Component

Cysteamine

Cysteamine. Experimental scope belongs to the associated record.

4 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

Where it participates (unsigned role)

  1. RNA-mediated reduction of endogenous human ADO in HepG2/C3A cells decreased hypotaurine production from cysteamine.

    Human 2-aminoethanethiol dioxygenase / ADO → Hypotaurine source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human liver-derived cultured cells.
    limitations
    Cysteamine can arise through CoA breakdown; this experiment does not show that B5 supplementation raises taurine.
    nutrient_topic
    Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
    plain_language
    Human-cell gene silencing supports the cysteamine pathway.
    primary_references
    Discovery and characterization of a second mammalian thiol dioxygenase, cysteamine dioxygenase. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17581819/ · DOI 10.1074/jbc.M703089200

    Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 65–71

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human liver-derived cultured cells. · source_derived_draft · unverified_draft

    ## taurine-ado-human-knockdown Human-cell gene silencing supports the cysteamine pathway. RNA-mediated reduction of endogenous human ADO in HepG2/C3A cells decreased hypotaurine production from cysteamine. Model: Human liver-derived cultured cells. Limitations: Cysteamine can arise through CoA breakdown; this experiment does not show that B5 supplementation raises taurine. Evidence access: Primary abstract Discovery and characterization of a second mammalian thiol dioxygenase, cysteamine dioxygenase. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17581819/ · DOI 10.1074/jbc.M703089200
    Complete structured claim and evidence

  2. Recombinant mouse Ado oxidized cysteamine to hypotaurine but did not oxidize cysteine in the tested assay.

    Mouse cysteamine dioxygenase / Ado → Hypotaurine source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Purified recombinant murine protein.
    limitations
    Do not assign the mouse enzyme kinetics directly to human ADO.
    nutrient_topic
    Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
    plain_language
    A separate enzyme provides a route from cysteamine.
    primary_references
    Discovery and characterization of a second mammalian thiol dioxygenase, cysteamine dioxygenase. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17581819/ · DOI 10.1074/jbc.M703089200

    Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 57–63

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Purified recombinant murine protein. · source_derived_draft · unverified_draft

    ## taurine-ado-mouse-enzyme A separate enzyme provides a route from cysteamine. Recombinant mouse Ado oxidized cysteamine to hypotaurine but did not oxidize cysteine in the tested assay. Model: Purified recombinant murine protein. Limitations: Do not assign the mouse enzyme kinetics directly to human ADO. Evidence access: Primary abstract Discovery and characterization of a second mammalian thiol dioxygenase, cysteamine dioxygenase. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17581819/ · DOI 10.1074/jbc.M703089200
    Complete structured claim and evidence

  3. After oral D-pantethine in the four cystinotic children, pantothenic acid and cysteamine appeared as products, while intact pantethine was not detected in plasma.

    Pantethine → Pantothenate (vitamin B5) source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    evidence_location
    Primary indexed abstract.
    experimental_model
    Pharmacokinetic/metabolic study in four children with nephropathic cystinosis
    exposure
    Historical oral D-pantethine exposures 70–1000 mg/kg/day.
    limitations
    Very high drug-like exposures in a rare disease; not nutritional dosing, ordinary healthy-person pharmacokinetics or proof of the mechanism behind lipid-trial effects. Rat intestinal-enzyme kinetic data in the same paper are not assigned to humans. The primary authors described rapid hydrolysis. This human observation does not by itself specify the reductive/disulfide steps or a human vanin isoform.
    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 administered derivative was rapidly converted; the blood exposure was not simply unchanged pantethine.
    primary_references
    [b5-clin-wittwer1985] Metabolism of pantethine in cystinosis. (1985). https://pubmed.ncbi.nlm.nih.gov/4056044/ DOI: 10.1172/jci112152
    tissue_or_cell_type
    Plasma after oral D-pantethine

    Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1467–1479

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Pharmacokinetic/metabolic study in four children with nephropathic cystinosis · source_derived_draft · unverified_draft

    ### b5-clin-pantethine-human-products After oral D-pantethine in the four cystinotic children, pantothenic acid and cysteamine appeared as products, while intact pantethine was not detected in plasma. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The administered derivative was rapidly converted; the blood exposure was not simply unchanged pantethine. organism: Homo sapiens tissue_or_cell_type: Plasma after oral D-pantethine experimental_model: Pharmacokinetic/metabolic study in four children with nephropathic cystinosis limitations: Very high drug-like exposures in a rare disease; not nutritional dosing, ordinary healthy-person pharmacokinetics or proof of the mechanism behind lipid-trial effects. Rat intestinal-enzyme kinetic data in the same paper are not assigned to humans. The primary authors described rapid hydrolysis. This human observation does not by itself specify the reductive/disulfide steps or a human vanin isoform. exposure: Historical oral D-pantethine exposures 70–1000 mg/kg/day. cross_nutrient: false evidence_location: Primary indexed abstract. [b5-clin-wittwer1985] Metabolism of pantethine in cystinosis. (1985). https://pubmed.ncbi.nlm.nih.gov/4056044/ DOI: 10.1172/jci112152
    Complete structured claim and evidence

  4. Radiolabeled cystine tracing in cystinotic fibroblasts supported formation of cysteamine-cysteine mixed disulfide during pantethine treatment.

    Pantethine → Cysteamine-cysteine mixed disulfide source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    evidence_location
    Primary indexed abstract, including metabolite-tracing conclusion.
    experimental_model
    Radiolabeled cystine metabolite-tracing experiment in cultured patient fibroblasts
    exposure
    Pantethine or cystamine treatment; specific concentration not retrieved from the primary abstract.
    limitations
    Disease-derived cultured cells; no molecular exporter is assigned without evidence. Formation and efflux of a mixed disulfide do not prove that pantothenate alone treats cystinosis.
    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 derivative changed accumulated cystine into a different disulfide product in these patient cells.
    primary_references
    [b5-clin-butler1984] Pantethine and cystamine deplete cystine from cystinotic fibroblasts via efflux of cysteamine-cysteine mixed disulfide. (1984). https://pubmed.ncbi.nlm.nih.gov/6746900/ DOI: 10.1172/jci111436
    tissue_or_cell_type
    Cystinotic fibroblast lysosomes and extracellular medium

    Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1495–1507

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Radiolabeled cystine metabolite-tracing experiment in cultured patient fibroblasts · source_derived_draft · unverified_draft

    ### b5-clin-pantethine-mixed-disulfide Radiolabeled cystine tracing in cystinotic fibroblasts supported formation of cysteamine-cysteine mixed disulfide during pantethine treatment. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The derivative changed accumulated cystine into a different disulfide product in these patient cells. organism: Homo sapiens tissue_or_cell_type: Cystinotic fibroblast lysosomes and extracellular medium experimental_model: Radiolabeled cystine metabolite-tracing experiment in cultured patient fibroblasts limitations: Disease-derived cultured cells; no molecular exporter is assigned without evidence. Formation and efflux of a mixed disulfide do not prove that pantothenate alone treats cystinosis. exposure: Pantethine or cystamine treatment; specific concentration not retrieved from the primary abstract. cross_nutrient: false evidence_location: Primary indexed abstract, including metabolite-tracing conclusion. [b5-clin-butler1984] Pantethine and cystamine deplete cystine from cystinotic fibroblasts via efflux of cysteamine-cysteine mixed disulfide. (1984). https://pubmed.ncbi.nlm.nih.gov/6746900/ DOI: 10.1172/jci111436
    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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