Component

Pyridoxine

Vitamin B6 form examined in transporter substrate assays.

24 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What it acts on

  1. Pyridoxine reduced MTT-measured viability of differentiated SH-SY5Y cells after 24 hours in a concentration-dependent manner.

    Pyridoxine → SH-SY5Y cell viability by MTT source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Differentiated human SH-SY5Y and CaCo-2 cells; isolated enzyme assays
    exposure
    Pyridoxine 0-5 micromolar for 24 hours.
    exposure-class
    Experimental excess pyridoxine; not dietary B6 deficiency · Pyridoxine
    limitations
    Tumor-derived cells and MTT endpoint; no oral-dose conversion or human toxicity threshold.
    nutrient_topic
    Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
    organism
    Homo sapiens
    plain_language
    Added pyridoxine harmed this experimental neuronal cell model.
    primary_references
    [vrolijk-2017-pn] The vitamin B6 paradox: Supplementation with high concentrations of pyridoxine leads to decreased vitamin B6 function (2017). https://doi.org/10.1016/j.tiv.2017.07.009 DOI: 10.1016/j.tiv.2017.07.009
    tissue_or_cell_type
    Differentiated SH-SY5Y neuroblastoma cells

    Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1232–1243

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Differentiated human SH-SY5Y and CaCo-2 cells; isolated enzyme assays · source_derived_draft · unverified_draft

    ### b6-neuro-pn-cell-viability Pyridoxine reduced MTT-measured viability of differentiated SH-SY5Y cells after 24 hours in a concentration-dependent manner. Condition category: normal nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Added pyridoxine harmed this experimental neuronal cell model. organism: Homo sapiens tissue_or_cell_type: Differentiated SH-SY5Y neuroblastoma cells experimental_model: Differentiated human SH-SY5Y and CaCo-2 cells; isolated enzyme assays limitations: Tumor-derived cells and MTT endpoint; no oral-dose conversion or human toxicity threshold. exposure: Pyridoxine 0-5 micromolar for 24 hours. exposure-class: Experimental excess pyridoxine; not dietary B6 deficiency [vrolijk-2017-pn] The vitamin B6 paradox: Supplementation with high concentrations of pyridoxine leads to decreased vitamin B6 function (2017). https://doi.org/10.1016/j.tiv.2017.07.009 DOI: 10.1016/j.tiv.2017.07.009
    Complete structured claim and evidence
  2. Pyridoxine inhibited the tested PLP-dependent bacterial tyrosine decarboxylase preparation.

    Experimental context and source evidence
    experimental_model
    Differentiated human SH-SY5Y and CaCo-2 cells; isolated enzyme assays
    exposure
    5 micromolar pyridoxine; commercial Streptococcus faecalis enzyme (current Enterococcus name).
    exposure-class
    Experimental excess pyridoxine; not dietary B6 deficiency · Pyridoxine
    limitations
    Not human GAD, DDC or PDXK; mechanism of human neuropathy remains unresolved.
    nutrient_topic
    Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
    organism
    Enterococcus faecalis (reported as Streptococcus faecalis)
    plain_language
    Pyridoxine interfered with one isolated B6-dependent enzyme.
    primary_references
    [vrolijk-2017-pn] The vitamin B6 paradox: Supplementation with high concentrations of pyridoxine leads to decreased vitamin B6 function (2017). https://doi.org/10.1016/j.tiv.2017.07.009 DOI: 10.1016/j.tiv.2017.07.009
    tissue_or_cell_type
    Cell-free bacterial enzyme

    Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1258–1269

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Differentiated human SH-SY5Y and CaCo-2 cells; isolated enzyme assays · source_derived_draft · unverified_draft

    ### b6-neuro-pn-enzyme-inhibition Pyridoxine inhibited the tested PLP-dependent bacterial tyrosine decarboxylase preparation. Condition category: normal nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Pyridoxine interfered with one isolated B6-dependent enzyme. organism: Enterococcus faecalis (reported as Streptococcus faecalis) tissue_or_cell_type: Cell-free bacterial enzyme experimental_model: Differentiated human SH-SY5Y and CaCo-2 cells; isolated enzyme assays limitations: Not human GAD, DDC or PDXK; mechanism of human neuropathy remains unresolved. exposure: 5 micromolar pyridoxine; commercial Streptococcus faecalis enzyme (current Enterococcus name). exposure-class: Experimental excess pyridoxine; not dietary B6 deficiency [vrolijk-2017-pn] The vitamin B6 paradox: Supplementation with high concentrations of pyridoxine leads to decreased vitamin B6 function (2017). https://doi.org/10.1016/j.tiv.2017.07.009 DOI: 10.1016/j.tiv.2017.07.009
    Complete structured claim and evidence
  3. All five volunteers developed sensory symptoms and quantitative sensory abnormalities; the 3 g/day group became symptomatic sooner than the 1 g/day group.

    Pyridoxine → Sensory neuropathy source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    Experimental excess, not nutrient deficiency
    experimental_model
    Five healthy volunteers prospectively followed during experimental pyridoxine excess.
    exposure
    Pyridoxine 1 or 3 g/day, stopped with clinical/laboratory abnormality; very high historical exposures.
    limitations
    Five volunteers at gram doses; cannot determine a lowest toxic dose, safe upper intake or equivalence of different B6 forms.
    nutrient_topic
    Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
    organism
    Homo sapiens
    plain_language
    At very high exposure, more pyridoxine produced earlier sensory toxicity.
    primary_references
    [b6-berger1992] Dose response, coasting, and differential fiber vulnerability in human toxic neuropathy: a prospective study of pyridoxine neurotoxicity (1992). https://pubmed.ncbi.nlm.nih.gov/1620347/ DOI: 10.1212/wnl.42.7.1367
    tissue_or_cell_type
    Peripheral sensory function

    Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1559–1570

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Five healthy volunteers prospectively followed during experimental pyridoxine excess. · source_derived_draft · unverified_draft

    ### b6-pyridoxine-dose-latency All five volunteers developed sensory symptoms and quantitative sensory abnormalities; the 3 g/day group became symptomatic sooner than the 1 g/day group. Condition category: normal nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: At very high exposure, more pyridoxine produced earlier sensory toxicity. organism: Homo sapiens tissue_or_cell_type: Peripheral sensory function experimental_model: Five healthy volunteers prospectively followed during experimental pyridoxine excess. limitations: Five volunteers at gram doses; cannot determine a lowest toxic dose, safe upper intake or equivalence of different B6 forms. exposure: Pyridoxine 1 or 3 g/day, stopped with clinical/laboratory abnormality; very high historical exposures. availability_state: Experimental excess, not nutrient deficiency [b6-berger1992] Dose response, coasting, and differential fiber vulnerability in human toxic neuropathy: a prospective study of pyridoxine neurotoxicity (1992). https://pubmed.ncbi.nlm.nih.gov/1620347/ DOI: 10.1212/wnl.42.7.1367
    Complete structured claim and evidence
  4. Pyridoxine reduced the erythrocyte AST activation coefficient and improved post-tryptophan-load urinary xanthurenate response.

