Component
Olvanil
Olvanil. 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)
Systemic 4-aminophenol and 4-hydroxy-3-methoxybenzylamine led to dose-dependent formation of AM404 and of arvanil and olvanil respectively in the mouse brain, the order of potency of these lipid metabolites as TRPV1 activators being arvanil equal to olvanil much greater than AM404, both parent amines displayed antinociceptive activity in rodent pain tests, formation of these metabolites and the antinociceptive effects were substantially reduced or disappeared in fatty acid amide hydrolase null mice, activity was lost in TRPV1 null mice, intracerebroventricular capsazepine eliminated the effects, and in the rat, inhibition of fatty acid amide hydrolase, TRPV1, cannabinoid CB1 receptors and spinal 5-HT3 or 5-HT1A receptors and chemical deletion of bulbospinal serotonergic pathways all prevented the action, giving a pharmacological profile identical to that previously reported for paracetamol.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/paracetamol-research/23940628.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "cc9d85547497bfdf88095aaeccf5a11cb9198140ebb35523d5da1b85f76e0a44", "start_char": 0, "end_char": 2208, "text_sha256": "cc9d85547497bfdf88095aaeccf5a11cb9198140ebb35523d5da1b85f76e0a44"}
- experimental_model
- Metabolite formation and antinociception for 4-aminophenol and a vanillylamine analogue across knockouts and pharmacological blockade
- exposure
- Systemic 4-aminophenol and 4-hydroxy-3-methoxybenzylamine, with fatty acid amide hydrolase, TRPV1, cannabinoid and serotonergic manipulations
- limitations
- The broadest test of the route: it reconstructs the whole chain from metabolite formation to descending pathway, and shows the profile of the metabolite matches that of the parent drug.
- nutrient_topic
- Paracetamol research collection; topical membership is not evidence of a direct clinical effect, and the drug is recorded separately from the metabolites NAPQI and AM404. · Paracetamol
- organism
- Mouse and rat
- plain_language
- Every step of the proposed chain was cut in turn, and cutting any of them stopped the painkilling.
- primary_references
- [apap-p23940628] Fatty acid amide hydrolase-dependent generation of antinociceptive drug metabolites acting on TRPV1 in the brain. (2013). https://pubmed.ncbi.nlm.nih.gov/23940628/ DOI: 10.1371/journal.pone.0070690
- tissue_or_cell_type
- Brain and spinal cord
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Metabolite formation and antinociception for 4-aminophenol and a vanillylamine analogue across knockouts and pharmacological blockade · source_derived_draft · unverified_draft
### apap-the-whole-chain Systemic 4-aminophenol and 4-hydroxy-3-methoxybenzylamine led to dose-dependent formation of AM404 and of arvanil and olvanil respectively in the mouse brain, the order of potency of these lipid metabolites as TRPV1 activators being arvanil equal to olvanil much greater than AM404, both parent amines displayed antinociceptive activity in rodent pain tests, formation of these metabolites and the antinociceptive effects were substantially reduced or disappeared in fatty acid amide hydrolase null mice, activity was lost in TRPV1 null mice, intracerebroventricular capsazepine eliminated the effects, and in the rat, inhibition of fatty acid amide hydrolase, TRPV1, cannabinoid CB1 receptors and spinal 5-HT3 or 5-HT1A receptors and chemical deletion of bulbospinal serotonergic pathways all prevented the action, giving a pharmacological profile identical to that previously reported for paracetamol. Condition category: normal nutrient_topic: Paracetamol research collection; topical membership is not evidence of a direct clinical effect, and the drug is recorded separately from the metabolites NAPQI and AM404. plain_language: Every step of the proposed chain was cut in turn, and cutting any of them stopped the painkilling. organism: Mouse and rat tissue_or_cell_type: Brain and spinal cord experimental_model: Metabolite formation and antinociception for 4-aminophenol and a vanillylamine analogue across knockouts and pharmacological blockade limitations: The broadest test of the route: it reconstructs the whole chain from metabolite formation to descending pathway, and shows the profile of the metabolite matches that of the parent drug. exposure: Systemic 4-aminophenol and 4-hydroxy-3-methoxybenzylamine, with fatty acid amide hydrolase, TRPV1, cannabinoid and serotonergic manipulations evidence_span: {"source_cache": "artifacts/paracetamol-research/23940628.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "cc9d85547497bfdf88095aaeccf5a11cb9198140ebb35523d5da1b85f76e0a44", "start_char": 0, "end_char": 2208, "text_sha256": "cc9d85547497bfdf88095aaeccf5a11cb9198140ebb35523d5da1b85f76e0a44"} [apap-p23940628] Fatty acid amide hydrolase-dependent generation of antinociceptive drug metabolites acting on TRPV1 in the brain. (2013). https://pubmed.ncbi.nlm.nih.gov/23940628/ DOI: 10.1371/journal.pone.0070690
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.