Component

Pyrithiamine

Experimental thiamine antagonist; exposure is distinct from dietary thiamine omission.

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

Where it participates (unsigned role)

  1. Reactive oxygen species assay signals were higher in thalamus and cortex on day 14 of pyrithiamine-assisted deficiency.

    Thiamine (vitamin B1) → Brain reactive oxygen species assay signal source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_location
    Abstract; Methods; Figure 1A
    evidence_span
    significantly elevated in thalamus and cortex on day 14
    experimental_model
    Male Sprague-Dawley rats, eight weeks old; thiamine-deficient chow plus daily pyrithiamine 0.25 mg/kg intraperitoneally; pair-fed thiamine-injected controls; days 13 and 14 brain assays.
    exposure
    Thiamine-deficient chow plus pyrithiamine, day 14 with seizures and absent righting reflex
    limitations
    The assay does not identify one oxidant species or its initiating enzyme; seizures can also influence the endpoint.
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Rattus norvegicus
    plain_language
    Late symptomatic depletion increased a marker of oxidant production in both sampled regions.
    primary_references
    [langlais-1997-brain-oxidants] Increased cerebral free radical production during thiamine deficiency (1997). https://pubmed.ncbi.nlm.nih.gov/9203158/ DOI: 10.1007/BF02674735
    tissue_or_cell_type
    Thalamus and cortex
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1155–1167

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Male Sprague-Dawley rats, eight weeks old; thiamine-deficient chow plus daily pyrithiamine 0.25 mg/kg intraperitoneally; pair-fed thiamine-injected controls; days 13 and 14 brain assays. · source_derived_draft · unverified_draft

    ### thiamine-def-brain-ros-increase Reactive oxygen species assay signals were higher in thalamus and cortex on day 14 of pyrithiamine-assisted deficiency. Condition category: nutrient_deficiency nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Late symptomatic depletion increased a marker of oxidant production in both sampled regions. organism: Rattus norvegicus tissue_or_cell_type: Thalamus and cortex experimental_model: Male Sprague-Dawley rats, eight weeks old; thiamine-deficient chow plus daily pyrithiamine 0.25 mg/kg intraperitoneally; pair-fed thiamine-injected controls; days 13 and 14 brain assays. limitations: The assay does not identify one oxidant species or its initiating enzyme; seizures can also influence the endpoint. evidence_location: Abstract; Methods; Figure 1A evidence_span: significantly elevated in thalamus and cortex on day 14 exposure: Thiamine-deficient chow plus pyrithiamine, day 14 with seizures and absent righting reflex [langlais-1997-brain-oxidants] Increased cerebral free radical production during thiamine deficiency (1997). https://pubmed.ncbi.nlm.nih.gov/9203158/ DOI: 10.1007/BF02674735
    Complete structured claim and evidence

  2. Medium from depleted astrocytes reduced glutamate uptake in naive recipient astrocytes by over 70% after 24 hours.

    Thiamine (vitamin B1) → Astrocyte glutamate uptake source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_location
    Results snippet: Effects of TD conditioned media on glutamate transport; Figure 1A
    evidence_span
    reduced by over 70% after 24 h
    experimental_model
    Newborn-rat astrocytes differentiated with dibutyryl cAMP; thiamine-free DMEM with 5% horse serum plus 10 micromolar pyrithiamine; conditioned-medium transfer and inflammatory-pathway inhibitors.
    exposure
    Thiamine-free medium plus pyrithiamine in cultured newborn-rat astrocytes
    limitations
    Conditioned medium is a mixture; this comparison alone cannot identify a secreted mediator or exclude carried-over medium components.
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Rattus norvegicus
    plain_language
    The culture environment from depleted cells transferred a defect in glutamate removal.
    primary_references
    [jhala-2014-astrocyte-inflammatory-signaling] Thiamine deficiency results in release of soluble factors that disrupt mitochondrial membrane potential and downregulate the glutamate transporter splice-variant GLT-1b in cultured astrocytes. (2014). https://www.sciencedirect.com/science/article/abs/pii/S0006291X14006482 DOI: 10.1016/j.bbrc.2014.04.017
    tissue_or_cell_type
    Cultured astrocytes
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1297–1309

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Newborn-rat astrocytes differentiated with dibutyryl cAMP; thiamine-free DMEM with 5% horse serum plus 10 micromolar pyrithiamine; conditioned-medium transfer and inflammatory-pathway inhibitors. · source_derived_draft · unverified_draft