    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    experimental_model
    Double-blind randomized placebo-controlled RA trial: 36 recruited, 33 baseline completers, 28 low-PLP patients eligible for supplementation.
    exposure
    Pyridoxine hydrochloride 50 mg/day or placebo for 30 days; historical trial exposure, not a regimen recommendation.
    limitations
    Challenge tests and erythrocyte saturation do not identify every tissue defect.
    nutrient_topic
    Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
    organism
    Homo sapiens
    plain_language
    Two B6-related functional tests improved, alongside blood vitamin levels.
    primary_references
    [b6-chiang2005-trial] Pyridoxine supplementation corrects vitamin B6 deficiency but does not improve inflammation in patients with rheumatoid arthritis (2005). https://pubmed.ncbi.nlm.nih.gov/16277693/ DOI: 10.1186/ar1839
    tissue_or_cell_type
    Human blood and whole-body measurements
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1473–1483

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind randomized placebo-controlled RA trial: 36 recruited, 33 baseline completers, 28 low-PLP patients eligible for supplementation. · source_derived_draft · unverified_draft

    ### b6-ra-functional-tests Pyridoxine reduced the erythrocyte AST activation coefficient and improved post-tryptophan-load urinary xanthurenate response. Condition category: biomarker_context nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Two B6-related functional tests improved, alongside blood vitamin levels. organism: Homo sapiens tissue_or_cell_type: Human blood and whole-body measurements experimental_model: Double-blind randomized placebo-controlled RA trial: 36 recruited, 33 baseline completers, 28 low-PLP patients eligible for supplementation. limitations: Challenge tests and erythrocyte saturation do not identify every tissue defect. exposure: Pyridoxine hydrochloride 50 mg/day or placebo for 30 days; historical trial exposure, not a regimen recommendation. [b6-chiang2005-trial] Pyridoxine supplementation corrects vitamin B6 deficiency but does not improve inflammation in patients with rheumatoid arthritis (2005). https://pubmed.ncbi.nlm.nih.gov/16277693/ DOI: 10.1186/ar1839
    Complete structured claim and evidence
  5. The overall post-methionine homocysteine treatment effect was a nonsignificant trend (P=0.086); an elevated-baseline subgroup showed a stronger signal.

    Pyridoxine → Homocysteine source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    cross_nutrient
    Methionine handling depends on more than circulating B6.
    experimental_model
    Double-blind randomized placebo-controlled RA trial: 36 recruited, 33 baseline completers, 28 low-PLP patients eligible for supplementation.
    exposure
    Pyridoxine hydrochloride 50 mg/day or placebo for 30 days; historical trial exposure, not a regimen recommendation.
    limitations
    Subgroup findings are exploratory; methotrexate, inflammation and enzyme differences can affect the challenge.
    nutrient_topic
    Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
    organism
    Homo sapiens
    plain_language
    The homocysteine test did not improve as consistently as the other B6 tests.
    primary_references
    [b6-chiang2005-trial] Pyridoxine supplementation corrects vitamin B6 deficiency but does not improve inflammation in patients with rheumatoid arthritis (2005). https://pubmed.ncbi.nlm.nih.gov/16277693/ DOI: 10.1186/ar1839
    tissue_or_cell_type
    Human blood and whole-body measurements
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1497–1508

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind randomized placebo-controlled RA trial: 36 recruited, 33 baseline completers, 28 low-PLP patients eligible for supplementation. · source_derived_draft · unverified_draft

    ### b6-ra-homocysteine-response-boundary The overall post-methionine homocysteine treatment effect was a nonsignificant trend (P=0.086); an elevated-baseline subgroup showed a stronger signal. Condition category: biomarker_context nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The homocysteine test did not improve as consistently as the other B6 tests. organism: Homo sapiens tissue_or_cell_type: Human blood and whole-body measurements experimental_model: Double-blind randomized placebo-controlled RA trial: 36 recruited, 33 baseline completers, 28 low-PLP patients eligible for supplementation. limitations: Subgroup findings are exploratory; methotrexate, inflammation and enzyme differences can affect the challenge. exposure: Pyridoxine hydrochloride 50 mg/day or placebo for 30 days; historical trial exposure, not a regimen recommendation. cross_nutrient: Methionine handling depends on more than circulating B6. [b6-chiang2005-trial] Pyridoxine supplementation corrects vitamin B6 deficiency but does not improve inflammation in patients with rheumatoid arthritis (2005). https://pubmed.ncbi.nlm.nih.gov/16277693/ DOI: 10.1186/ar1839
    Complete structured claim and evidence
  6. The 2005 trial found no suppression of IL-6 or TNF production despite improved B6 markers.

    Pyridoxine → IL6 source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    experimental_model
    Double-blind randomized placebo-controlled RA trial: 36 recruited, 33 baseline completers, 28 low-PLP patients eligible for supplementation.
    exposure
    Pyridoxine hydrochloride 50 mg/day or placebo for 30 days; historical trial exposure, not a regimen recommendation.
    limitations
    Small short trial; a null finding is not proof that no population can respond. The CRP/ESR/RF table-versus-narrative reporting ambiguity is retained separately as an open question.
    nutrient_topic
    Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
    organism
    Homo sapiens
    plain_language
    Correcting the vitamin measurements did not resolve the measured inflammation.
    primary_references
    [b6-chiang2005-trial] Pyridoxine supplementation corrects vitamin B6 deficiency but does not improve inflammation in patients with rheumatoid arthritis (2005). https://pubmed.ncbi.nlm.nih.gov/16277693/ DOI: 10.1186/ar1839
    tissue_or_cell_type
    Human blood and whole-body measurements
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1485–1495

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind randomized placebo-controlled RA trial: 36 recruited, 33 baseline completers, 28 low-PLP patients eligible for supplementation. · source_derived_draft · unverified_draft

    ### b6-ra-no-cytokine-suppression The 2005 trial found no suppression of IL-6 or TNF production despite improved B6 markers. Condition category: biomarker_context nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Correcting the vitamin measurements did not resolve the measured inflammation. organism: Homo sapiens tissue_or_cell_type: Human blood and whole-body measurements experimental_model: Double-blind randomized placebo-controlled RA trial: 36 recruited, 33 baseline completers, 28 low-PLP patients eligible for supplementation. limitations: Small short trial; a null finding is not proof that no population can respond. The CRP/ESR/RF table-versus-narrative reporting ambiguity is retained separately as an open question. exposure: Pyridoxine hydrochloride 50 mg/day or placebo for 30 days; historical trial exposure, not a regimen recommendation. [b6-chiang2005-trial] Pyridoxine supplementation corrects vitamin B6 deficiency but does not improve inflammation in patients with rheumatoid arthritis (2005). https://pubmed.ncbi.nlm.nih.gov/16277693/ DOI: 10.1186/ar1839
    Complete structured claim and evidence
  7. Supplementation improved plasma and erythrocyte PLP compared with placebo.

