Component
Cytosolic free NAD+/NADH ratio
Cytosolic free NAD+/NADH ratio. 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 acts on it
Ethanol administration caused an immediate decrease in the NAD+/NADH ratio of both cytoplasm and mitochondria, which persisted over the 30 minutes studied.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/alcohol-research/4342558.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dce57aa8128b432a841f087e3c4e70963b8fe318e462df980e6cdd66ed4af79d", "start_char": 0, "end_char": 959, "text_sha256": "dce57aa8128b432a841f087e3c4e70963b8fe318e462df980e6cdd66ed4af79d"}
- experimental_model
- Freeze-clamped liver metabolite measurement in starved rats after ethanol
- exposure
- Single ethanol dose, sampled over 30 minutes in fed and starved animals
- limitations
- The classic redox measurement. Metabolite ratios are calculated from near-equilibrium assumptions rather than measured directly, which the authors state.
- 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
- Rat
- plain_language
- Burning alcohol floods the cell with the reduced form of the carrier that every other pathway needs oxidised.
- primary_references
- [alcohol-p4342558] The time-course of the effects of ethanol on the redox and phosphorylation states of rat liver. (1972). https://pubmed.ncbi.nlm.nih.gov/4342558/ DOI: 10.1042/bj1270387
- tissue_or_cell_type
- Liver
Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 98–109
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Freeze-clamped liver metabolite measurement in starved rats after ethanol · source_derived_draft · unverified_draft
### alcohol-redox-shift Ethanol administration caused an immediate decrease in the NAD+/NADH ratio of both cytoplasm and mitochondria, which persisted over the 30 minutes studied. Condition category: normal 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: Burning alcohol floods the cell with the reduced form of the carrier that every other pathway needs oxidised. organism: Rat tissue_or_cell_type: Liver experimental_model: Freeze-clamped liver metabolite measurement in starved rats after ethanol limitations: The classic redox measurement. Metabolite ratios are calculated from near-equilibrium assumptions rather than measured directly, which the authors state. exposure: Single ethanol dose, sampled over 30 minutes in fed and starved animals evidence_span: {"source_cache": "artifacts/alcohol-research/4342558.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dce57aa8128b432a841f087e3c4e70963b8fe318e462df980e6cdd66ed4af79d", "start_char": 0, "end_char": 959, "text_sha256": "dce57aa8128b432a841f087e3c4e70963b8fe318e462df980e6cdd66ed4af79d"} [alcohol-p4342558] The time-course of the effects of ethanol on the redox and phosphorylation states of rat liver. (1972). https://pubmed.ncbi.nlm.nih.gov/4342558/ DOI: 10.1042/bj1270387
Complete structured claim and evidence
Where it participates (unsigned role)
The ethanol-induced hepatic redox change was attenuated after chronic alcohol consumption in baboons, with metabolic consequences measured both in vivo and in vitro.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/alcohol-research/6793493.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5105956fd640dc7b32bd1d5e54a0df98bc5eb8d332220e27578ce5e631536fbe", "start_char": 0, "end_char": 986, "text_sha256": "5105956fd640dc7b32bd1d5e54a0df98bc5eb8d332220e27578ce5e631536fbe"}
- experimental_model
- Baboons fed alcohol chronically, with in vivo and in vitro redox measurement
- exposure
- Chronic alcohol consumption compared with acute administration
- limitations
- A primate chronic-feeding model. It shows the redox change is not fixed, which bears on reading any single acute measurement as the steady state.
- 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
- Baboon
- plain_language
- The redox hit shrinks with habitual drinking, so a first-drink measurement does not describe a heavy drinker.
- primary_references
- [alcohol-p6793493] Attenuation of the ethanol-induced hepatic redox change after chronic alcohol consumption in baboons: metabolic consequences in vivo and in vitro. (1981). https://pubmed.ncbi.nlm.nih.gov/6793493/ DOI: 10.1002/hep.1840010106
- tissue_or_cell_type
- Liver
Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 124–135
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Baboons fed alcohol chronically, with in vivo and in vitro redox measurement · source_derived_draft · unverified_draft
### alcohol-redox-adaptation The ethanol-induced hepatic redox change was attenuated after chronic alcohol consumption in baboons, with metabolic consequences measured both in vivo and in vitro. Condition category: normal 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 redox hit shrinks with habitual drinking, so a first-drink measurement does not describe a heavy drinker. organism: Baboon tissue_or_cell_type: Liver experimental_model: Baboons fed alcohol chronically, with in vivo and in vitro redox measurement limitations: A primate chronic-feeding model. It shows the redox change is not fixed, which bears on reading any single acute measurement as the steady state. exposure: Chronic alcohol consumption compared with acute administration evidence_span: {"source_cache": "artifacts/alcohol-research/6793493.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5105956fd640dc7b32bd1d5e54a0df98bc5eb8d332220e27578ce5e631536fbe", "start_char": 0, "end_char": 986, "text_sha256": "5105956fd640dc7b32bd1d5e54a0df98bc5eb8d332220e27578ce5e631536fbe"} [alcohol-p6793493] Attenuation of the ethanol-induced hepatic redox change after chronic alcohol consumption in baboons: metabolic consequences in vivo and in vitro. (1981). https://pubmed.ncbi.nlm.nih.gov/6793493/ DOI: 10.1002/hep.1840010106
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.