Component
tert-butyl hydroperoxide
tert-butyl hydroperoxide. 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)
Increasing the peroxide product of the cyclooxygenase, prostaglandin G2, by elevating the concentration of either enzyme or substrate reverses the inhibitory action of acetaminophen, as does adding prostaglandin G2 itself, 0.3 micromolar 12-hydroperoxyeicosatetraenoic acid which is a major product of the platelet completely reverses the action on synthase-1, and inhibition in endothelial cells is abrogated by tert-butyl hydroperoxide, supporting the hypothesis that hydroperoxide concentration contributes to the cellular selectivity.
Experimental context and source evidence
- availability_state
- biomarker_context Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/paracetamol-research/12011469.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7e599890f658a63c52471fbc7e6853d7db6a5ecbe892241a39c8a633b3ab2d0d", "start_char": 0, "end_char": 1561, "text_sha256": "7e599890f658a63c52471fbc7e6853d7db6a5ecbe892241a39c8a633b3ab2d0d"}
- experimental_model
- Interleukin-1-alpha-stimulated human endothelial cells and human platelets compared, with hydroperoxide addition
- exposure
- Acetaminophen with 2 micromolar arachidonic acid, and with prostaglandin G2, 12-hydroperoxyeicosatetraenoic acid or tert-butyl hydroperoxide added back
- limitations
- The decisive record of the chapter: it measures a 435-fold difference between two human cell types, shows it is not isoform selectivity, and reverses it by adding the peroxide back.
- 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
- Human
- plain_language
- Put the peroxide back and the drug stops working, which is why the platelet is untouched.
- primary_references
- [apap-p12011469] Determinants of the cellular specificity of acetaminophen as an inhibitor of prostaglandin H(2) synthases. (2002). https://pubmed.ncbi.nlm.nih.gov/12011469/ DOI: 10.1073/pnas.102588199
- tissue_or_cell_type
- Endothelium and platelets
- trigger_kind
- biomarker_context Imported condition classification; unverified.
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Interleukin-1-alpha-stimulated human endothelial cells and human platelets compared, with hydroperoxide addition · source_derived_draft · unverified_draft
### apap-peroxide-reverses-it Increasing the peroxide product of the cyclooxygenase, prostaglandin G2, by elevating the concentration of either enzyme or substrate reverses the inhibitory action of acetaminophen, as does adding prostaglandin G2 itself, 0.3 micromolar 12-hydroperoxyeicosatetraenoic acid which is a major product of the platelet completely reverses the action on synthase-1, and inhibition in endothelial cells is abrogated by tert-butyl hydroperoxide, supporting the hypothesis that hydroperoxide concentration contributes to the cellular selectivity. Condition category: biomarker_context 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: Put the peroxide back and the drug stops working, which is why the platelet is untouched. organism: Human tissue_or_cell_type: Endothelium and platelets experimental_model: Interleukin-1-alpha-stimulated human endothelial cells and human platelets compared, with hydroperoxide addition limitations: The decisive record of the chapter: it measures a 435-fold difference between two human cell types, shows it is not isoform selectivity, and reverses it by adding the peroxide back. exposure: Acetaminophen with 2 micromolar arachidonic acid, and with prostaglandin G2, 12-hydroperoxyeicosatetraenoic acid or tert-butyl hydroperoxide added back evidence_span: {"source_cache": "artifacts/paracetamol-research/12011469.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7e599890f658a63c52471fbc7e6853d7db6a5ecbe892241a39c8a633b3ab2d0d", "start_char": 0, "end_char": 1561, "text_sha256": "7e599890f658a63c52471fbc7e6853d7db6a5ecbe892241a39c8a633b3ab2d0d"} [apap-p12011469] Determinants of the cellular specificity of acetaminophen as an inhibitor of prostaglandin H(2) synthases. (2002). https://pubmed.ncbi.nlm.nih.gov/12011469/ DOI: 10.1073/pnas.102588199
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.