Component

Secondary vitamin B6 deficiency associated with hyperprolinemia type II

Context-specific entity; species, compartment and exposure are stated on each claim.

1 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 acts on it

  1. The study was prompted by B6 deficiency and seizures in a child with hyperprolinemia type II; the adduct experiments support P5C-mediated cofactor inactivation as a contributing mechanism.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Human index-case context combined with in-vitro chemical mechanism.
    limitations
    Contribution to seizures is an interpretation; the paper does not establish controlled efficacy or a universal treatment dose.
    nutrient_topic
    L-Proline collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Proline
    plain_language
    A breakdown disorder can create a secondary cofactor problem.
    primary_references
    Pyridoxal phosphate de-activation by pyrroline-5-carboxylic acid. Increased risk of vitamin B6 deficiency and seizures in hyperprolinemia type II. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11134058/ · DOI 10.1074/jbc.M010860200
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Proline: synthesis, collagen processing, redox metabolism and cross-nutrient mechanisms (2026-09-19) · lines 126–132

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human index-case context combined with in-vitro chemical mechanism. · source_derived_draft · unverified_draft

    ## l-proline-p5c-clinical-link A breakdown disorder can create a secondary cofactor problem. The study was prompted by B6 deficiency and seizures in a child with hyperprolinemia type II; the adduct experiments support P5C-mediated cofactor inactivation as a contributing mechanism. Model: Human index-case context combined with in-vitro chemical mechanism. Limitations: Contribution to seizures is an interpretation; the paper does not establish controlled efficacy or a universal treatment dose. Evidence access: Primary abstract Pyridoxal phosphate de-activation by pyrroline-5-carboxylic acid. Increased risk of vitamin B6 deficiency and seizures in hyperprolinemia type II. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11134058/ · DOI 10.1074/jbc.M010860200
    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