    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    experimental_model
    Double-blind randomized placebo-controlled RA trial: 36 recruited, 33 baseline completers, 28 low-PLP patients eligible for supplementation.
    exposure
    Pyridoxine hydrochloride 50 mg/day or placebo for 30 days; historical trial exposure, not a regimen recommendation.
    limitations
    Selected low-PLP RA patients; blood response is not direct all-organ cofactor measurement.
    nutrient_topic
    Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
    organism
    Homo sapiens
    plain_language
    The measured B6 pools responded to added pyridoxine.
    primary_references
    [b6-chiang2005-trial] Pyridoxine supplementation corrects vitamin B6 deficiency but does not improve inflammation in patients with rheumatoid arthritis (2005). https://pubmed.ncbi.nlm.nih.gov/16277693/ DOI: 10.1186/ar1839
    tissue_or_cell_type
    Human blood and whole-body measurements
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1461–1471

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind randomized placebo-controlled RA trial: 36 recruited, 33 baseline completers, 28 low-PLP patients eligible for supplementation. · source_derived_draft · unverified_draft

    ### b6-ra-vitamer-response Supplementation improved plasma and erythrocyte PLP compared with placebo. Condition category: biomarker_context nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The measured B6 pools responded to added pyridoxine. organism: Homo sapiens tissue_or_cell_type: Human blood and whole-body measurements experimental_model: Double-blind randomized placebo-controlled RA trial: 36 recruited, 33 baseline completers, 28 low-PLP patients eligible for supplementation. limitations: Selected low-PLP RA patients; blood response is not direct all-organ cofactor measurement. exposure: Pyridoxine hydrochloride 50 mg/day or placebo for 30 days; historical trial exposure, not a regimen recommendation. [b6-chiang2005-trial] Pyridoxine supplementation corrects vitamin B6 deficiency but does not improve inflammation in patients with rheumatoid arthritis (2005). https://pubmed.ncbi.nlm.nih.gov/16277693/ DOI: 10.1186/ar1839
    Complete structured claim and evidence
  8. After long-term 1250–1750 mg/day exposure, the reported patient recovered sensory function and nerve potentials following reduction to 500 mg/day.

    Pyridoxine → Sensory neuropathy source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Single patient with homocystinuria and long-term high-dose pyridoxine exposure.
    exposure
    1250–1750 mg/day for 20 years; subsequently reduced to 500 mg/day. Case history, not evidence that the reduced dose is safe generally.
    limitations
    Single homocystinuria case; does not establish universal reversibility or safety of 500 mg/day. The article background statement about 50 mg is not treated as an experimentally determined threshold.
    nutrient_topic
    Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
    organism
    Homo sapiens
    plain_language
    Recovery was possible in this individual despite long exposure.
    primary_references
    [b6-echanizlaguna2018] Regressive pyridoxine-induced sensory neuronopathy in a patient with homocystinuria (2018). https://pubmed.ncbi.nlm.nih.gov/29954767/ DOI: 10.1136/bcr-2018-225059
    tissue_or_cell_type
    Peripheral sensory nerves

    Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1596–1606

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Single patient with homocystinuria and long-term high-dose pyridoxine exposure. · source_derived_draft · unverified_draft

    ### b6-toxicity-case-recovery After long-term 1250–1750 mg/day exposure, the reported patient recovered sensory function and nerve potentials following reduction to 500 mg/day. Condition category: normal nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Recovery was possible in this individual despite long exposure. organism: Homo sapiens tissue_or_cell_type: Peripheral sensory nerves experimental_model: Single patient with homocystinuria and long-term high-dose pyridoxine exposure. limitations: Single homocystinuria case; does not establish universal reversibility or safety of 500 mg/day. The article background statement about 50 mg is not treated as an experimentally determined threshold. exposure: 1250–1750 mg/day for 20 years; subsequently reduced to 500 mg/day. Case history, not evidence that the reduced dose is safe generally. [b6-echanizlaguna2018] Regressive pyridoxine-induced sensory neuronopathy in a patient with homocystinuria (2018). https://pubmed.ncbi.nlm.nih.gov/29954767/ DOI: 10.1136/bcr-2018-225059
    Complete structured claim and evidence
  9. Symptoms progressed for two to three weeks after pyridoxine withdrawal despite normalized serum PLP.

    Pyridoxine → Sensory neuropathy source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Five healthy volunteers prospectively followed during experimental pyridoxine excess.
    exposure
    Pyridoxine 1 or 3 g/day, stopped with clinical/laboratory abnormality; very high historical exposures.
    limitations
    Demonstrates clinical timing; does not identify the molecular injury mechanism or prove irreversible damage.
    nutrient_topic
    Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
    organism
    Homo sapiens
    plain_language
    A blood vitamin level returned to normal before the nerve symptoms stopped worsening.
    primary_references
    [b6-berger1992] Dose response, coasting, and differential fiber vulnerability in human toxic neuropathy: a prospective study of pyridoxine neurotoxicity (1992). https://pubmed.ncbi.nlm.nih.gov/1620347/ DOI: 10.1212/wnl.42.7.1367
    tissue_or_cell_type
    Peripheral sensory function after exposure withdrawal

    Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1584–1594

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Five healthy volunteers prospectively followed during experimental pyridoxine excess. · source_derived_draft · unverified_draft

    ### b6-toxicity-coasting Symptoms progressed for two to three weeks after pyridoxine withdrawal despite normalized serum PLP. Condition category: normal nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A blood vitamin level returned to normal before the nerve symptoms stopped worsening. organism: Homo sapiens tissue_or_cell_type: Peripheral sensory function after exposure withdrawal experimental_model: Five healthy volunteers prospectively followed during experimental pyridoxine excess. limitations: Demonstrates clinical timing; does not identify the molecular injury mechanism or prove irreversible damage. exposure: Pyridoxine 1 or 3 g/day, stopped with clinical/laboratory abnormality; very high historical exposures. [b6-berger1992] Dose response, coasting, and differential fiber vulnerability in human toxic neuropathy: a prospective study of pyridoxine neurotoxicity (1992). https://pubmed.ncbi.nlm.nih.gov/1620347/ DOI: 10.1212/wnl.42.7.1367
    Complete structured claim and evidence
  10. Thermal thresholds changed before or more strongly than vibration thresholds in the lower-dose group; sensory nerve-potential changes lagged thresholds in two of three subjects.

    Pyridoxine → Quantitative sensory thresholds source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Five healthy volunteers prospectively followed during experimental pyridoxine excess.
    exposure
    Pyridoxine 1 or 3 g/day, stopped with clinical/laboratory abnormality; very high historical exposures.
    limitations
    Small experimental groups; not a diagnostic screening protocol.
    nutrient_topic
    Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
    organism
    Homo sapiens
    plain_language
    Different nerve tests detected the developing injury at different times.
    primary_references
    [b6-berger1992] Dose response, coasting, and differential fiber vulnerability in human toxic neuropathy: a prospective study of pyridoxine neurotoxicity (1992). https://pubmed.ncbi.nlm.nih.gov/1620347/ DOI: 10.1212/wnl.42.7.1367
    tissue_or_cell_type
    Peripheral sensory nerve function

    Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1572–1582

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Five healthy volunteers prospectively followed during experimental pyridoxine excess. · source_derived_draft · unverified_draft

    ### b6-toxicity-early-sensory-tests Thermal thresholds changed before or more strongly than vibration thresholds in the lower-dose group; sensory nerve-potential changes lagged thresholds in two of three subjects. Condition category: normal nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Different nerve tests detected the developing injury at different times. organism: Homo sapiens tissue_or_cell_type: Peripheral sensory nerve function experimental_model: Five healthy volunteers prospectively followed during experimental pyridoxine excess. limitations: Small experimental groups; not a diagnostic screening protocol. exposure: Pyridoxine 1 or 3 g/day, stopped with clinical/laboratory abnormality; very high historical exposures. [b6-berger1992] Dose response, coasting, and differential fiber vulnerability in human toxic neuropathy: a prospective study of pyridoxine neurotoxicity (1992). https://pubmed.ncbi.nlm.nih.gov/1620347/ DOI: 10.1212/wnl.42.7.1367
    Complete structured claim and evidence
  11. Caco-2 pyridoxine uptake was energy-dependent and sodium-independent; saturation occurred at pH 5.5 (apparent Km 11.99 micromolar), but not pH 7.4.

