Component

Vigabatrin

Vigabatrin

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

What it acts on

  1. Vigabatrin formed a covalent adduct involving pig GABA-AT Lys329 and its PLP cofactor.

    Vigabatrin → Pig GABA aminotransferase / ABAT source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    experimental_model
    Pig liver GABA aminotransferase; inhibitor complexes and spectroscopy
    exposure
    Inhibitor-treated purified enzyme.
    limitations
    Does not establish systemic B6 depletion.
    nutrient_topic
    Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
    organism
    Sus scrofa
    plain_language
    The drug traps the enzyme together with its B6 cofactor.
    primary_references
    [storici-2004-gaba-at] Structures of gamma-aminobutyric acid (GABA) aminotransferase, a pyridoxal 5'-phosphate, and [2Fe-2S] cluster-containing enzyme, complexed with gamma-ethynyl-GABA and with the antiepilepsy drug vigabatrin (2004). https://doi.org/10.1074/jbc.M305884200 DOI: 10.1074/jbc.M305884200
    tissue_or_cell_type
    Pig liver enzyme
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1096–1106

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Pig liver GABA aminotransferase; inhibitor complexes and spectroscopy · source_derived_draft · unverified_draft

    ### b6-neuro-vigabatrin-plp-adduct Vigabatrin formed a covalent adduct involving pig GABA-AT Lys329 and its PLP cofactor. Condition category: machinery_impairment nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The drug traps the enzyme together with its B6 cofactor. organism: Sus scrofa tissue_or_cell_type: Pig liver enzyme experimental_model: Pig liver GABA aminotransferase; inhibitor complexes and spectroscopy limitations: Does not establish systemic B6 depletion. exposure: Inhibitor-treated purified enzyme. [storici-2004-gaba-at] Structures of gamma-aminobutyric acid (GABA) aminotransferase, a pyridoxal 5'-phosphate, and [2Fe-2S] cluster-containing enzyme, complexed with gamma-ethynyl-GABA and with the antiepilepsy drug vigabatrin (2004). https://doi.org/10.1074/jbc.M305884200 DOI: 10.1074/jbc.M305884200
    Complete structured claim and evidence

  2. Out of 88 patients exposed to vigabatrin in infancy, 28 were able to perform formal visual field testing, mild vigabatrin-attributed visual field defect was found in four patients and severe defect in one, median vigabatrin treatment duration for those with normal visual field was 11 months compared to 19 months for those with the defect, optical coherence tomography showed concomitant attenuated retinal nerve fiber layer in three children, and the overall prevalence after exposure in infancy is lower than the 52% which has been reported after exposure in adulthood while the risk increases with longer treatment duration.

    Vigabatrin → Vigabatrin-attributed visual field defect source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/gaba-research/34716587.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "30459a805ac23ba0a6f0cb4c9484da96a968609466a4bb1fc7c41636542ba887", "start_char": 0, "end_char": 1403, "text_sha256": "30459a805ac23ba0a6f0cb4c9484da96a968609466a4bb1fc7c41636542ba887"}
    experimental_model
    Retrospective population-based perimetry and optical coherence tomography at school age in children exposed in infancy
    exposure
    Vigabatrin given for infantile spasms, with visual fields and retinal nerve fibre layer measured years later
    limitations
    Only 28 of 88 exposed patients could perform formal visual field testing, which limits the prevalence estimate in both directions.
    nutrient_topic
    GABA research collection; topical membership is not evidence of a direct clinical effect, and the sign of a GABA response depends on the chloride gradient of the cell it was measured in. · Gamma-aminobutyric acid
    organism
    Human
    plain_language
    The drug that raises brain GABA costs some patients their peripheral vision, and the longer they take it the likelier that is.
    primary_references
    [gb-p34716587] Visual field defects after vigabatrin treatment during infancy: retrospective population-based study. (2022). https://pubmed.ncbi.nlm.nih.gov/34716587/ DOI: 10.1111/dmcn.15099
    tissue_or_cell_type
    Retina

