Component
Transketolase activity
Transketolase activity. Species, exposure and limitations are retained in each linked 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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What acts on it
Thiamine deficiency impairs oxidative metabolic pathways and contributes to ethanol-induced neurotoxicity, with poor nutrition contributing to the alcoholic syndrome.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/alcohol-research/28225048.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "14985f03480c03e14fe75f00e454323cd6f5d414f3775e5ee0d4d4da7825e8c6", "start_char": 0, "end_char": 1824, "text_sha256": "14985f03480c03e14fe75f00e454323cd6f5d414f3775e5ee0d4d4da7825e8c6"}
- experimental_model
- Review of thiamine deficiency and oxidative metabolic pathways in ethanol neurotoxicity
- exposure
- Chronic alcohol use with poor nutrition
- limitations
- A review, labelled as such, linking the coenzyme role to the clinical syndrome. Marchiafava-Bignami disease is rare, so the clinical anchor is narrow.
- nutrient_topic
- Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. · Ethanol
- organism
- Human
- plain_language
- Without the coenzyme the pathways that burn sugar for the brain stall.
- primary_references
- [alcohol-p28225048] Thiamine deficiency, oxidative metabolic pathways and ethanol-induced neurotoxicity: how poor nutrition contributes to the alcoholic syndrome, as Marchiafava-Bignami disease. (2017). https://pubmed.ncbi.nlm.nih.gov/28225048/ DOI: 10.1038/ejcn.2016.267
- tissue_or_cell_type
- Brain
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 748–759
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Review of thiamine deficiency and oxidative metabolic pathways in ethanol neurotoxicity · source_derived_draft · unverified_draft
### alcohol-thiamine-oxidative-pathways Thiamine deficiency impairs oxidative metabolic pathways and contributes to ethanol-induced neurotoxicity, with poor nutrition contributing to the alcoholic syndrome. Condition category: nutrient_deficiency nutrient_topic: Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. plain_language: Without the coenzyme the pathways that burn sugar for the brain stall. organism: Human tissue_or_cell_type: Brain experimental_model: Review of thiamine deficiency and oxidative metabolic pathways in ethanol neurotoxicity limitations: A review, labelled as such, linking the coenzyme role to the clinical syndrome. Marchiafava-Bignami disease is rare, so the clinical anchor is narrow. exposure: Chronic alcohol use with poor nutrition evidence_span: {"source_cache": "artifacts/alcohol-research/28225048.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "14985f03480c03e14fe75f00e454323cd6f5d414f3775e5ee0d4d4da7825e8c6", "start_char": 0, "end_char": 1824, "text_sha256": "14985f03480c03e14fe75f00e454323cd6f5d414f3775e5ee0d4d4da7825e8c6"} [alcohol-p28225048] Thiamine deficiency, oxidative metabolic pathways and ethanol-induced neurotoxicity: how poor nutrition contributes to the alcoholic syndrome, as Marchiafava-Bignami disease. (2017). https://pubmed.ncbi.nlm.nih.gov/28225048/ DOI: 10.1038/ejcn.2016.267
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.