    Pyridoxine → Intestinal pyridoxine uptake source_derived_draftungraded
    Experimental context and source evidence
    evidence_location
    Indexed abstract: pH-dependent saturation and sodium independence
    experimental_model
    Human Caco-2 intestinal epithelial cells.
    exposure
    Radiotracer uptake at controlled extracellular pH.
    limitations
    Carrier identity was not established; uptake behavior alone does not identify a transporter gene.
    nutrient_topic
    Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
    organism
    Homo sapiens
    plain_language
    Acidic conditions exposed a saturable uptake component.
    primary_references
    [said2003] A carrier-mediated mechanism for pyridoxine uptake by human intestinal epithelial Caco-2 cells: regulation by a PKA-mediated pathway. (2003). https://pubmed.ncbi.nlm.nih.gov/12867360/ DOI: 10.1152/ajpcell.00204.2003
    tissue_or_cell_type
    Caco-2 cells

    Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 111–122

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human Caco-2 intestinal epithelial cells. · source_derived_draft · unverified_draft

    ### b6-transport-caco2-pn-uptake Caco-2 pyridoxine uptake was energy-dependent and sodium-independent; saturation occurred at pH 5.5 (apparent Km 11.99 micromolar), but not pH 7.4. Condition category: normal nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Acidic conditions exposed a saturable uptake component. organism: Homo sapiens tissue_or_cell_type: Caco-2 cells experimental_model: Human Caco-2 intestinal epithelial cells. limitations: Carrier identity was not established; uptake behavior alone does not identify a transporter gene. exposure: Radiotracer uptake at controlled extracellular pH. evidence_location: Indexed abstract: pH-dependent saturation and sodium independence [said2003] A carrier-mediated mechanism for pyridoxine uptake by human intestinal epithelial Caco-2 cells: regulation by a PKA-mediated pathway. (2003). https://pubmed.ncbi.nlm.nih.gov/12867360/ DOI: 10.1152/ajpcell.00204.2003
    Complete structured claim and evidence
  12. Polarized Caco-2 cells supplied apically with PN generated PL and released more PL basolaterally than apically.

    Pyridoxine → Pyridoxal source_derived_draftungraded
    Experimental context and source evidence
    evidence_location
    Results: Incubation with pyridoxine; Figure 4
    experimental_model
    Polarized human Caco-2 monolayers; human intestinal lysates.
    exposure
    100 or 1000 nM PN; 6-48 h.
    limitations
    Vitamer measurements establish net conversion; individual enzyme fluxes were not separately perturbed.
    nutrient_topic
    Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
    organism
    Homo sapiens
    plain_language
    Enterocytes can process a precursor before releasing pyridoxal.
    primary_references
    [albersen2013] The intestine plays a substantial role in human vitamin B6 metabolism: a Caco-2 cell model. (2013). https://pubmed.ncbi.nlm.nih.gov/23342087/ DOI: 10.1371/journal.pone.0054113
    tissue_or_cell_type
    Polarized Caco-2 monolayers

    Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 124–135

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Polarized human Caco-2 monolayers; human intestinal lysates. · source_derived_draft · unverified_draft

    ### b6-transport-enterocyte-pn-to-pl Polarized Caco-2 cells supplied apically with PN generated PL and released more PL basolaterally than apically. Condition category: normal nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Enterocytes can process a precursor before releasing pyridoxal. organism: Homo sapiens tissue_or_cell_type: Polarized Caco-2 monolayers experimental_model: Polarized human Caco-2 monolayers; human intestinal lysates. limitations: Vitamer measurements establish net conversion; individual enzyme fluxes were not separately perturbed. exposure: 100 or 1000 nM PN; 6-48 h. evidence_location: Results: Incubation with pyridoxine; Figure 4 [albersen2013] The intestine plays a substantial role in human vitamin B6 metabolism: a Caco-2 cell model. (2013). https://pubmed.ncbi.nlm.nih.gov/23342087/ DOI: 10.1371/journal.pone.0054113
    Complete structured claim and evidence
  13. Evening pyridoxine did not significantly change melatonin onset, peak, mean or AUC relative to placebo.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/melatonin-research/12080281.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "04727c17cd3152a4749ec25ff15b36b827efb885501ce058d436fbbea1e9e7a9", "start_char": 0, "end_char": 1222, "text_sha256": "04727c17cd3152a4749ec25ff15b36b827efb885501ce058d436fbbea1e9e7a9"}
    experimental_model
    Placebo-controlled evening pyridoxine experiment
    exposure
    100 mg pyridoxine at 17:00; evening/night sampling
    limitations
    Acute exposure in healthy men. Null supplementation response does not negate the enzymatic requirement for PLP or settle effects in B6 deficiency.
    nutrient_topic
    Melatonin research collection; topical membership is not evidence of a direct dietary effect. · Melatonin
    organism
    Twelve healthy men
    plain_language
    An enzyme needs B6, but giving extra B6 did not increase the hormone in this experiment.
    primary_references
    [melatonin-p12080281] The effect of pyridoxine administration on melatonin secretion in normal men. (2002). https://pubmed.ncbi.nlm.nih.gov/12080281/
    tissue_or_cell_type
    Melatonin secretion, temperature and polysomnography

    Melatonin: synthesis, receptors, circadian timing and nutrient interactions (2026-09-17) · lines 773–784

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Placebo-controlled evening pyridoxine experiment · source_derived_draft · unverified_draft

    ### melatonin-b6-secretion-null Evening pyridoxine did not significantly change melatonin onset, peak, mean or AUC relative to placebo. Condition category: normal nutrient_topic: Melatonin research collection; topical membership is not evidence of a direct dietary effect. plain_language: An enzyme needs B6, but giving extra B6 did not increase the hormone in this experiment. organism: Twelve healthy men tissue_or_cell_type: Melatonin secretion, temperature and polysomnography experimental_model: Placebo-controlled evening pyridoxine experiment limitations: Acute exposure in healthy men. Null supplementation response does not negate the enzymatic requirement for PLP or settle effects in B6 deficiency. exposure: 100 mg pyridoxine at 17:00; evening/night sampling evidence_span: {"source_cache": "artifacts/melatonin-research/12080281.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "04727c17cd3152a4749ec25ff15b36b827efb885501ce058d436fbbea1e9e7a9", "start_char": 0, "end_char": 1222, "text_sha256": "04727c17cd3152a4749ec25ff15b36b827efb885501ce058d436fbbea1e9e7a9"} [melatonin-p12080281] The effect of pyridoxine administration on melatonin secretion in normal men. (2002). https://pubmed.ncbi.nlm.nih.gov/12080281/
    Complete structured claim and evidence
  14. Sleep amount and architecture were similar after pyridoxine and placebo.

