matrix, degradation and analytical methods differ from the cactus pear study. NOx is not itself a measurement of a betanin mechanism.
- nutrient_topic
- Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
- organism
- Ten healthy men in a randomized crossover study
- plain_language
- Betanin was undetectable at all sampled plasma time points after beetroot juice or whole beetroot in this crossover study.
- primary_references
- The plasma bioavailability of nitrate and betanin from Beta vulgaris rubra in humans. (2017). https://pubmed.ncbi.nlm.nih.gov/26873098/ DOI: 10.1007/s00394-016-1173-5
- route
- Oral food/drink
- tissue
- Venous plasma
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 527–535
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Ten healthy men in a randomized crossover study · source_derived_draft · unverified_draft
## betalains-beetroot-pk-null Betanin was undetectable at all sampled plasma time points after beetroot juice or whole beetroot in this crossover study. Model/species: Ten healthy men in a randomized crossover study Tissue: Venous plasma Exposure: 250 mL beetroot juice or 300 g whole beetroot versus placebo Route: Oral food/drink Duration: Baseline and 1, 2, 3, 5 and 8 h Limits: An undetectable parent compound is not proof of zero absorption. Food matrix, degradation and analytical methods differ from the cactus pear study. NOx is not itself a measurement of a betanin mechanism. Primary reference: The plasma bioavailability of nitrate and betanin from Beta vulgaris rubra in humans. (2017). https://pubmed.ncbi.nlm.nih.gov/26873098/ DOI: 10.1007/s00394-016-1173-5
Complete structured claim and evidenceAfter cactus pear ingestion, plasma betanin peaked at 3 h and was undetectable by 12 h.
Experimental context and source evidence
- dose
- Single 500 g cactus pear pulp meal: 28 mg indicaxanthin and 16 mg betanin
- duration
- Plasma/urine followed for 12 h
- evidence_access
- Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
- evidence_scope
- literature_reviewed; source-derived curation, not universally established human effects
- experimental_model
- Eight healthy human volunteers
- limitations
- Whole-food exposure cannot attribute the LDL response exclusively to either pigment; urinary recovery is not absolute absorption.
- nutrient_topic
- Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
- organism
- Eight healthy human volunteers
- plain_language
- After cactus pear ingestion, plasma betanin peaked at 3 h and was undetectable by 12 h.
- primary_references
- Absorption, excretion, and distribution of dietary antioxidant betalains in LDLs: potential health effects of betalains in humans. (2004). https://pubmed.ncbi.nlm.nih.gov/15447903/ DOI: 10.1093/ajcn/80.4.941
- route
- Oral whole food
- tissue
- Plasma, urine and isolated LDL
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 497–505
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Eight healthy human volunteers · source_derived_draft · unverified_draft
## betalains-betanin-human-pk After cactus pear ingestion, plasma betanin peaked at 3 h and was undetectable by 12 h. Model/species: Eight healthy human volunteers Tissue: Plasma, urine and isolated LDL Exposure: Single 500 g cactus pear pulp meal: 28 mg indicaxanthin and 16 mg betanin Route: Oral whole food Duration: Plasma/urine followed for 12 h Limits: Whole-food exposure cannot attribute the LDL response exclusively to either pigment; urinary recovery is not absolute absorption. Primary reference: Absorption, excretion, and distribution of dietary antioxidant betalains in LDLs: potential health effects of betalains in humans. (2004). https://pubmed.ncbi.nlm.nih.gov/15447903/ DOI: 10.1093/ajcn/80.4.941
Complete structured claim and evidenceLDL isolated 3 and 5 h after cactus pear ingestion resisted ex vivo oxidation more strongly; LDL vitamin E and beta-carotene levels were unchanged.
Experimental context and source evidence
- dose
- Single 500 g cactus pear pulp meal: 28 mg indicaxanthin and 16 mg betanin
- duration
- Plasma/urine followed for 12 h
- evidence_access
- Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
- evidence_scope
- literature_reviewed; source-derived curation, not universally established human effects
- experimental_model
- Eight healthy human volunteers
- limitations
- Whole-food exposure cannot attribute the LDL response exclusively to either pigment; urinary recovery is not absolute absorption.
- nutrient_topic
- Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
- organism
- Eight healthy human volunteers
- plain_language
- LDL isolated 3 and 5 h after cactus pear ingestion resisted ex vivo oxidation more strongly; LDL vitamin E and beta-carotene levels were unchanged.
- primary_references
- Absorption, excretion, and distribution of dietary antioxidant betalains in LDLs: potential health effects of betalains in humans. (2004). https://pubmed.ncbi.nlm.nih.gov/15447903/ DOI: 10.1093/ajcn/80.4.941
- route
- Oral whole food
- tissue
- Plasma, urine and isolated LDL
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 517–525
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Eight healthy human volunteers · source_derived_draft · unverified_draft
## betalains-human-food-ldl LDL isolated 3 and 5 h after cactus pear ingestion resisted ex vivo oxidation more strongly; LDL vitamin E and beta-carotene levels were unchanged. Model/species: Eight healthy human volunteers Tissue: Plasma, urine and isolated LDL Exposure: Single 500 g cactus pear pulp meal: 28 mg indicaxanthin and 16 mg betanin Route: Oral whole food Duration: Plasma/urine followed for 12 h Limits: Whole-food exposure cannot attribute the LDL response exclusively to either pigment; urinary recovery is not absolute absorption. Primary reference: Absorption, excretion, and distribution of dietary antioxidant betalains in LDLs: potential health effects of betalains in humans. (2004). https://pubmed.ncbi.nlm.nih.gov/15447903/ DOI: 10.1093/ajcn/80.4.941
Complete structured claim and evidenceUnidentified products generated by MPO/nitrite oxidation of betanin also inhibited LDL oxidation in the assay.
Experimental context and source evidence
- dose
- Experimental betanin addition; concentration not specified in accessed abstract
- duration
- Oxidation time courses; duration not specified in accessed abstract
- evidence_access
- Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
- evidence_scope
- literature_reviewed; source-derived curation, not universally established human effects
- experimental_model
- Isolated human LDL and MPO/nitrite biochemical system
- limitations
- Oxidation products were not chemically identified; clinical LDL lowering was not tested.
- nutrient_topic
- Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
- organism
- Isolated human LDL and MPO/nitrite biochemical system
- plain_language
- Unidentified products generated by MPO/nitrite oxidation of betanin also inhibited LDL oxidation in the assay.
- primary_references
- Betanin inhibits the myeloperoxidase/nitrite-induced oxidation of human low-density lipoproteins. (2007). https://pubmed.ncbi.nlm.nih.gov/17364963/ DOI: 10.1080/10715760601038783
- route
- In vitro addition
- tissue
- LDL lipid compartment
Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 197–205
Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Isolated human LDL and MPO/nitrite biochemical system · source_derived_draft · unverified_draft
## betalains-oxidation-products Unidentified products generated by MPO/nitrite oxidation of betanin also inhibited LDL oxidation in the assay. Model/species: Isolated human LDL and MPO/nitrite biochemical system Tissue: LDL lipid compartment Exposure: Experimental betanin addition; concentration not specified in accessed abstract Route: In vitro addition Duration: Oxidation time courses; duration not specified in accessed abstract Limits: Oxidation products were not chemically identified; clinical LDL lowering was not tested. Primary reference: Betanin inhibits the myeloperoxidase/nitrite-induced oxidation of human low-density lipoproteins. (2007). https://pubmed.ncbi.nlm.nih.gov/17364963/ DOI: 10.1080/10715760601038783
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.