    GABA: a ligand with no sign of its own, the cofactor that limits its synthesis, the barrier that keeps it out of the brain, and the immune settings where the same molecule protects and harms (2026-09-22) · lines 170–181

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Retrospective population-based perimetry and optical coherence tomography at school age in children exposed in infancy · source_derived_draft · unverified_draft

    ### gb-duration-drives-the-field-loss Out of 88 patients exposed to vigabatrin in infancy, 28 were able to perform formal visual field testing, mild vigabatrin-attributed visual field defect was found in four patients and severe defect in one, median vigabatrin treatment duration for those with normal visual field was 11 months compared to 19 months for those with the defect, optical coherence tomography showed concomitant attenuated retinal nerve fiber layer in three children, and the overall prevalence after exposure in infancy is lower than the 52% which has been reported after exposure in adulthood while the risk increases with longer treatment duration. Condition category: normal nutrient_topic: GABA research collection; topical membership is not evidence of a direct clinical effect, and the sign of a GABA response depends on the chloride gradient of the cell it was measured in. plain_language: The drug that raises brain GABA costs some patients their peripheral vision, and the longer they take it the likelier that is. organism: Human tissue_or_cell_type: Retina experimental_model: Retrospective population-based perimetry and optical coherence tomography at school age in children exposed in infancy limitations: Only 28 of 88 exposed patients could perform formal visual field testing, which limits the prevalence estimate in both directions. exposure: Vigabatrin given for infantile spasms, with visual fields and retinal nerve fibre layer measured years later evidence_span: {"source_cache": "artifacts/gaba-research/34716587.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "30459a805ac23ba0a6f0cb4c9484da96a968609466a4bb1fc7c41636542ba887", "start_char": 0, "end_char": 1403, "text_sha256": "30459a805ac23ba0a6f0cb4c9484da96a968609466a4bb1fc7c41636542ba887"} [gb-p34716587] Visual field defects after vigabatrin treatment during infancy: retrospective population-based study. (2022). https://pubmed.ncbi.nlm.nih.gov/34716587/ DOI: 10.1111/dmcn.15099
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. A close relationship between vigabatrin-induced retinal toxicity and light exposure was observed, vigabatrin-treated mice reared in darkness preserved better visual function and retinal architectures as verified by optokinetic tests, optical coherence tomography and electroretinography, the retinal taurine level of vigabatrin-treated mice exposed to light was significantly lower than that of vigabatrin mice reared in darkness, and the vigabatrin-induced morphological and functional impairments could be partially alleviated by taurine treatment.

    Retinal taurine concentration → Retinal function measured by electroretinography and optokinetic testing source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/gaba-research/27941319.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "92835398ef34fe87d3c084d1933722427a474b40c88c30ada21a6ede8f4d875a", "start_char": 0, "end_char": 1596, "text_sha256": "92835398ef34fe87d3c084d1933722427a474b40c88c30ada21a6ede8f4d875a"}
    experimental_model
    Electroretinography, optical coherence tomography and optokinetic testing in mice reared in light or darkness
    exposure
    Vigabatrin with and without light exposure, and with taurine supplementation
    limitations
    A mouse study. It identifies two contributing factors and shows partial rescue, not that taurine prevents the human visual field defect.
    nutrient_topic
    GABA research collection; topical membership is not evidence of a direct clinical effect, and the sign of a GABA response depends on the chloride gradient of the cell it was measured in. · Gamma-aminobutyric acid
    organism
    Mouse
    plain_language
    The retinal damage needed light to happen, went with a fall in retinal taurine, and was partly undone by giving taurine back.
    primary_references
    [gb-p27941319] The Vigabatrin Induced Retinal Toxicity is Associated with Photopic Exposure and Taurine Deficiency: An In Vivo Study. (2016). https://pubmed.ncbi.nlm.nih.gov/27941319/ DOI: 10.1159/000453143
    tissue_or_cell_type
    Retina

