Component

3-Hydroxy-L-kynurenine

KMO hydroxylation product and intermediate toward quinolinate.

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

Read recorded mechanisms Open recursive mind map

How nutrients influence it

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

How nutrients reach it in more than one step

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

Tracing routes…

What it does

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

Recorded relationships

What acts on it

  1. Human KYNU cleaves 3-hydroxykynurenine to 3-hydroxyanthranilate and alanine using PLP.

    Human kynureninase / KYNU → 3-Hydroxy-L-kynurenine source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    PLP-dependent KYNU follows the FAD-dependent KMO step, connecting B6 and B2 with tryptophan-niacin metabolism.
    existing_related_claim_ids
    ["5570a502-6ebf-5397-bf2a-0148727e7695"]
    experimental_model
    Recombinant human KYNU crystallography and biochemical characterization
    limitations
    KYNU does not directly make NAD; subsequent enzymes and dietary niacin also contribute.
    nutrient_topic
    Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
    organism
    Homo sapiens
    plain_language
    This B6-dependent step processes the product of upstream KMO chemistry.
    primary_references
    [b6-kynu-2007] Crystal Structure of Homo Sapiens Kynureninase (2007). https://pmc.ncbi.nlm.nih.gov/articles/PMC2531291/ DOI: 10.1021/bi0616697
    tissue_or_cell_type
    Purified recombinant protein; no intact tissue

    Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 885–896

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human KYNU crystallography and biochemical characterization · source_derived_draft · unverified_draft

    ### b6-met-kynu-hydrolysis Human KYNU cleaves 3-hydroxykynurenine to 3-hydroxyanthranilate and alanine using PLP. Condition category: normal nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: This B6-dependent step processes the product of upstream KMO chemistry. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Recombinant human KYNU crystallography and biochemical characterization limitations: KYNU does not directly make NAD; subsequent enzymes and dietary niacin also contribute. cross_nutrient: PLP-dependent KYNU follows the FAD-dependent KMO step, connecting B6 and B2 with tryptophan-niacin metabolism. existing_related_claim_ids: ["5570a502-6ebf-5397-bf2a-0148727e7695"] [b6-kynu-2007] Crystal Structure of Homo Sapiens Kynureninase (2007). https://pmc.ncbi.nlm.nih.gov/articles/PMC2531291/ DOI: 10.1021/bi0616697
    Complete structured claim and evidence

  2. 3-Hydroxykynurenine increased 39% fasting and 34% after meals; kynurenic acid decreased 22% and 20%, respectively.

    Vitamin B6 → 3-Hydroxy-L-kynurenine source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    B6-dependent kynurenine reactions intersect the tryptophan-to-niacin network; conversion to NAD was not measured.
    experimental_model
    Twenty-three healthy adults; paired pre/postprandial LC-MS/MS metabolite profiling.
    exposure
    28 days below 0.35 mg/day B6. Related restriction research program; do not count paper totals as independent trial replications.
    limitations
    Does not measure brain neurotransmitters, tissue NAD synthesis or diagnose niacin deficiency.
    nutrient_topic
    Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
    organism
    Homo sapiens
    plain_language
    Different branches of tryptophan processing left a detectable blood pattern.
    primary_references
    [b6-dasilva2013] Metabolite profile analysis reveals functional effects of 28-day vitamin B-6 restriction on one-carbon metabolism and tryptophan catabolic pathways in healthy men and women (2013). https://pubmed.ncbi.nlm.nih.gov/23966327/ DOI: 10.3945/jn.113.180588
    tissue_or_cell_type
    Human blood and whole-body measurements
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1436–1447

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Twenty-three healthy adults; paired pre/postprandial LC-MS/MS metabolite profiling. · source_derived_draft · unverified_draft

