Component
Triacsin C, an acyl-CoA synthetase 1 inhibitor
Triacsin C, an acyl-CoA synthetase 1 inhibitor. 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.
Where it participates (unsigned role)
In hepatocytes isolated from rats with adjuvant-induced arthritis the chiral inversion rate constant of R- to S-ibuprofen and the metabolic rate constants of both enantiomers were significantly decreased to about 64 to 80% of control values, while adding serum from each group abolished the difference; adjuvant-induced arthritis decreased messenger RNA levels of acyl-coenzyme A synthetase isoforms but not of 2-arylpropionyl-CoA epimerase, and chiral inversion was inhibited by triacsin C, a specific inhibitor of acyl-CoA synthetase 1.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/ibuprofen-research/18988084.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "49f5377220f47f04a74dc5e1cd5408a0b175eafbf602e536e57d80a9e8eb1f3a", "start_char": 0, "end_char": 1381, "text_sha256": "49f5377220f47f04a74dc5e1cd5408a0b175eafbf602e536e57d80a9e8eb1f3a"}
- experimental_model
- Freshly isolated hepatocytes from control rats and rats with adjuvant-induced arthritis
- exposure
- S- or R-ibuprofen incubated with hepatocytes, with and without serum, and with triacsin C
- limitations
- Tests whether the disease being treated changes the handling of the drug. Isolated hepatocytes, and the serum arm shows the effect disappears when serum is added back.
- nutrient_topic
- Ibuprofen research collection; topical membership is not evidence of a direct clinical effect, and the racemate is recorded separately from each of its two enantiomers. · Ibuprofen
- organism
- Rat
- plain_language
- The inflammation the drug is prescribed for slows down the step that makes the drug active.
- primary_references
- [ibu-p18988084] Impaired intrinsic chiral inversion activity of ibuprofen in rats with adjuvant-induced arthritis. (2008). https://pubmed.ncbi.nlm.nih.gov/18988084/ DOI: 10.1080/00498250802483768
- tissue_or_cell_type
- Hepatocytes
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Freshly isolated hepatocytes from control rats and rats with adjuvant-induced arthritis · source_derived_draft · unverified_draft
### ibu-arthritis-slows-inversion In hepatocytes isolated from rats with adjuvant-induced arthritis the chiral inversion rate constant of R- to S-ibuprofen and the metabolic rate constants of both enantiomers were significantly decreased to about 64 to 80% of control values, while adding serum from each group abolished the difference; adjuvant-induced arthritis decreased messenger RNA levels of acyl-coenzyme A synthetase isoforms but not of 2-arylpropionyl-CoA epimerase, and chiral inversion was inhibited by triacsin C, a specific inhibitor of acyl-CoA synthetase 1. Condition category: machinery_impairment nutrient_topic: Ibuprofen research collection; topical membership is not evidence of a direct clinical effect, and the racemate is recorded separately from each of its two enantiomers. plain_language: The inflammation the drug is prescribed for slows down the step that makes the drug active. organism: Rat tissue_or_cell_type: Hepatocytes experimental_model: Freshly isolated hepatocytes from control rats and rats with adjuvant-induced arthritis limitations: Tests whether the disease being treated changes the handling of the drug. Isolated hepatocytes, and the serum arm shows the effect disappears when serum is added back. exposure: S- or R-ibuprofen incubated with hepatocytes, with and without serum, and with triacsin C evidence_span: {"source_cache": "artifacts/ibuprofen-research/18988084.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "49f5377220f47f04a74dc5e1cd5408a0b175eafbf602e536e57d80a9e8eb1f3a", "start_char": 0, "end_char": 1381, "text_sha256": "49f5377220f47f04a74dc5e1cd5408a0b175eafbf602e536e57d80a9e8eb1f3a"} [ibu-p18988084] Impaired intrinsic chiral inversion activity of ibuprofen in rats with adjuvant-induced arthritis. (2008). https://pubmed.ncbi.nlm.nih.gov/18988084/ DOI: 10.1080/00498250802483768
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.