    GABA: a ligand with no sign of its own, the cofactor that limits its synthesis, the barrier that keeps it out of the brain, and the immune settings where the same molecule protects and harms (2026-09-22) · lines 183–194

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Electroretinography, optical coherence tomography and optokinetic testing in mice reared in light or darkness · source_derived_draft · unverified_draft

    ### gb-light-and-taurine-both-matter A close relationship between vigabatrin-induced retinal toxicity and light exposure was observed, vigabatrin-treated mice reared in darkness preserved better visual function and retinal architectures as verified by optokinetic tests, optical coherence tomography and electroretinography, the retinal taurine level of vigabatrin-treated mice exposed to light was significantly lower than that of vigabatrin mice reared in darkness, and the vigabatrin-induced morphological and functional impairments could be partially alleviated by taurine treatment. Condition category: normal nutrient_topic: GABA research collection; topical membership is not evidence of a direct clinical effect, and the sign of a GABA response depends on the chloride gradient of the cell it was measured in. plain_language: The retinal damage needed light to happen, went with a fall in retinal taurine, and was partly undone by giving taurine back. organism: Mouse tissue_or_cell_type: Retina experimental_model: Electroretinography, optical coherence tomography and optokinetic testing in mice reared in light or darkness limitations: A mouse study. It identifies two contributing factors and shows partial rescue, not that taurine prevents the human visual field defect. exposure: Vigabatrin with and without light exposure, and with taurine supplementation evidence_span: {"source_cache": "artifacts/gaba-research/27941319.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "92835398ef34fe87d3c084d1933722427a474b40c88c30ada21a6ede8f4d875a", "start_char": 0, "end_char": 1596, "text_sha256": "92835398ef34fe87d3c084d1933722427a474b40c88c30ada21a6ede8f4d875a"} [gb-p27941319] The Vigabatrin Induced Retinal Toxicity is Associated with Photopic Exposure and Taurine Deficiency: An In Vivo Study. (2016). https://pubmed.ncbi.nlm.nih.gov/27941319/ DOI: 10.1159/000453143
    Complete structured claim and evidence

  2. AOA treatment during beta-alanine feeding raised circulating beta-alanine and muscle/heart carnosine and anserine; selective GABA-T inhibition with vigabatrin did not.

    Aminooxyacetic acid / AOA → Mouse skeletal-muscle histidine dipeptide content source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Mice; beta-alanine 0.1% in drinking water for two weeks.
    limitations
    Broad inhibitor experiment; not an intervention recommendation.
    nutrient_topic
    Carnosine collection; isomer, preparation, species, exposure and manipulation remain explicit. · L-Carnosine / beta-alanyl-L-histidine
    plain_language
    Blocking multiple precursor-disposal routes changed tissue peptide stores.
    primary_references
    Carnosine and anserine homeostasis in skeletal muscle and heart is controlled by β-alanine transamination. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27062388/ · DOI 10.1113/JP272050

    Carnosine: synthesis, transport, carbonyl chemistry and nutrient interactions (2026-09-19) · lines 140–146

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mice; beta-alanine 0.1% in drinking water for two weeks. · source_derived_draft · unverified_draft

    ## carnosine-transamination-block Blocking multiple precursor-disposal routes changed tissue peptide stores. AOA treatment during beta-alanine feeding raised circulating beta-alanine and muscle/heart carnosine and anserine; selective GABA-T inhibition with vigabatrin did not. Model: Mice; beta-alanine 0.1% in drinking water for two weeks. Limitations: Broad inhibitor experiment; not an intervention recommendation. Evidence access: Primary abstract Carnosine and anserine homeostasis in skeletal muscle and heart is controlled by β-alanine transamination. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27062388/ · DOI 10.1113/JP272050
    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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