    Pyridoxine → Polysomnographic total sleep time source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/melatonin-research/12080281.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "04727c17cd3152a4749ec25ff15b36b827efb885501ce058d436fbbea1e9e7a9", "start_char": 0, "end_char": 1222, "text_sha256": "04727c17cd3152a4749ec25ff15b36b827efb885501ce058d436fbbea1e9e7a9"}
    experimental_model
    Placebo-controlled evening pyridoxine experiment
    exposure
    100 mg pyridoxine at 17:00; evening/night sampling
    limitations
    Acute exposure in healthy men. Null supplementation response does not negate the enzymatic requirement for PLP or settle effects in B6 deficiency.
    nutrient_topic
    Melatonin research collection; topical membership is not evidence of a direct dietary effect. · Melatonin
    organism
    Twelve healthy men
    plain_language
    A plausible precursor pathway did not guarantee an observable sleep improvement.
    primary_references
    [melatonin-p12080281] The effect of pyridoxine administration on melatonin secretion in normal men. (2002). https://pubmed.ncbi.nlm.nih.gov/12080281/
    tissue_or_cell_type
    Melatonin secretion, temperature and polysomnography

    Melatonin: synthesis, receptors, circadian timing and nutrient interactions (2026-09-17) · lines 786–797

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Placebo-controlled evening pyridoxine experiment · source_derived_draft · unverified_draft

    ### melatonin-b6-sleep-null Sleep amount and architecture were similar after pyridoxine and placebo. Condition category: normal nutrient_topic: Melatonin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A plausible precursor pathway did not guarantee an observable sleep improvement. organism: Twelve healthy men tissue_or_cell_type: Melatonin secretion, temperature and polysomnography experimental_model: Placebo-controlled evening pyridoxine experiment limitations: Acute exposure in healthy men. Null supplementation response does not negate the enzymatic requirement for PLP or settle effects in B6 deficiency. exposure: 100 mg pyridoxine at 17:00; evening/night sampling evidence_span: {"source_cache": "artifacts/melatonin-research/12080281.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "04727c17cd3152a4749ec25ff15b36b827efb885501ce058d436fbbea1e9e7a9", "start_char": 0, "end_char": 1222, "text_sha256": "04727c17cd3152a4749ec25ff15b36b827efb885501ce058d436fbbea1e9e7a9"} [melatonin-p12080281] The effect of pyridoxine administration on melatonin secretion in normal men. (2002). https://pubmed.ncbi.nlm.nih.gov/12080281/
    Complete structured claim and evidence

What acts on it

  1. Purified recombinant human PDXK phosphorylated pyridoxine to its corresponding 5-prime phosphate.

    Pyridoxal kinase / PDXK → Pyridoxine source_derived_draftungraded
    Experimental context and source evidence
    evidence_location
    Indexed abstract and publisher abstract; human enzyme findings only
    experimental_model
    Purified recombinant human and E. coli pyridoxal kinases.
    exposure
    Purified-enzyme substrate kinetics.
    limitations
    Model-specific evidence; no dietary threshold or treatment benefit established.
    nutrient_topic
    Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
    organism
    Homo sapiens
    plain_language
    PDXK adds phosphate to this B6 precursor.
    primary_references
    [disalvo2004] Expression, purification, and kinetic constants for human and Escherichia coli pyridoxal kinases. (2004). https://pubmed.ncbi.nlm.nih.gov/15249053/ DOI: 10.1016/j.pep.2004.04.021
    tissue_or_cell_type
    Purified human enzyme

    Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 163–174

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified recombinant human and E. coli pyridoxal kinases. · source_derived_draft · unverified_draft

    ### b6-transport-pdxk-pn Purified recombinant human PDXK phosphorylated pyridoxine to its corresponding 5-prime phosphate. Condition category: normal nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: PDXK adds phosphate to this B6 precursor. organism: Homo sapiens tissue_or_cell_type: Purified human enzyme experimental_model: Purified recombinant human and E. coli pyridoxal kinases. limitations: Model-specific evidence; no dietary threshold or treatment benefit established. exposure: Purified-enzyme substrate kinetics. evidence_location: Indexed abstract and publisher abstract; human enzyme findings only [disalvo2004] Expression, purification, and kinetic constants for human and Escherichia coli pyridoxal kinases. (2004). https://pubmed.ncbi.nlm.nih.gov/15249053/ DOI: 10.1016/j.pep.2004.04.021
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Catalytically active recombinant human pyridoxal phosphatase hydrolyzed pyridoxine-phosphate.

    Experimental context and source evidence
    evidence_location
    Indexed abstract: cloning and substrate hydrolysis
    experimental_model
    Recombinant human pyridoxal phosphatase expressed in E. coli.
    exposure
    Recombinant-enzyme characterization.
    limitations
    Model-specific evidence; no dietary threshold or treatment benefit established.
    nutrient_topic
    Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
    organism
    Homo sapiens
    plain_language
    PDXP removes phosphate from a B6 vitamer.
    primary_references
    [jang2003] Human pyridoxal phosphatase. Molecular cloning, functional expression, and tissue distribution. (2003). https://pubmed.ncbi.nlm.nih.gov/14522954/ DOI: 10.1074/jbc.m309619200
    tissue_or_cell_type
    Purified recombinant human enzyme

    Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 269–280

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human pyridoxal phosphatase expressed in E. coli. · source_derived_draft · unverified_draft

    ### b6-transport-pdxp-pnp Catalytically active recombinant human pyridoxal phosphatase hydrolyzed pyridoxine-phosphate. Condition category: normal nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: PDXP removes phosphate from a B6 vitamer. organism: Homo sapiens tissue_or_cell_type: Purified recombinant human enzyme experimental_model: Recombinant human pyridoxal phosphatase expressed in E. coli. limitations: Model-specific evidence; no dietary threshold or treatment benefit established. exposure: Recombinant-enzyme characterization. evidence_location: Indexed abstract: cloning and substrate hydrolysis [jang2003] Human pyridoxal phosphatase. Molecular cloning, functional expression, and tissue distribution. (2003). https://pubmed.ncbi.nlm.nih.gov/14522954/ DOI: 10.1074/jbc.m309619200
    Complete structured claim and evidence
  2. After a 100 nM D3-PN pulse, labeled PLP appeared in whole cells but scarcely in SLC25A38-null mitochondria.

    Human SLC25A38 knockout genotype → PLP source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_location
    Figure 4A-B
    experimental_model
    Human K562 knockout cells, Mito-IP, LC-MS and isotope tracing.
    exposure
    100 nM D3-PN, one-hour tracing after 10 nM PN conditioning.
    limitations
    Import, retention and indirect regulation remain alternatives.
    nutrient_topic
    Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
    organism
    Homo sapiens
    plain_language
    Synthesis persisted while mitochondrial accumulation failed.
    primary_references
    [pena2025] SLC25A38 is required for mitochondrial pyridoxal 5'-phosphate (PLP) accumulation. (2025). https://pubmed.ncbi.nlm.nih.gov/39856062/ DOI: 10.1038/s41467-025-56130-3
    tissue_or_cell_type
    K562 cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 465–476

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human K562 knockout cells, Mito-IP, LC-MS and isotope tracing. · source_derived_draft · unverified_draft

    ### b6-transport-slc25a38-tracer After a 100 nM D3-PN pulse, labeled PLP appeared in whole cells but scarcely in SLC25A38-null mitochondria. Condition category: machinery_impairment nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Synthesis persisted while mitochondrial accumulation failed. organism: Homo sapiens tissue_or_cell_type: K562 cells experimental_model: Human K562 knockout cells, Mito-IP, LC-MS and isotope tracing. limitations: Import, retention and indirect regulation remain alternatives. exposure: 100 nM D3-PN, one-hour tracing after 10 nM PN conditioning. evidence_location: Figure 4A-B [pena2025] SLC25A38 is required for mitochondrial pyridoxal 5'-phosphate (PLP) accumulation. (2025). https://pubmed.ncbi.nlm.nih.gov/39856062/ DOI: 10.1038/s41467-025-56130-3
    Complete structured claim and evidence
  3. Human SLC19A3 expression increased pyridoxine uptake at pH 5.5; transport favored acidic over neutral/basic conditions.