    ### thiamine-def-conditioned-medium-uptake Medium from depleted astrocytes reduced glutamate uptake in naive recipient astrocytes by over 70% after 24 hours. Condition category: nutrient_deficiency nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The culture environment from depleted cells transferred a defect in glutamate removal. organism: Rattus norvegicus tissue_or_cell_type: Cultured astrocytes experimental_model: Newborn-rat astrocytes differentiated with dibutyryl cAMP; thiamine-free DMEM with 5% horse serum plus 10 micromolar pyrithiamine; conditioned-medium transfer and inflammatory-pathway inhibitors. limitations: Conditioned medium is a mixture; this comparison alone cannot identify a secreted mediator or exclude carried-over medium components. evidence_location: Results snippet: Effects of TD conditioned media on glutamate transport; Figure 1A evidence_span: reduced by over 70% after 24 h exposure: Thiamine-free medium plus pyrithiamine in cultured newborn-rat astrocytes [jhala-2014-astrocyte-inflammatory-signaling] Thiamine deficiency results in release of soluble factors that disrupt mitochondrial membrane potential and downregulate the glutamate transporter splice-variant GLT-1b in cultured astrocytes. (2014). https://www.sciencedirect.com/science/article/abs/pii/S0006291X14006482 DOI: 10.1016/j.bbrc.2014.04.017
    Complete structured claim and evidence

  3. N-acetylcysteine co-treatment prevented the loss of EAAT2 protein in medial thalamus of the depleted rats.

    N-Acetyl-L-cysteine → Rat excitatory amino acid transporter 2 / Slc1a2 source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_location
    Rat Model of TD; Results; Figures 6-7
    evidence_span
    NAC prevented downregulation of the transporter protein
    experimental_model
    Male Sprague-Dawley rats; thiamine-deficient diet plus pyrithiamine 0.5 mg/kg/day, with or without N-acetylcysteine 163 mg/kg/day intraperitoneally; day-14 symptomatic stage; pair-fed controls.
    exposure
    Pyrithiamine-assisted depletion with pharmacological N-acetylcysteine co-treatment
    limitations
    N-acetylcysteine has multiple actions; this does not prove a specific glutathione mechanism or support a human dosing recommendation.
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Rattus norvegicus
    plain_language
    An antioxidant intervention preserved a glutamate transporter in this experimental model.
    primary_references
    [hazell-2010-human-astrocytes] Loss of astrocytic glutamate transporters in Wernicke encephalopathy (2010). https://pmc.ncbi.nlm.nih.gov/articles/PMC3388119/ DOI: 10.1002/glia.20908
    tissue_or_cell_type
    Medial thalamus
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1283–1295

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Male Sprague-Dawley rats; thiamine-deficient diet plus pyrithiamine 0.5 mg/kg/day, with or without N-acetylcysteine 163 mg/kg/day intraperitoneally; day-14 symptomatic stage; pair-fed controls. · source_derived_draft · unverified_draft

    ### thiamine-def-nac-preserves-rat-eaat2 N-acetylcysteine co-treatment prevented the loss of EAAT2 protein in medial thalamus of the depleted rats. Condition category: nutrient_deficiency nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: An antioxidant intervention preserved a glutamate transporter in this experimental model. organism: Rattus norvegicus tissue_or_cell_type: Medial thalamus experimental_model: Male Sprague-Dawley rats; thiamine-deficient diet plus pyrithiamine 0.5 mg/kg/day, with or without N-acetylcysteine 163 mg/kg/day intraperitoneally; day-14 symptomatic stage; pair-fed controls. limitations: N-acetylcysteine has multiple actions; this does not prove a specific glutathione mechanism or support a human dosing recommendation. evidence_location: Rat Model of TD; Results; Figures 6-7 evidence_span: NAC prevented downregulation of the transporter protein exposure: Pyrithiamine-assisted depletion with pharmacological N-acetylcysteine co-treatment [hazell-2010-human-astrocytes] Loss of astrocytic glutamate transporters in Wernicke encephalopathy (2010). https://pmc.ncbi.nlm.nih.gov/articles/PMC3388119/ DOI: 10.1002/glia.20908
    Complete structured claim and evidence

  4. Before neurological signs, total high-energy phosphates were 89% of control in diencephalon and 91% in lower brainstem; after signs, 76% and 79%.

