Component

Delta1-piperideine-6-carboxylate

Independent small molecule record; interpretation is limited by each linked claim and its study context.

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

Read recorded mechanisms Open recursive mind map

How nutrients influence it

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

How nutrients reach it in more than one step

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

Tracing routes…

What it does

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

Recorded relationships

What it acts on

  1. P6C reacts with PLP to form a Knoevenagel condensation product that inactivates the cofactor.

    Delta1-piperideine-6-carboxylate → PLP source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    Direct lysine-metabolite to vitamin-B6 antagonism.
    experimental_model
    Affected children, expressed human ALDH7A1 variants and metabolite chemistry
    exposure
    Biochemical P6C-PLP reaction.
    limitations
    Direct chemistry supports sequestration; it does not quantify PLP loss in every neuronal compartment.
    nutrient_topic
    Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
    organism
    Homo sapiens
    plain_language
    The accumulated lysine metabolite chemically traps activated B6.
    primary_references
    [mills-2006-aldh7a1] Mutations in antiquitin in individuals with pyridoxine-dependent seizures (2006). https://doi.org/10.1038/nm1366 DOI: 10.1038/nm1366
    tissue_or_cell_type
    Cell-free chemistry
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1171–1182

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Affected children, expressed human ALDH7A1 variants and metabolite chemistry · source_derived_draft · unverified_draft

    ### b6-neuro-p6c-plp-sequestration P6C reacts with PLP to form a Knoevenagel condensation product that inactivates the cofactor. Condition category: machinery_impairment nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The accumulated lysine metabolite chemically traps activated B6. organism: Homo sapiens tissue_or_cell_type: Cell-free chemistry experimental_model: Affected children, expressed human ALDH7A1 variants and metabolite chemistry limitations: Direct chemistry supports sequestration; it does not quantify PLP loss in every neuronal compartment. exposure: Biochemical P6C-PLP reaction. cross_nutrient: Direct lysine-metabolite to vitamin-B6 antagonism. [mills-2006-aldh7a1] Mutations in antiquitin in individuals with pyridoxine-dependent seizures (2006). https://doi.org/10.1038/nm1366 DOI: 10.1038/nm1366
    Complete structured claim and evidence

  2. P6C and acetoacetate form 2-OPP in chemical incubations including plasma.

    Delta1-piperideine-6-carboxylate → 2S,6S-/2S,6R-6-(2-Oxopropyl)piperidine-2-carboxylate source_derived_draftungraded
    Experimental context and source evidence
    affected_machinery
    ALDH7A1
    availability_state
    machinery_impairment Imported condition classification; unverified.
    deficiency_not_equivalent
    Dietary lysine deficiency
    experimental_model
    Chemical incubations in aqueous solutions and human biological matrices
    limitations
    In-vivo formation is inferred; patient flux was not measured.
    organism
    Homo sapiens
    plain_language
    An accumulated intermediate can react with a ketone body.
    primary_references
    [engelke2021] Untargeted metabolomics and infrared ion spectroscopy identify biomarkers for pyridoxine-dependent epilepsy (2021). https://www.jci.org/articles/view/148272 DOI: 10.1172/JCI148272
    tissue_or_cell_type
    Body-fluid reaction model
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Lysine: mechanism-first literature curation (2026-09-17) · lines 302–312

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Chemical incubations in aqueous solutions and human biological matrices · source_derived_draft · unverified_draft

    ### p6c-acetoacetate-2opp P6C and acetoacetate form 2-OPP in chemical incubations including plasma. Plain language: An accumulated intermediate can react with a ketone body. Condition category: machinery_impairment organism: Homo sapiens tissue_or_cell_type: Body-fluid reaction model experimental_model: Chemical incubations in aqueous solutions and human biological matrices limitations: In-vivo formation is inferred; patient flux was not measured. affected_machinery: ALDH7A1 deficiency_not_equivalent: Dietary lysine deficiency [engelke2021] Untargeted metabolomics and infrared ion spectroscopy identify biomarkers for pyridoxine-dependent epilepsy (2021). https://www.jci.org/articles/view/148272 DOI: 10.1172/JCI148272
    Complete structured claim and evidence