    ### b6-restriction-kynurenine-profile 3-Hydroxykynurenine increased 39% fasting and 34% after meals; kynurenic acid decreased 22% and 20%, respectively. Condition category: nutrient_deficiency nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Different branches of tryptophan processing left a detectable blood pattern. organism: Homo sapiens tissue_or_cell_type: Human blood and whole-body measurements experimental_model: Twenty-three healthy adults; paired pre/postprandial LC-MS/MS metabolite profiling. limitations: Does not measure brain neurotransmitters, tissue NAD synthesis or diagnose niacin deficiency. exposure: 28 days below 0.35 mg/day B6. Related restriction research program; do not count paper totals as independent trial replications. cross_nutrient: B6-dependent kynurenine reactions intersect the tryptophan-to-niacin network; conversion to NAD was not measured. [b6-dasilva2013] Metabolite profile analysis reveals functional effects of 28-day vitamin B-6 restriction on one-carbon metabolism and tryptophan catabolic pathways in healthy men and women (2013). https://pubmed.ncbi.nlm.nih.gov/23966327/ DOI: 10.3945/jn.113.180588
    Complete structured claim and evidence

  3. Riboflavin-deficient baboons excreted approximately one tenth as much urinary 3-hydroxykynurenine in the reported dietary comparison.

    Riboflavin (vitamin B2) → 3-Hydroxy-L-kynurenine source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    Dietary B2 status influences a tryptophan/niacin-pathway readout.
    evidence_location
    Abstract
    experimental_model
    Dietary riboflavin-deficient, pyridoxine-deficient, pair-fed and natural-diet baboons; urinary and erythrocyte measurements.
    exposure
    Experimental riboflavin-deficient diet
    limitations
    Indexed abstract does not give diet duration or group size; urinary output is not a direct tissue KMO flux measurement.
    nutrient_topic
    Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
    organism
    Papio species (baboon)
    plain_language
    Dietary B2 deficiency changed a measured tryptophan-pathway product.
    primary_references
    [verjee1975] Tryptophan metabolism in baboons: effect of riboflavin and pyridoxine deficiency. (1975). https://pubmed.ncbi.nlm.nih.gov/23659/
    tissue_or_cell_type
    Urine
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1276–1288

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dietary riboflavin-deficient, pyridoxine-deficient, pair-fed and natural-diet baboons; urinary and erythrocyte measurements. · source_derived_draft · unverified_draft

    ### b2-baboon-urinary-hydroxykynurenine Riboflavin-deficient baboons excreted approximately one tenth as much urinary 3-hydroxykynurenine in the reported dietary comparison. Condition category: nutrient_deficiency nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Dietary B2 deficiency changed a measured tryptophan-pathway product. organism: Papio species (baboon) tissue_or_cell_type: Urine experimental_model: Dietary riboflavin-deficient, pyridoxine-deficient, pair-fed and natural-diet baboons; urinary and erythrocyte measurements. limitations: Indexed abstract does not give diet duration or group size; urinary output is not a direct tissue KMO flux measurement. exposure: Experimental riboflavin-deficient diet cross_nutrient: Dietary B2 status influences a tryptophan/niacin-pathway readout. evidence_location: Abstract [verjee1975] Tryptophan metabolism in baboons: effect of riboflavin and pyridoxine deficiency. (1975). https://pubmed.ncbi.nlm.nih.gov/23659/
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Human KMO membrane assays measured kynurenine conversion to 3-hydroxykynurenine with NADPH; at 200 micromolar NADPH, kynurenine Km was 2 micromolar.

    Human kynurenine 3-monooxygenase / KMO → L-Kynurenine source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    B2-FAD and nicotinamide-containing NADPH support a branch upstream of de novo niacin synthesis.
    evidence_location
    Fig 2f and Methods: kinetic assays; interpret species separately
    experimental_model
    Human KMO in Sf9 membrane preparations; mass-spectrometry kinetics; separate P. fluorescens KMO crystallography.
    exposure
    Purified-enzyme assay
    limitations
    Human functional assays and bacterial structures are distinct evidence; this experiment did not test dietary B2 restriction or total NAD synthesis.
    nutrient_topic
    Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
    organism
    Homo sapiens
    plain_language
    A flavin enzyme directs tryptophan-derived kynurenine into the hydroxylated branch.
    primary_references
    [hutchinson2017] Structural and mechanistic basis of differentiated inhibitors of the acute pancreatitis target kynurenine-3-monooxygenase. (2017). https://pubmed.ncbi.nlm.nih.gov/28604669/ DOI: 10.1038/ncomms15827
    tissue_or_cell_type
    Sf9 membrane fraction expressing human KMO

    Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1234–1246

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human KMO in Sf9 membrane preparations; mass-spectrometry kinetics; separate P. fluorescens KMO crystallography. · source_derived_draft · unverified_draft

    ### b2-kmo-kynurenine-hydroxylation Human KMO membrane assays measured kynurenine conversion to 3-hydroxykynurenine with NADPH; at 200 micromolar NADPH, kynurenine Km was 2 micromolar. Condition category: normal nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A flavin enzyme directs tryptophan-derived kynurenine into the hydroxylated branch. organism: Homo sapiens tissue_or_cell_type: Sf9 membrane fraction expressing human KMO experimental_model: Human KMO in Sf9 membrane preparations; mass-spectrometry kinetics; separate P. fluorescens KMO crystallography. limitations: Human functional assays and bacterial structures are distinct evidence; this experiment did not test dietary B2 restriction or total NAD synthesis. exposure: Purified-enzyme assay cross_nutrient: B2-FAD and nicotinamide-containing NADPH support a branch upstream of de novo niacin synthesis. evidence_location: Fig 2f and Methods: kinetic assays; interpret species separately [hutchinson2017] Structural and mechanistic basis of differentiated inhibitors of the acute pancreatitis target kynurenine-3-monooxygenase. (2017). https://pubmed.ncbi.nlm.nih.gov/28604669/ DOI: 10.1038/ncomms15827
    Complete structured claim and evidence

  2. Kmo knockout reduced quinolinate to about 3% of wild-type liver content but about 80% of wild-type brain content.

    Mouse kynurenine 3-monooxygenase / Kmo → Quinolinic acid source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    A B2-dependent step feeds the tryptophan-to-niacin pathway with tissue-specific dependence.
    evidence_location
    Results: liver Fig 4 and brain Fig 7; matching abstract conclusion
    experimental_model
    Constitutive Kmo knockout and wild-type mice, approximately two months old; liver and brain metabolite assays.
    exposure
    Constitutive Kmo deletion
    limitations
    Genetic deletion; alternative routes were proposed but not all directly traced.
    nutrient_topic
    Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
    organism
    Mus musculus
    plain_language
    Removing this enzyme affected downstream metabolites differently across tissues.
    primary_references
    [giorgini2013] Targeted deletion of kynurenine 3-monooxygenase in mice: a new tool for studying kynurenine pathway metabolism in periphery and brain. (2013). https://pubmed.ncbi.nlm.nih.gov/24189070/ DOI: 10.1074/jbc.m113.503813
    tissue_or_cell_type
    Liver and brain
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1248–1260

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Constitutive Kmo knockout and wild-type mice, approximately two months old; liver and brain metabolite assays. · source_derived_draft · unverified_draft

    ### b2-kmo-loss-quinolinate-tissue Kmo knockout reduced quinolinate to about 3% of wild-type liver content but about 80% of wild-type brain content. Condition category: machinery_impairment nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing this enzyme affected downstream metabolites differently across tissues. organism: Mus musculus tissue_or_cell_type: Liver and brain experimental_model: Constitutive Kmo knockout and wild-type mice, approximately two months old; liver and brain metabolite assays. limitations: Genetic deletion; alternative routes were proposed but not all directly traced. exposure: Constitutive Kmo deletion cross_nutrient: A B2-dependent step feeds the tryptophan-to-niacin pathway with tissue-specific dependence. evidence_location: Results: liver Fig 4 and brain Fig 7; matching abstract conclusion [giorgini2013] Targeted deletion of kynurenine 3-monooxygenase in mice: a new tool for studying kynurenine pathway metabolism in periphery and brain. (2013). https://pubmed.ncbi.nlm.nih.gov/24189070/ DOI: 10.1074/jbc.m113.503813
    Complete structured claim and evidence

In the sources

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

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