    Thiamine (vitamin B1) → Brain high-energy phosphate content source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_location
    Abstract
    evidence_span
    before the onset of neurological signs
    experimental_model
    Adult male Wistar rats with pyrithiamine-induced acute thiamine-deficient encephalopathy; microwave fixation and regional ATP/phosphocreatine assays before and after neurological signs.
    exposure
    Pyrithiamine-induced severe thiamine deficiency in rats
    limitations
    Combined thiamine withdrawal and pyrithiamine exposure; not an estimate for mild dietary insufficiency or a human blood threshold.
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Rattus norvegicus
    plain_language
    Energy reserves fell early in two vulnerable brain regions.
    primary_references
    [aikawa-1984-brain-energy] Low energy levels in thiamine-deficient encephalopathy. (1984). https://pubmed.ncbi.nlm.nih.gov/6726285/ DOI: 10.1097/00005072-198405000-00006
    tissue_or_cell_type
    Diencephalon and lower brainstem
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1070–1082

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Adult male Wistar rats with pyrithiamine-induced acute thiamine-deficient encephalopathy; microwave fixation and regional ATP/phosphocreatine assays before and after neurological signs. · source_derived_draft · unverified_draft

    ### thiamine-def-regional-energy-loss Before neurological signs, total high-energy phosphates were 89% of control in diencephalon and 91% in lower brainstem; after signs, 76% and 79%. Condition category: nutrient_deficiency nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Energy reserves fell early in two vulnerable brain regions. organism: Rattus norvegicus tissue_or_cell_type: Diencephalon and lower brainstem experimental_model: Adult male Wistar rats with pyrithiamine-induced acute thiamine-deficient encephalopathy; microwave fixation and regional ATP/phosphocreatine assays before and after neurological signs. limitations: Combined thiamine withdrawal and pyrithiamine exposure; not an estimate for mild dietary insufficiency or a human blood threshold. evidence_location: Abstract evidence_span: before the onset of neurological signs exposure: Pyrithiamine-induced severe thiamine deficiency in rats [aikawa-1984-brain-energy] Low energy levels in thiamine-deficient encephalopathy. (1984). https://pubmed.ncbi.nlm.nih.gov/6726285/ DOI: 10.1097/00005072-198405000-00006
    Complete structured claim and evidence

  5. Acute symptomatic rats had thalamic dialysate glutamate of 3.37 versus 0.93 micromolar in controls, with no corresponding cortical increase.

    Thiamine (vitamin B1) → Extracellular brain glutamate concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_location
    Abstract
    evidence_span
    precedes the appearance of histological lesions
    experimental_model
    Awake freely moving rats with pyrithiamine-induced deficiency; microdialysis of ventral posterior medial thalamus and contralateral frontoparietal cortex, compared with pair-fed controls.
    exposure
    Pyrithiamine-induced deficiency within six hours of loss of righting reflexes
    limitations
    Microdialysis alone cannot assign increased release versus impaired uptake or prove NMDA-mediated cell death. Combined thiamine withdrawal and pyrithiamine exposure; not an estimate for mild dietary insufficiency or a human blood threshold.
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Rattus norvegicus
    plain_language
    Glutamate accumulated outside cells in a vulnerable region before visible tissue lesions.
    primary_references
    [hazell-1993-extracellular-glutamate] Cerebral vulnerability is associated with selective increase in extracellular glutamate concentration in experimental thiamine deficiency (1993). https://pubmed.ncbi.nlm.nih.gov/8103080/ DOI: 10.1111/j.1471-4159.1993.tb03635.x
    tissue_or_cell_type
    Ventral posterior medial thalamus versus frontoparietal cortex
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1141–1153

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Awake freely moving rats with pyrithiamine-induced deficiency; microdialysis of ventral posterior medial thalamus and contralateral frontoparietal cortex, compared with pair-fed controls. · source_derived_draft · unverified_draft

    ### thiamine-def-thalamic-extracellular-glutamate Acute symptomatic rats had thalamic dialysate glutamate of 3.37 versus 0.93 micromolar in controls, with no corresponding cortical increase. Condition category: nutrient_deficiency nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Glutamate accumulated outside cells in a vulnerable region before visible tissue lesions. organism: Rattus norvegicus tissue_or_cell_type: Ventral posterior medial thalamus versus frontoparietal cortex experimental_model: Awake freely moving rats with pyrithiamine-induced deficiency; microdialysis of ventral posterior medial thalamus and contralateral frontoparietal cortex, compared with pair-fed controls. limitations: Microdialysis alone cannot assign increased release versus impaired uptake or prove NMDA-mediated cell death. Combined thiamine withdrawal and pyrithiamine exposure; not an estimate for mild dietary insufficiency or a human blood threshold. evidence_location: Abstract evidence_span: precedes the appearance of histological lesions exposure: Pyrithiamine-induced deficiency within six hours of loss of righting reflexes [hazell-1993-extracellular-glutamate] Cerebral vulnerability is associated with selective increase in extracellular glutamate concentration in experimental thiamine deficiency (1993). https://pubmed.ncbi.nlm.nih.gov/8103080/ DOI: 10.1111/j.1471-4159.1993.tb03635.x
    Complete structured claim and evidence

In the sources

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