  3. Accumulated P6C reacts with PLP through Knoevenagel condensation, reducing cofactor availability.

    Delta1-piperideine-6-carboxylate → PLP source_derived_draftungraded
    Experimental context and source evidence
    affected_machinery
    ALDH7A1 upstream clearance
    availability_state
    machinery_impairment Imported condition classification; unverified.
    deficiency_not_equivalent
    Dietary lysine or vitamin B6 deficiency
    experimental_model
    Chemical mechanism associated with human ALDH7A1 disease
    limitations
    Secondary cofactor loss does not demonstrate primary dietary vitamin B6 or lysine deficiency.
    organism
    Homo sapiens
    plain_language
    A lysine metabolite can trap active vitamin B6.
    primary_references
    [mills2006] Mutations in antiquitin in individuals with pyridoxine-dependent seizures. (2006). https://pubmed.ncbi.nlm.nih.gov/16491085/ DOI: 10.1038/nm1366
    tissue_or_cell_type
    PDE-ALDH7A1 biochemical context
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Lysine: mechanism-first literature curation (2026-09-17) · lines 266–276

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Chemical mechanism associated with human ALDH7A1 disease · source_derived_draft · unverified_draft

    ### p6c-plp-trapping Accumulated P6C reacts with PLP through Knoevenagel condensation, reducing cofactor availability. Plain language: A lysine metabolite can trap active vitamin B6. Condition category: machinery_impairment organism: Homo sapiens tissue_or_cell_type: PDE-ALDH7A1 biochemical context experimental_model: Chemical mechanism associated with human ALDH7A1 disease limitations: Secondary cofactor loss does not demonstrate primary dietary vitamin B6 or lysine deficiency. affected_machinery: ALDH7A1 upstream clearance deficiency_not_equivalent: Dietary lysine or vitamin B6 deficiency [mills2006] Mutations in antiquitin in individuals with pyridoxine-dependent seizures. (2006). https://pubmed.ncbi.nlm.nih.gov/16491085/ DOI: 10.1038/nm1366
    Complete structured claim and evidence

What acts on it

  1. The antiquitin defect was linked to accumulation of alpha-AASA/P6C in the lysine degradation pathway.

    Biallelic ALDH7A1 disease genotypes studied by Mills 2006 → Delta1-piperideine-6-carboxylate source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    Lysine catabolism generates the metabolite that can sequester PLP.
    experimental_model
    Affected children, expressed human ALDH7A1 variants and metabolite chemistry
    exposure
    ALDH7A1-associated disease and metabolite analysis.
    limitations
    This is inherited pathway failure, not lysine toxicity in healthy people.
    nutrient_topic
    Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
    organism
    Homo sapiens
    plain_language
    A blocked lysine pathway builds up B6-reactive metabolites.
    primary_references
    [mills-2006-aldh7a1] Mutations in antiquitin in individuals with pyridoxine-dependent seizures (2006). https://doi.org/10.1038/nm1366 DOI: 10.1038/nm1366
    tissue_or_cell_type
    Patient biological samples and biochemical pathway analysis
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1158–1169

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Affected children, expressed human ALDH7A1 variants and metabolite chemistry · source_derived_draft · unverified_draft

    ### b6-neuro-aldh7a1-metabolite-accumulation The antiquitin defect was linked to accumulation of alpha-AASA/P6C in the lysine degradation pathway. Condition category: machinery_impairment nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A blocked lysine pathway builds up B6-reactive metabolites. organism: Homo sapiens tissue_or_cell_type: Patient biological samples and biochemical pathway analysis experimental_model: Affected children, expressed human ALDH7A1 variants and metabolite chemistry limitations: This is inherited pathway failure, not lysine toxicity in healthy people. exposure: ALDH7A1-associated disease and metabolite analysis. cross_nutrient: Lysine catabolism generates the metabolite that can sequester PLP. [mills-2006-aldh7a1] Mutations in antiquitin in individuals with pyridoxine-dependent seizures (2006). https://doi.org/10.1038/nm1366 DOI: 10.1038/nm1366
    Complete structured claim and evidence

  2. Alpha-aminoadipate semialdehyde interconverts with its cyclic Schiff base P6C.

    alpha-Aminoadipate semialdehyde → Delta1-piperideine-6-carboxylate source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Biochemical characterization
    limitations
    The two chemical species are separate entities connected by equilibrium.
    organism
    Homo sapiens
    plain_language
    One intermediate exists in open-chain and ring forms.
    primary_references
    [mills2006] Mutations in antiquitin in individuals with pyridoxine-dependent seizures. (2006). https://pubmed.ncbi.nlm.nih.gov/16491085/ DOI: 10.1038/nm1366
    tissue_or_cell_type
    Lysine-catabolizing compartments and body fluids