    Experimental context and source evidence
    cross_nutrient
    A pH-dependent shared transport route links B1 and the pyridoxine form of B6.
    evidence-scope
    Cultured epithelial cells
    evidence_locator
    Figures 1-3, 6 and 9
    evidence_spans
    [{"source_document": "artifacts/thiamine_transport_sources/yamashiro-2020-pyridoxine-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1718}]
    experimental_model
    Human transporter constructs in MDCKII/HEK293 cells; radiotracer uptake at pH 5.5.
    extracellular-pH
    5.5
    limitations
    No systemic B6 transport fraction or supplementation benefit established.
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Human proteins; canine and human cell hosts
    plain_language
    The B1 carrier can also carry one B6 form under acidic conditions.
    primary_references
    [yamashiro-2020-pyridoxine] pH-dependent pyridoxine transport by SLC19A2 and SLC19A3: Implications for absorption in acidic microclimates (2020). https://pmc.ncbi.nlm.nih.gov/articles/PMC7863892/ DOI: 10.1074/jbc.RA120.013610
    tissue_or_cell_type
    Cultured epithelial cells

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 631–645

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human transporter constructs in MDCKII/HEK293 cells; radiotracer uptake at pH 5.5. · source_derived_draft · unverified_draft

    ### b1-slc19a3-pyridoxine-transport Human SLC19A3 expression increased pyridoxine uptake at pH 5.5; transport favored acidic over neutral/basic conditions. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The B1 carrier can also carry one B6 form under acidic conditions. organism: Human proteins; canine and human cell hosts tissue_or_cell_type: Cultured epithelial cells experimental_model: Human transporter constructs in MDCKII/HEK293 cells; radiotracer uptake at pH 5.5. limitations: No systemic B6 transport fraction or supplementation benefit established. cross_nutrient: A pH-dependent shared transport route links B1 and the pyridoxine form of B6. evidence_spans: [{"source_document": "artifacts/thiamine_transport_sources/yamashiro-2020-pyridoxine-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1718}] evidence_locator: Figures 1-3, 6 and 9 extracellular-pH: 5.5 evidence-scope: Cultured epithelial cells [yamashiro-2020-pyridoxine] pH-dependent pyridoxine transport by SLC19A2 and SLC19A3: Implications for absorption in acidic microclimates (2020). https://pmc.ncbi.nlm.nih.gov/articles/PMC7863892/ DOI: 10.1074/jbc.RA120.013610
    Complete structured claim and evidence
  4. Thiamine inhibited SLC19A2- and SLC19A3-mediated pyridoxine uptake in acidic-pH transfectant assays.

    Thiamine (vitamin B1) → Cellular pyridoxine uptake source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Direct B1-to-pyridoxine transport inhibition is demonstrated in vitro, with pH and exposure limitations.
    evidence-scope
    Cultured epithelial cells
    evidence_locator
    Figures 1-3, 6 and 9
    evidence_spans
    [{"source_document": "artifacts/thiamine_transport_sources/yamashiro-2020-pyridoxine-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1718}]
    experimental_model
    Human transporter constructs in MDCKII/HEK293 cells; radiotracer uptake at pH 5.5.
    extracellular-pH
    5.5
    limitations
    Assay inhibition does not show clinical B6 deficiency from dietary thiamine.
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Human proteins; canine and human cell hosts
    plain_language
    B1 reduced uptake of a B6 form in these transporter experiments.
    primary_references
    [yamashiro-2020-pyridoxine] pH-dependent pyridoxine transport by SLC19A2 and SLC19A3: Implications for absorption in acidic microclimates (2020). https://pmc.ncbi.nlm.nih.gov/articles/PMC7863892/ DOI: 10.1074/jbc.RA120.013610
    tissue_or_cell_type
    Cultured epithelial cells

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 647–661

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human transporter constructs in MDCKII/HEK293 cells; radiotracer uptake at pH 5.5. · source_derived_draft · unverified_draft

    ### b1-thiamine-inhibits-pyridoxine-uptake Thiamine inhibited SLC19A2- and SLC19A3-mediated pyridoxine uptake in acidic-pH transfectant assays. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: B1 reduced uptake of a B6 form in these transporter experiments. organism: Human proteins; canine and human cell hosts tissue_or_cell_type: Cultured epithelial cells experimental_model: Human transporter constructs in MDCKII/HEK293 cells; radiotracer uptake at pH 5.5. limitations: Assay inhibition does not show clinical B6 deficiency from dietary thiamine. cross_nutrient: Direct B1-to-pyridoxine transport inhibition is demonstrated in vitro, with pH and exposure limitations. evidence_spans: [{"source_document": "artifacts/thiamine_transport_sources/yamashiro-2020-pyridoxine-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1718}] evidence_locator: Figures 1-3, 6 and 9 extracellular-pH: 5.5 evidence-scope: Cultured epithelial cells [yamashiro-2020-pyridoxine] pH-dependent pyridoxine transport by SLC19A2 and SLC19A3: Implications for absorption in acidic microclimates (2020). https://pmc.ncbi.nlm.nih.gov/articles/PMC7863892/ DOI: 10.1074/jbc.RA120.013610
    Complete structured claim and evidence
  5. Cheilosis and angular stomatitis occurred during the low-niacin/tryptophan regimen even with approximately 2 mg/day total riboflavin and supplemental pyridoxine; these lesions were not specific evidence of B2 deficiency.

    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    Riboflavin (vitamin B2) (supplied_co_nutrient); Pyridoxine (supplied_co_nutrient)
    evidence_span
    {"source_cache": "artifacts/niacin-clinical-sources/goldsmith1952.txt", "locator": "Primary full report; exact character range, zero-based and end-exclusive", "file_sha256": "2d4004fb5985f80c8e44909506e1aa05b6eefd838f4c28102beac30fb3092bc5", "start_char": 15452, "end_char": 16019, "text_sha256": "66c68d7739e59c3e98f30fe0757f468a7952746f7dfe082138dfa6727fa54bf4"}
    experimental_model
    Historical metabolic-ward restriction; seven women, with three prolonged corn-diet cases developing pellagra
    exposure
    Corn diet about 4.7 mg niacin and 190 mg tryptophan/day; other B-vitamin supplements; 40–135 days depending on subject; subsequent niacinamide or DL-tryptophan
    limitations
    Very small nonrandomized historical experiment. Diets and exposure durations differed; signs were not universal. Nitrogen balance did not prove niacin sufficiency. This does not establish a modern intake threshold or demonstrate a corn toxin.
    nutrient_topic
    Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
    organism
    Homo sapiens
    plain_language
    A sore mouth can arise from different nutrient problems. The appearance alone did not identify which vitamin was lacking.
    primary_references
    [nia-clin-goldsmith1952] Studies of niacin requirement in man. I. Experimental pellagra in subjects on corn diets low in niacin and tryptophan. (1952). https://pubmed.ncbi.nlm.nih.gov/14938430/ DOI: 10.1172/jci102638
    supplementary_evidence_spans
    [{"source_cache": "artifacts/niacin-clinical-sources/goldsmith1952.txt", "start_char": 8901, "end_char": 9290, "file_sha256": "2d4004fb5985f80c8e44909506e1aa05b6eefd838f4c28102beac30fb3092bc5", "text_sha256": "59d1a659822aca95688b5e36bd07b41ea700bfbfdc92b40005acf11bd540b046", "locator": "Methods: supplied B-vitamin quantities"}, {"source_cache": "artifacts/niacin-clinical-sources/goldsmith1952.txt", "start_char": 31540, "end_char": 31811, "file_sha256": "2d4004fb5985f80c8e44909506e1aa05b6eefd838f4c28102beac30fb3092bc5", "text_sha256": "ff226f4114a9dec08a00118aa9df933b8246dc89bcf362b2569c089b511d9d3e", "locator": "Discussion: riboflavin and pyridoxine supplements"}]
    tissue_or_cell_type
    Skin, oral and intestinal mucosa
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 1205–1218

