Component

Recovery of platelet cyclooxygenase activity after aspirin

Recovery of platelet cyclooxygenase activity after aspirin. Species, exposure and limitations are retained in each linked claim.

4 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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.

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.

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What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What acts on it

  1. Megakaryocyte thromboxane production was depressed by 70% and that of platelets by 85% at two hours after 20 milligrams per kilogram oral aspirin, full megakaryocyte thromboxane recovery occurred by 72 hours and preceded complete platelet recovery by 24 hours, megakaryocyte synthesis showed substantial recovery by 36 hours while platelet recovery did not begin for 24 hours, and the authors conclude that thromboxane synthesis develops in rat megakaryocytes after approximately 48 hours of cytoplasmic differentiation toward platelet shedding.

    Megakaryocyte → Recovery of platelet cyclooxygenase activity after aspirin source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/aspirin-research/6812167.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "fd3cbdc85225aabdb23690613d2ba4bd49151f144c362d6121721eb45e969389", "start_char": 0, "end_char": 1366, "text_sha256": "fd3cbdc85225aabdb23690613d2ba4bd49151f144c362d6121721eb45e969389"}
    experimental_model
    Radioimmunoassay of megakaryocyte and platelet thromboxane B2 recovery in rats after a single oral aspirin dose
    exposure
    20 milligrams per kilogram oral aspirin dissolved in dimethyl sulphoxide
    limitations
    Follows the precursor cell rather than the platelet, which is where the recovery kinetics are actually set. A rat study and the maturation timing is inferred from transit times.
    nutrient_topic
    Aspirin research collection; topical membership is not evidence of a direct clinical effect, and aspirin is recorded separately from salicylate, the metabolite it becomes. · Aspirin / acetylsalicylic acid
    organism
    Rat
    plain_language
    The marrow recovers first and the blood follows, because new platelets have to be built and released.
    primary_references
    [asa-p6812167] Aspirin inhibits rat megakaryocyte thromboxane synthesis. (1982). https://pubmed.ncbi.nlm.nih.gov/6812167/ DOI: 10.1016/0090-6980(82)90128-9
    tissue_or_cell_type
    Bone marrow megakaryocytes and platelets

    Aspirin: the serine it acetylates, the enzyme that acetylation creates, the dose that separates platelet from vessel wall, and the metabolite that is a different drug (2026-09-22) · lines 416–427

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Radioimmunoassay of megakaryocyte and platelet thromboxane B2 recovery in rats after a single oral aspirin dose · source_derived_draft · unverified_draft

    ### asa-recovery-starts-in-the-marrow Megakaryocyte thromboxane production was depressed by 70% and that of platelets by 85% at two hours after 20 milligrams per kilogram oral aspirin, full megakaryocyte thromboxane recovery occurred by 72 hours and preceded complete platelet recovery by 24 hours, megakaryocyte synthesis showed substantial recovery by 36 hours while platelet recovery did not begin for 24 hours, and the authors conclude that thromboxane synthesis develops in rat megakaryocytes after approximately 48 hours of cytoplasmic differentiation toward platelet shedding. Condition category: normal nutrient_topic: Aspirin research collection; topical membership is not evidence of a direct clinical effect, and aspirin is recorded separately from salicylate, the metabolite it becomes. plain_language: The marrow recovers first and the blood follows, because new platelets have to be built and released. organism: Rat tissue_or_cell_type: Bone marrow megakaryocytes and platelets experimental_model: Radioimmunoassay of megakaryocyte and platelet thromboxane B2 recovery in rats after a single oral aspirin dose limitations: Follows the precursor cell rather than the platelet, which is where the recovery kinetics are actually set. A rat study and the maturation timing is inferred from transit times. exposure: 20 milligrams per kilogram oral aspirin dissolved in dimethyl sulphoxide evidence_span: {"source_cache": "artifacts/aspirin-research/6812167.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "fd3cbdc85225aabdb23690613d2ba4bd49151f144c362d6121721eb45e969389", "start_char": 0, "end_char": 1366, "text_sha256": "fd3cbdc85225aabdb23690613d2ba4bd49151f144c362d6121721eb45e969389"} [asa-p6812167] Aspirin inhibits rat megakaryocyte thromboxane synthesis. (1982). https://pubmed.ncbi.nlm.nih.gov/6812167/ DOI: 10.1016/0090-6980(82)90128-9
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Platelet function and prostaglandin synthesis recovered completely 26 hours after ingestion of ibuprofen but remained compromised 26 hours after taking aspirin, and when 650 milligrams of aspirin was administered after ibuprofen, platelet function and cyclooxygenase activity recovered as completely at 26 hours as in platelets exposed to ibuprofen alone, so prior exposure to ibuprofen in vivo completely protected cyclooxygenase from the irreversible effects of aspirin.