    L-Lysine: mechanism-first literature curation (2026-09-17) · lines 94–102

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

    ### aasa-p6c-equilibrium Alpha-aminoadipate semialdehyde interconverts with its cyclic Schiff base P6C. Plain language: One intermediate exists in open-chain and ring forms. Condition category: normal organism: Homo sapiens tissue_or_cell_type: Lysine-catabolizing compartments and body fluids experimental_model: Biochemical characterization limitations: The two chemical species are separate entities connected by equilibrium. [mills2006] Mutations in antiquitin in individuals with pyridoxine-dependent seizures. (2006). https://pubmed.ncbi.nlm.nih.gov/16491085/ DOI: 10.1038/nm1366
    Complete structured claim and evidence

  3. Human peroxisomal PIPOX oxidizes L-pipecolate to P6C.

    L-Pipecolate → Delta1-piperideine-6-carboxylate source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Human cDNA cloning and expressed enzyme
    limitations
    Enzyme capability does not establish that this route predominates in human brain; see conflict.
    organism
    Homo sapiens
    plain_language
    Pipecolate can join the common lysine breakdown route.
    primary_references
    [ijlst2000] Molecular cloning and expression of human L-pipecolate oxidase (2000). https://pubmed.ncbi.nlm.nih.gov/10772957/ DOI: 10.1006/bbrc.2000.2575
    tissue_or_cell_type
    Peroxisomes

    L-Lysine: mechanism-first literature curation (2026-09-17) · lines 146–154

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human cDNA cloning and expressed enzyme · source_derived_draft · unverified_draft

    ### pipox-pipecolate-oxidation Human peroxisomal PIPOX oxidizes L-pipecolate to P6C. Plain language: Pipecolate can join the common lysine breakdown route. Condition category: normal organism: Homo sapiens tissue_or_cell_type: Peroxisomes experimental_model: Human cDNA cloning and expressed enzyme limitations: Enzyme capability does not establish that this route predominates in human brain; see conflict. [ijlst2000] Molecular cloning and expression of human L-pipecolate oxidase (2000). https://pubmed.ncbi.nlm.nih.gov/10772957/ DOI: 10.1006/bbrc.2000.2575
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. ALDH7A1 deficiency reduces aldehyde clearance, increasing AASA and its equilibrium partner P6C.

    Antiquitin / ALDH7A1 → alpha-Aminoadipate semialdehyde source_derived_draftungraded
    Experimental context and source evidence
    affected_machinery
    ALDH7A1
    availability_state
    machinery_impairment Imported condition classification; unverified.
    deficiency_not_equivalent
    Dietary lysine deficiency
    experimental_model
    Human patient biochemical and genetic evidence
    limitations
    Inherited enzyme failure is distinct from inadequate lysine intake.
    organism
    Homo sapiens
    plain_language
    An enzyme block allows reactive lysine metabolites to accumulate.
    primary_references
    [mills2006] Mutations in antiquitin in individuals with pyridoxine-dependent seizures. (2006). https://pubmed.ncbi.nlm.nih.gov/16491085/ DOI: 10.1038/nm1366
    tissue_or_cell_type
    Affected tissues and body fluids
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Lysine: mechanism-first literature curation (2026-09-17) · lines 254–264

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human patient biochemical and genetic evidence · source_derived_draft · unverified_draft

    ### aldh7a1-metabolite-accumulation ALDH7A1 deficiency reduces aldehyde clearance, increasing AASA and its equilibrium partner P6C. Plain language: An enzyme block allows reactive lysine metabolites to accumulate. Condition category: machinery_impairment organism: Homo sapiens tissue_or_cell_type: Affected tissues and body fluids experimental_model: Human patient biochemical and genetic evidence limitations: Inherited enzyme failure is distinct from inadequate lysine intake. affected_machinery: ALDH7A1 deficiency_not_equivalent: Dietary lysine deficiency [mills2006] Mutations in antiquitin in individuals with pyridoxine-dependent seizures. (2006). https://pubmed.ncbi.nlm.nih.gov/16491085/ DOI: 10.1038/nm1366
    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.

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