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Historical metabolic-ward restriction; seven women, with three prolonged corn-diet cases developing pellagra · source_derived_draft · unverified_draft

    ### nia-clin-pellagra-riboflavin-context Cheilosis and angular stomatitis occurred during the low-niacin/tryptophan regimen even with approximately 2 mg/day total riboflavin and supplemental pyridoxine; these lesions were not specific evidence of B2 deficiency. Condition category: nutrient_deficiency nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A sore mouth can arise from different nutrient problems. The appearance alone did not identify which vitamin was lacking. organism: Homo sapiens tissue_or_cell_type: Skin, oral and intestinal mucosa experimental_model: Historical metabolic-ward restriction; seven women, with three prolonged corn-diet cases developing pellagra limitations: Very small nonrandomized historical experiment. Diets and exposure durations differed; signs were not universal. Nitrogen balance did not prove niacin sufficiency. This does not establish a modern intake threshold or demonstrate a corn toxin. exposure: Corn diet about 4.7 mg niacin and 190 mg tryptophan/day; other B-vitamin supplements; 40–135 days depending on subject; subsequent niacinamide or DL-tryptophan cross_nutrient: Riboflavin (vitamin B2) (supplied_co_nutrient); Pyridoxine (supplied_co_nutrient) evidence_span: {"source_cache": "artifacts/niacin-clinical-sources/goldsmith1952.txt", "locator": "Primary full report; exact character range, zero-based and end-exclusive", "file_sha256": "2d4004fb5985f80c8e44909506e1aa05b6eefd838f4c28102beac30fb3092bc5", "start_char": 15452, "end_char": 16019, "text_sha256": "66c68d7739e59c3e98f30fe0757f468a7952746f7dfe082138dfa6727fa54bf4"} supplementary_evidence_spans: [{"source_cache": "artifacts/niacin-clinical-sources/goldsmith1952.txt", "start_char": 8901, "end_char": 9290, "file_sha256": "2d4004fb5985f80c8e44909506e1aa05b6eefd838f4c28102beac30fb3092bc5", "text_sha256": "59d1a659822aca95688b5e36bd07b41ea700bfbfdc92b40005acf11bd540b046", "locator": "Methods: supplied B-vitamin quantities"}, {"source_cache": "artifacts/niacin-clinical-sources/goldsmith1952.txt", "start_char": 31540, "end_char": 31811, "file_sha256": "2d4004fb5985f80c8e44909506e1aa05b6eefd838f4c28102beac30fb3092bc5", "text_sha256": "ff226f4114a9dec08a00118aa9df933b8246dc89bcf362b2569c089b511d9d3e", "locator": "Discussion: riboflavin and pyridoxine supplements"}] [nia-clin-goldsmith1952] Studies of niacin requirement in man. I. Experimental pellagra in subjects on corn diets low in niacin and tryptophan. (1952). https://pubmed.ncbi.nlm.nih.gov/14938430/ DOI: 10.1172/jci102638
    Complete structured claim and evidence
  6. The five men receiving B5/B6-deficient diet plus both antagonists failed to respond to tetanus and typhoid O immunization and had little typhoid H response.

    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    true
    evidence_location
    Publisher primary Summary at https://www.sciencedirect.com/science/article/abs/pii/S0002916523345945 ; full article not retrieved.
    experimental_model
    Historical two-stage combined B5/B6 depletion experiment in male volunteers
    exposure
    First stage: two controls, two diet-only deficient men and one receiving diet plus both antagonists. Second stage: five men received B5/B6-deficient diet plus omega-methyl pantothenic acid and desoxypyridoxine; exact doses not available in the publisher summary.
    limitations
    Combined nutrient restriction plus antivitamins cannot identify the separate contribution of B5 or B6, a synergistic effect, or a universal immune defect. Reimmunization also changes prior antigen exposure.
    nutrient_topic
    Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
    organism
    Homo sapiens
    plain_language
    Combined depletion and antivitamins impaired some antibody responses.
    primary_references
    [b5-clin-hodges1962] Factors affecting human antibody response. V. Combined deficiencies of pantothenic acid and pyridoxine. (1962). https://pubmed.ncbi.nlm.nih.gov/13907960/ DOI: 10.1093/ajcn/11.3.187
    tissue_or_cell_type
    Immunization responses and serum proteins
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1327–1339

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Historical two-stage combined B5/B6 depletion experiment in male volunteers · source_derived_draft · unverified_draft

    ### b5-clin-combined-antibody-loss The five men receiving B5/B6-deficient diet plus both antagonists failed to respond to tetanus and typhoid O immunization and had little typhoid H response. Condition category: nutrient_deficiency nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Combined depletion and antivitamins impaired some antibody responses. organism: Homo sapiens tissue_or_cell_type: Immunization responses and serum proteins experimental_model: Historical two-stage combined B5/B6 depletion experiment in male volunteers limitations: Combined nutrient restriction plus antivitamins cannot identify the separate contribution of B5 or B6, a synergistic effect, or a universal immune defect. Reimmunization also changes prior antigen exposure. exposure: First stage: two controls, two diet-only deficient men and one receiving diet plus both antagonists. Second stage: five men received B5/B6-deficient diet plus omega-methyl pantothenic acid and desoxypyridoxine; exact doses not available in the publisher summary. cross_nutrient: true evidence_location: Publisher primary Summary at https://www.sciencedirect.com/science/article/abs/pii/S0002916523345945 ; full article not retrieved. [b5-clin-hodges1962] Factors affecting human antibody response. V. Combined deficiencies of pantothenic acid and pyridoxine. (1962). https://pubmed.ncbi.nlm.nih.gov/13907960/ DOI: 10.1093/ajcn/11.3.187
    Complete structured claim and evidence
  7. After vitamins were restored and the five subjects were reimmunized, tetanus and typhoid antibody responses were reported as normal.

