Component
Erythrocyte pyridoxal 5′-phosphate synthesis
Erythrocyte pyridoxal 5′-phosphate synthesis. 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
Acetaldehyde, but not ethanol, impaired net formation of PLP from pyridoxal, pyridoxine and pyridoxine phosphate by erythrocytes, and the effect was abolished when the B6-phosphate phosphatase was inhibited by 80 mM phosphate, while pyridoxal kinase and pyridoxine phosphate oxidase activities were not decreased.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/alcohol-research/4359937.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1df4485150b1be55f3e5214c424f960ff627cfc317e643c86a0f6747efed8b08", "start_char": 0, "end_char": 1650, "text_sha256": "1df4485150b1be55f3e5214c424f960ff627cfc317e643c86a0f6747efed8b08"}
- experimental_model
- Plasma PLP in 66 alcoholic subjects without liver abnormality, plus erythrocyte enzyme assays
- exposure
- Chronic alcohol abuse; acetaldehyde and ethanol applied to erythrocytes
- limitations
- Selecting subjects without abnormal liver function isolates the vitamin effect from liver disease. The phosphatase mechanism is shown in erythrocytes, not liver.
- 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
- It is the breakdown product that destroys the vitamin, and it works by exposing it to a phosphatase rather than by blocking its synthesis.
- primary_references
- [alcohol-p4359937] Vitamin B6 metabolism in chronic alcohol abuse. Pyridoxal phosphate levels in plasma and the effects of acetaldehyde on pyridoxal phosphate synthesis and degradation in human erythrocytes. (1974). https://pubmed.ncbi.nlm.nih.gov/4359937/ DOI: 10.1172/jci107607
- tissue_or_cell_type
- Plasma and erythrocytes
- 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 644–655
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Plasma PLP in 66 alcoholic subjects without liver abnormality, plus erythrocyte enzyme assays · source_derived_draft · unverified_draft
### alcohol-acetaldehyde-not-ethanol Acetaldehyde, but not ethanol, impaired net formation of PLP from pyridoxal, pyridoxine and pyridoxine phosphate by erythrocytes, and the effect was abolished when the B6-phosphate phosphatase was inhibited by 80 mM phosphate, while pyridoxal kinase and pyridoxine phosphate oxidase activities were not decreased. 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: It is the breakdown product that destroys the vitamin, and it works by exposing it to a phosphatase rather than by blocking its synthesis. organism: Human tissue_or_cell_type: Plasma and erythrocytes experimental_model: Plasma PLP in 66 alcoholic subjects without liver abnormality, plus erythrocyte enzyme assays limitations: Selecting subjects without abnormal liver function isolates the vitamin effect from liver disease. The phosphatase mechanism is shown in erythrocytes, not liver. exposure: Chronic alcohol abuse; acetaldehyde and ethanol applied to erythrocytes evidence_span: {"source_cache": "artifacts/alcohol-research/4359937.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1df4485150b1be55f3e5214c424f960ff627cfc317e643c86a0f6747efed8b08", "start_char": 0, "end_char": 1650, "text_sha256": "1df4485150b1be55f3e5214c424f960ff627cfc317e643c86a0f6747efed8b08"} [alcohol-p4359937] Vitamin B6 metabolism in chronic alcohol abuse. Pyridoxal phosphate levels in plasma and the effects of acetaldehyde on pyridoxal phosphate synthesis and degradation in human erythrocytes. (1974). https://pubmed.ncbi.nlm.nih.gov/4359937/ DOI: 10.1172/jci107607
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.