Component
Platelet activation
Platelet responsiveness measured by activation or aggregation assays.
4 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
Curcumin inhibited PAF- and arachidonic-acid-driven platelet aggregation in vitro.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/curcumin-research/10484074.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a7f693540f3a0c4db6b93f1ce8c2adaadd1647a6234091da685497bdf66c2b1a", "start_char": 0, "end_char": 1375, "text_sha256": "a7f693540f3a0c4db6b93f1ce8c2adaadd1647a6234091da685497bdf66c2b1a"}
- experimental_model
- Isolated platelet aggregation and signaling assays
- exposure
- Curcumin: PAF/arachidonic-acid aggregation IC50 about 20-25 micromolar, thromboxane IC50 about 70 micromolar
- limitations
- In-vitro concentrations are not proof of clinical bleeding risk or an anticoagulant treatment effect; fluorescence-based calcium readout is assay-specific.
- nutrient_topic
- Curcumin research collection; topical membership is not evidence of a direct dietary effect. · Curcumin
- organism
- Platelets; donor species not resolved in indexed abstract
- plain_language
- The platelet response was smaller in the assay.
- primary_references
- [curcumin-p10484074] Inhibitory effect of curcumin, a food spice from turmeric, on platelet-activating factor- and arachidonic acid-mediated platelet aggregation through inhibition of thromboxane formation and Ca2+ signaling. (1999). https://pubmed.ncbi.nlm.nih.gov/10484074/ DOI: 10.1016/s0006-2952(99)00206-3
- tissue_or_cell_type
- Platelet activation and calcium signaling
Curcumin: metabolism, signaling and nutrient connections (2026-09-17) · lines 983–994
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated platelet aggregation and signaling assays · source_derived_draft · unverified_draft
### curcumin-platelet-aggregation Curcumin inhibited PAF- and arachidonic-acid-driven platelet aggregation in vitro. Condition category: normal nutrient_topic: Curcumin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The platelet response was smaller in the assay. organism: Platelets; donor species not resolved in indexed abstract tissue_or_cell_type: Platelet activation and calcium signaling experimental_model: Isolated platelet aggregation and signaling assays limitations: In-vitro concentrations are not proof of clinical bleeding risk or an anticoagulant treatment effect; fluorescence-based calcium readout is assay-specific. exposure: Curcumin: PAF/arachidonic-acid aggregation IC50 about 20-25 micromolar, thromboxane IC50 about 70 micromolar evidence_span: {"source_cache": "artifacts/curcumin-research/10484074.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a7f693540f3a0c4db6b93f1ce8c2adaadd1647a6234091da685497bdf66c2b1a", "start_char": 0, "end_char": 1375, "text_sha256": "a7f693540f3a0c4db6b93f1ce8c2adaadd1647a6234091da685497bdf66c2b1a"} [curcumin-p10484074] Inhibitory effect of curcumin, a food spice from turmeric, on platelet-activating factor- and arachidonic acid-mediated platelet aggregation through inhibition of thromboxane formation and Ca2+ signaling. (1999). https://pubmed.ncbi.nlm.nih.gov/10484074/ DOI: 10.1016/s0006-2952(99)00206-3
Complete structured claim and evidenceGpx3-deficient mice showed increased platelet responsiveness.
Experimental context and source evidence
- cell_type
- platelets and plasma
- experimental_model
- Gpx3 knockout
- limitations
- Not a selenium-supplementation trial.
- organism
- mouse
Selenium: literature corrections and mechanism additions · lines 690–700
Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Gpx3 knockout · secondary_verified · secondary_verified
## gpx3-loss-increases-platelet-activation GPX3 loss made platelets more reactive in this model. Gpx3-deficient mice showed increased platelet responsiveness. Organism: mouse Cell type: platelets and plasma Experimental model: Gpx3 knockout Limitations: Not a selenium-supplementation trial. Primary reference: [Glutathione Peroxidase-3 Deficiency Promotes Platelet-dependent Thrombosis in vivo](https://pmc.ncbi.nlm.nih.gov/articles/PMC3107543/)
Complete structured claim and evidence
Where it participates (unsigned role)
Gpx3 deficiency increased platelet-dependent thrombosis after experimental vascular provocation.
Experimental context and source evidence
- cell_type
- arterial injury model
- experimental_model
- Gpx3 knockout
- limitations
- Does not establish a human selenium cutoff.
- organism
- mouse
Selenium: literature corrections and mechanism additions · lines 702–712
Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Gpx3 knockout · secondary_verified · secondary_verified
## gpx3-loss-increases-provoked-thrombosis GPX3-deficient mice formed more thrombus after vascular injury. Gpx3 deficiency increased platelet-dependent thrombosis after experimental vascular provocation. Organism: mouse Cell type: arterial injury model Experimental model: Gpx3 knockout Limitations: Does not establish a human selenium cutoff. Primary reference: [Glutathione Peroxidase-3 Deficiency Promotes Platelet-dependent Thrombosis in vivo](https://pmc.ncbi.nlm.nih.gov/articles/PMC3107543/)
Complete structured claim and evidenceRedox and platelet measurements support GPX3 preservation of NO-mediated platelet restraint.
Experimental context and source evidence
- cell_type
- plasma and platelets
- experimental_model
- Gpx3 knockout
- limitations
- Individual oxidant intermediates were not fully isolated.
- organism
- mouse
Selenium: literature corrections and mechanism additions · lines 714–724
Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Gpx3 knockout · secondary_verified · secondary_verified
## gpx3-supports-no-platelet-restraint GPX3 may help preserve nitric oxide's platelet-inhibitory signal. Redox and platelet measurements support GPX3 preservation of NO-mediated platelet restraint. Organism: mouse Cell type: plasma and platelets Experimental model: Gpx3 knockout Limitations: Individual oxidant intermediates were not fully isolated. Primary reference: [Glutathione Peroxidase-3 Deficiency Promotes Platelet-dependent Thrombosis in vivo](https://pmc.ncbi.nlm.nih.gov/articles/PMC3107543/)
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.