    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    true
    evidence_location
    Publisher primary Summary at https://www.sciencedirect.com/science/article/abs/pii/S0002916523345945 ; full article not retrieved.
    experimental_model
    Historical two-stage combined B5/B6 depletion experiment in male volunteers
    exposure
    First stage: two controls, two diet-only deficient men and one receiving diet plus both antagonists. Second stage: five men received B5/B6-deficient diet plus omega-methyl pantothenic acid and desoxypyridoxine; exact doses not available in the publisher summary.
    limitations
    Combined nutrient restriction plus antivitamins cannot identify the separate contribution of B5 or B6, a synergistic effect, or a universal immune defect. Reimmunization also changes prior antigen exposure. This is not a blinded comparison of B5 alone, B6 alone or their interaction.
    nutrient_topic
    Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
    organism
    Homo sapiens
    plain_language
    Responses recovered after combined vitamin restoration and another immunization.
    primary_references
    [b5-clin-hodges1962] Factors affecting human antibody response. V. Combined deficiencies of pantothenic acid and pyridoxine. (1962). https://pubmed.ncbi.nlm.nih.gov/13907960/ DOI: 10.1093/ajcn/11.3.187
    tissue_or_cell_type
    Immunization responses and serum proteins
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1355–1367

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Historical two-stage combined B5/B6 depletion experiment in male volunteers · source_derived_draft · unverified_draft

    ### b5-clin-combined-immune-recovery After vitamins were restored and the five subjects were reimmunized, tetanus and typhoid antibody responses were reported as normal. Condition category: nutrient_deficiency nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Responses recovered after combined vitamin restoration and another immunization. organism: Homo sapiens tissue_or_cell_type: Immunization responses and serum proteins experimental_model: Historical two-stage combined B5/B6 depletion experiment in male volunteers limitations: Combined nutrient restriction plus antivitamins cannot identify the separate contribution of B5 or B6, a synergistic effect, or a universal immune defect. Reimmunization also changes prior antigen exposure. This is not a blinded comparison of B5 alone, B6 alone or their interaction. exposure: First stage: two controls, two diet-only deficient men and one receiving diet plus both antagonists. Second stage: five men received B5/B6-deficient diet plus omega-methyl pantothenic acid and desoxypyridoxine; exact doses not available in the publisher summary. cross_nutrient: true evidence_location: Publisher primary Summary at https://www.sciencedirect.com/science/article/abs/pii/S0002916523345945 ; full article not retrieved. [b5-clin-hodges1962] Factors affecting human antibody response. V. Combined deficiencies of pantothenic acid and pyridoxine. (1962). https://pubmed.ncbi.nlm.nih.gov/13907960/ DOI: 10.1093/ajcn/11.3.187
    Complete structured claim and evidence
  8. The same five men retained strong antibody responses to polio immunization despite their impaired tetanus and typhoid responses.

    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    true
    evidence_location
    Publisher primary Summary at https://www.sciencedirect.com/science/article/abs/pii/S0002916523345945 ; full article not retrieved.
    experimental_model
    Historical two-stage combined B5/B6 depletion experiment in male volunteers
    exposure
    First stage: two controls, two diet-only deficient men and one receiving diet plus both antagonists. Second stage: five men received B5/B6-deficient diet plus omega-methyl pantothenic acid and desoxypyridoxine; exact doses not available in the publisher summary.
    limitations
    Combined nutrient restriction plus antivitamins cannot identify the separate contribution of B5 or B6, a synergistic effect, or a universal immune defect. Reimmunization also changes prior antigen exposure.
    nutrient_topic
    Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
    organism
    Homo sapiens
    plain_language
    The immune impairment did not affect every tested antigen equally.
    primary_references
    [b5-clin-hodges1962] Factors affecting human antibody response. V. Combined deficiencies of pantothenic acid and pyridoxine. (1962). https://pubmed.ncbi.nlm.nih.gov/13907960/ DOI: 10.1093/ajcn/11.3.187
    tissue_or_cell_type
    Immunization responses and serum proteins
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1341–1353

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Historical two-stage combined B5/B6 depletion experiment in male volunteers · source_derived_draft · unverified_draft

    ### b5-clin-combined-polio-preserved The same five men retained strong antibody responses to polio immunization despite their impaired tetanus and typhoid responses. Condition category: nutrient_deficiency nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The immune impairment did not affect every tested antigen equally. organism: Homo sapiens tissue_or_cell_type: Immunization responses and serum proteins experimental_model: Historical two-stage combined B5/B6 depletion experiment in male volunteers limitations: Combined nutrient restriction plus antivitamins cannot identify the separate contribution of B5 or B6, a synergistic effect, or a universal immune defect. Reimmunization also changes prior antigen exposure. exposure: First stage: two controls, two diet-only deficient men and one receiving diet plus both antagonists. Second stage: five men received B5/B6-deficient diet plus omega-methyl pantothenic acid and desoxypyridoxine; exact doses not available in the publisher summary. cross_nutrient: true evidence_location: Publisher primary Summary at https://www.sciencedirect.com/science/article/abs/pii/S0002916523345945 ; full article not retrieved. [b5-clin-hodges1962] Factors affecting human antibody response. V. Combined deficiencies of pantothenic acid and pyridoxine. (1962). https://pubmed.ncbi.nlm.nih.gov/13907960/ DOI: 10.1093/ajcn/11.3.187
    Complete structured claim and evidence
  9. The two men receiving the B5/B6-deficient diet without antagonists in the first stage showed minor abnormalities but no impairment of antibody production in that stage.

    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    true
    evidence_location
    Publisher primary Summary at https://www.sciencedirect.com/science/article/abs/pii/S0002916523345945 ; full article not retrieved.
    experimental_model
    Historical two-stage combined B5/B6 depletion experiment in male volunteers
    exposure
    First stage: two controls, two diet-only deficient men and one receiving diet plus both antagonists. Second stage: five men received B5/B6-deficient diet plus omega-methyl pantothenic acid and desoxypyridoxine; exact doses not available in the publisher summary.
    limitations
    Combined nutrient restriction plus antivitamins cannot identify the separate contribution of B5 or B6, a synergistic effect, or a universal immune defect. Reimmunization also changes prior antigen exposure. Only two subjects; not proof that prolonged isolated dietary deficiency cannot impair immunity.
    nutrient_topic
    Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
    organism
    Homo sapiens
    plain_language
    Diet-only restriction gave a different result from the later antivitamin regimen.
    primary_references
    [b5-clin-hodges1962] Factors affecting human antibody response. V. Combined deficiencies of pantothenic acid and pyridoxine. (1962). https://pubmed.ncbi.nlm.nih.gov/13907960/ DOI: 10.1093/ajcn/11.3.187
    tissue_or_cell_type
    Immunization responses and serum proteins
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1369–1381

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Historical two-stage combined B5/B6 depletion experiment in male volunteers · source_derived_draft · unverified_draft

    ### b5-clin-diet-only-immune-result The two men receiving the B5/B6-deficient diet without antagonists in the first stage showed minor abnormalities but no impairment of antibody production in that stage. Condition category: nutrient_deficiency nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Diet-only restriction gave a different result from the later antivitamin regimen. organism: Homo sapiens tissue_or_cell_type: Immunization responses and serum proteins experimental_model: Historical two-stage combined B5/B6 depletion experiment in male volunteers limitations: Combined nutrient restriction plus antivitamins cannot identify the separate contribution of B5 or B6, a synergistic effect, or a universal immune defect. Reimmunization also changes prior antigen exposure. Only two subjects; not proof that prolonged isolated dietary deficiency cannot impair immunity. exposure: First stage: two controls, two diet-only deficient men and one receiving diet plus both antagonists. Second stage: five men received B5/B6-deficient diet plus omega-methyl pantothenic acid and desoxypyridoxine; exact doses not available in the publisher summary. cross_nutrient: true evidence_location: Publisher primary Summary at https://www.sciencedirect.com/science/article/abs/pii/S0002916523345945 ; full article not retrieved. [b5-clin-hodges1962] Factors affecting human antibody response. V. Combined deficiencies of pantothenic acid and pyridoxine. (1962). https://pubmed.ncbi.nlm.nih.gov/13907960/ DOI: 10.1093/ajcn/11.3.187
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards