Component
Experimental Adh4-null mouse genotype
Experimental Adh4-null mouse genotype. Species, exposure and limitations are retained in each linked claim.
2 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 it acts on
Retinoic acid production following retinol administration was reduced 8.5-fold in Adh4-null mice and 4.8-fold in Adh1-null mice, showing overlapping roles for Adh1 and Adh4 in both ethanol and retinol metabolism.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/alcohol-research/10358022.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c1e4e6f0703d814d36609e71a38be53f7c36bebcfdcd3a60c52ea49625369305", "start_char": 0, "end_char": 1272, "text_sha256": "c1e4e6f0703d814d36609e71a38be53f7c36bebcfdcd3a60c52ea49625369305"}
- experimental_model
- Adh1, Adh3 and Adh4 null mutant mice with ethanol, formaldehyde and retinol challenges
- exposure
- Intoxicating ethanol dose, formaldehyde LD50, and retinol administration
- limitations
- A clean three-gene dissection showing which enzyme does which job. It is a mouse gene family that does not map one-to-one onto the human one.
- 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
- Mouse
- plain_language
- The same enzymes that clear alcohol also turn vitamin A into its signalling form.
- primary_references
- [alcohol-p10358022] Metabolic deficiencies in alcohol dehydrogenase Adh1, Adh3, and Adh4 null mutant mice. Overlapping roles of Adh1 and Adh4 in ethanol clearance and metabolism of retinol to retinoic acid. (1999). https://pubmed.ncbi.nlm.nih.gov/10358022/ DOI: 10.1074/jbc.274.24.16796
- tissue_or_cell_type
- Liver and embryo
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 241–252
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Adh1, Adh3 and Adh4 null mutant mice with ethanol, formaldehyde and retinol challenges · source_derived_draft · unverified_draft
### alcohol-adh-retinoic-acid Retinoic acid production following retinol administration was reduced 8.5-fold in Adh4-null mice and 4.8-fold in Adh1-null mice, showing overlapping roles for Adh1 and Adh4 in both ethanol and retinol metabolism. Condition category: machinery_impairment 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: The same enzymes that clear alcohol also turn vitamin A into its signalling form. organism: Mouse tissue_or_cell_type: Liver and embryo experimental_model: Adh1, Adh3 and Adh4 null mutant mice with ethanol, formaldehyde and retinol challenges limitations: A clean three-gene dissection showing which enzyme does which job. It is a mouse gene family that does not map one-to-one onto the human one. exposure: Intoxicating ethanol dose, formaldehyde LD50, and retinol administration evidence_span: {"source_cache": "artifacts/alcohol-research/10358022.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c1e4e6f0703d814d36609e71a38be53f7c36bebcfdcd3a60c52ea49625369305", "start_char": 0, "end_char": 1272, "text_sha256": "c1e4e6f0703d814d36609e71a38be53f7c36bebcfdcd3a60c52ea49625369305"} [alcohol-p10358022] Metabolic deficiencies in alcohol dehydrogenase Adh1, Adh3, and Adh4 null mutant mice. Overlapping roles of Adh1 and Adh4 in ethanol clearance and metabolism of retinol to retinoic acid. (1999). https://pubmed.ncbi.nlm.nih.gov/10358022/ DOI: 10.1074/jbc.274.24.16796
Complete structured claim and evidence
Where it participates (unsigned role)
Following an intoxicating dose of ethanol, Adh1-null mice and to a lesser extent Adh4-null mice, but not Adh3-null mice, showed significant reductions in blood ethanol clearance, and ethanol-induced sleep was significantly longer only in Adh1-null mice.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/alcohol-research/10358022.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c1e4e6f0703d814d36609e71a38be53f7c36bebcfdcd3a60c52ea49625369305", "start_char": 0, "end_char": 1272, "text_sha256": "c1e4e6f0703d814d36609e71a38be53f7c36bebcfdcd3a60c52ea49625369305"}
- experimental_model
- Adh1, Adh3 and Adh4 null mutant mice with ethanol, formaldehyde and retinol challenges
- exposure
- Intoxicating ethanol dose, formaldehyde LD50, and retinol administration
- limitations
- A clean three-gene dissection showing which enzyme does which job. It is a mouse gene family that does not map one-to-one onto the human one.
- 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
- Mouse
- plain_language
- Remove the main enzyme and the animal stays drunk longer.
- primary_references
- [alcohol-p10358022] Metabolic deficiencies in alcohol dehydrogenase Adh1, Adh3, and Adh4 null mutant mice. Overlapping roles of Adh1 and Adh4 in ethanol clearance and metabolism of retinol to retinoic acid. (1999). https://pubmed.ncbi.nlm.nih.gov/10358022/ DOI: 10.1074/jbc.274.24.16796
- tissue_or_cell_type
- Liver and embryo
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 228–239
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Adh1, Adh3 and Adh4 null mutant mice with ethanol, formaldehyde and retinol challenges · source_derived_draft · unverified_draft
### alcohol-adh1-clearance Following an intoxicating dose of ethanol, Adh1-null mice and to a lesser extent Adh4-null mice, but not Adh3-null mice, showed significant reductions in blood ethanol clearance, and ethanol-induced sleep was significantly longer only in Adh1-null mice. Condition category: machinery_impairment 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: Remove the main enzyme and the animal stays drunk longer. organism: Mouse tissue_or_cell_type: Liver and embryo experimental_model: Adh1, Adh3 and Adh4 null mutant mice with ethanol, formaldehyde and retinol challenges limitations: A clean three-gene dissection showing which enzyme does which job. It is a mouse gene family that does not map one-to-one onto the human one. exposure: Intoxicating ethanol dose, formaldehyde LD50, and retinol administration evidence_span: {"source_cache": "artifacts/alcohol-research/10358022.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c1e4e6f0703d814d36609e71a38be53f7c36bebcfdcd3a60c52ea49625369305", "start_char": 0, "end_char": 1272, "text_sha256": "c1e4e6f0703d814d36609e71a38be53f7c36bebcfdcd3a60c52ea49625369305"} [alcohol-p10358022] Metabolic deficiencies in alcohol dehydrogenase Adh1, Adh3, and Adh4 null mutant mice. Overlapping roles of Adh1 and Adh4 in ethanol clearance and metabolism of retinol to retinoic acid. (1999). https://pubmed.ncbi.nlm.nih.gov/10358022/ DOI: 10.1074/jbc.274.24.16796
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.