    Ibuprofen → Aspirin / acetylsalicylic acid source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/aspirin-research/6411052.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a685344a88574182dbad6f8d70308dce88384a63ed0c561ccaec4d522000b132", "start_char": 0, "end_char": 1551, "text_sha256": "a685344a88574182dbad6f8d70308dce88384a63ed0c561ccaec4d522000b132"}
    experimental_model
    Platelet aggregation and cyclooxygenase activity in subjects given ibuprofen before aspirin, in vitro and in vivo
    exposure
    Ibuprofen ingestion followed by 650 milligrams of aspirin, with recovery followed to 26 hours
    limitations
    The observation is clean and has been confirmed since. The authors’ inference from it, that aspirin must act on the heme group rather than by acetylating the protein, is contradicted by the mutant and crystallographic records in this collection and is not adopted here.
    nutrient_topic
    Aspirin research collection; topical membership is not evidence of a direct clinical effect, and aspirin is recorded separately from salicylate, the metabolite it becomes. · Aspirin / acetylsalicylic acid
    organism
    Human
    plain_language
    Take ibuprofen first and aspirin never gets its chance; the protection wears off in a day like ibuprofen, not like aspirin.
    primary_references
    [asa-p6411052] Ibuprofen protects platelet cyclooxygenase from irreversible inhibition by aspirin. (1983). https://pubmed.ncbi.nlm.nih.gov/6411052/ DOI: 10.1161/01.atv.3.4.383
    tissue_or_cell_type
    Platelets
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    Aspirin: the serine it acetylates, the enzyme that acetylation creates, the dose that separates platelet from vessel wall, and the metabolite that is a different drug (2026-09-22) · lines 442–453

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Platelet aggregation and cyclooxygenase activity in subjects given ibuprofen before aspirin, in vitro and in vivo · source_derived_draft · unverified_draft

    ### asa-ibuprofen-blocks-aspirin Platelet function and prostaglandin synthesis recovered completely 26 hours after ingestion of ibuprofen but remained compromised 26 hours after taking aspirin, and when 650 milligrams of aspirin was administered after ibuprofen, platelet function and cyclooxygenase activity recovered as completely at 26 hours as in platelets exposed to ibuprofen alone, so prior exposure to ibuprofen in vivo completely protected cyclooxygenase from the irreversible effects of aspirin. Condition category: biomarker_context nutrient_topic: Aspirin research collection; topical membership is not evidence of a direct clinical effect, and aspirin is recorded separately from salicylate, the metabolite it becomes. plain_language: Take ibuprofen first and aspirin never gets its chance; the protection wears off in a day like ibuprofen, not like aspirin. organism: Human tissue_or_cell_type: Platelets experimental_model: Platelet aggregation and cyclooxygenase activity in subjects given ibuprofen before aspirin, in vitro and in vivo limitations: The observation is clean and has been confirmed since. The authors’ inference from it, that aspirin must act on the heme group rather than by acetylating the protein, is contradicted by the mutant and crystallographic records in this collection and is not adopted here. exposure: Ibuprofen ingestion followed by 650 milligrams of aspirin, with recovery followed to 26 hours evidence_span: {"source_cache": "artifacts/aspirin-research/6411052.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a685344a88574182dbad6f8d70308dce88384a63ed0c561ccaec4d522000b132", "start_char": 0, "end_char": 1551, "text_sha256": "a685344a88574182dbad6f8d70308dce88384a63ed0c561ccaec4d522000b132"} [asa-p6411052] Ibuprofen protects platelet cyclooxygenase from irreversible inhibition by aspirin. (1983). https://pubmed.ncbi.nlm.nih.gov/6411052/ DOI: 10.1161/01.atv.3.4.383
    Complete structured claim and evidence

  2. In human megakaryocytic cell lines a single 10 micromolar aspirin exposure suppressed thromboxane B2 by 90% and 85% respectively with full recovery within 48 to 72 hours, selective cyclooxygenase-1 inhibition by SC-560 reduced thromboxane B2 by more than 75% whereas cyclooxygenase-2 inhibition by NS-398 had minimal effect, and repeated exposure every 24 hours produced concentration- and time-dependent suppression reaching 89% by day 2 at 1 micromolar and 73% by day 4 at 0.1 micromolar, with delayed recovery likely reflecting de novo synthesis of cyclooxygenase-1 protein.

    Cyclooxygenase-1 (PTGS1) → Thromboxane A2 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/aspirin-research/41265381.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "88710110438cddd108a51822aeb63c5f0a8125192eecc85eeeaf1edf3c3d85cc", "start_char": 0, "end_char": 2110, "text_sha256": "88710110438cddd108a51822aeb63c5f0a8125192eecc85eeeaf1edf3c3d85cc"}
    experimental_model
    Aspirin pharmacodynamics in MEG-01 and CHRF-288-11 human megakaryocytic cell lines with selective isoform inhibitors
    exposure
    Single and repeated aspirin exposures from 0.1 to 10 micromolar, with SC-560 and NS-398 as isoform probes
    limitations
    A surrogate for a tissue that cannot ethically be sampled repeatedly. Cell lines rather than primary megakaryocytes, which the authors state.
    nutrient_topic
    Aspirin research collection; topical membership is not evidence of a direct clinical effect, and aspirin is recorded separately from salicylate, the metabolite it becomes. · Aspirin / acetylsalicylic acid
    organism
    Human cells
    plain_language
    The precursor cell makes its thromboxane with the first enzyme, and has to build new enzyme to recover.
    primary_references
    [asa-p41265381] Aspirin inhibition and recovery of cyclooxygenase activity and thromboxane biosynthesis in human megakaryocytes: a translational surrogate model. (2025). https://pubmed.ncbi.nlm.nih.gov/41265381/ DOI: 10.1016/j.jpet.2025.103762
    tissue_or_cell_type
    Megakaryocytic cell lines

    Aspirin: the serine it acetylates, the enzyme that acetylation creates, the dose that separates platelet from vessel wall, and the metabolite that is a different drug (2026-09-22) · lines 429–440

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Aspirin pharmacodynamics in MEG-01 and CHRF-288-11 human megakaryocytic cell lines with selective isoform inhibitors · source_derived_draft · unverified_draft

    ### asa-megakaryocyte-cox1 In human megakaryocytic cell lines a single 10 micromolar aspirin exposure suppressed thromboxane B2 by 90% and 85% respectively with full recovery within 48 to 72 hours, selective cyclooxygenase-1 inhibition by SC-560 reduced thromboxane B2 by more than 75% whereas cyclooxygenase-2 inhibition by NS-398 had minimal effect, and repeated exposure every 24 hours produced concentration- and time-dependent suppression reaching 89% by day 2 at 1 micromolar and 73% by day 4 at 0.1 micromolar, with delayed recovery likely reflecting de novo synthesis of cyclooxygenase-1 protein. Condition category: normal nutrient_topic: Aspirin research collection; topical membership is not evidence of a direct clinical effect, and aspirin is recorded separately from salicylate, the metabolite it becomes. plain_language: The precursor cell makes its thromboxane with the first enzyme, and has to build new enzyme to recover. organism: Human cells tissue_or_cell_type: Megakaryocytic cell lines experimental_model: Aspirin pharmacodynamics in MEG-01 and CHRF-288-11 human megakaryocytic cell lines with selective isoform inhibitors limitations: A surrogate for a tissue that cannot ethically be sampled repeatedly. Cell lines rather than primary megakaryocytes, which the authors state. exposure: Single and repeated aspirin exposures from 0.1 to 10 micromolar, with SC-560 and NS-398 as isoform probes evidence_span: {"source_cache": "artifacts/aspirin-research/41265381.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "88710110438cddd108a51822aeb63c5f0a8125192eecc85eeeaf1edf3c3d85cc", "start_char": 0, "end_char": 2110, "text_sha256": "88710110438cddd108a51822aeb63c5f0a8125192eecc85eeeaf1edf3c3d85cc"} [asa-p41265381] Aspirin inhibition and recovery of cyclooxygenase activity and thromboxane biosynthesis in human megakaryocytes: a translational surrogate model. (2025). https://pubmed.ncbi.nlm.nih.gov/41265381/ DOI: 10.1016/j.jpet.2025.103762
    Complete structured claim and evidence

  3. Following ingestion of 650 milligrams of acetylsalicylate as compressed tablets, platelet cyclooxygenase activity was inhibited 95% within 45 minutes, enzyme activity was observed to increase within 8 hours and reached 10% of control level by 24 hours, a pattern suggesting that only circulating platelets are affected by ingestion; enteric-coated tablets gave comparable inhibition with a delayed onset reflecting delayed appearance of acetylsalicylate in plasma, and returned to control along a similar pattern.

    Aspirin / acetylsalicylic acid → The cyclooxygenase activity of prostaglandin endoperoxide synthase source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/aspirin-research/7355437.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "01e0a159576fdabca8185271b0d6acd2e790cff32c06ba1e68906afb3a63544a", "start_char": 0, "end_char": 909, "text_sha256": "01e0a159576fdabca8185271b0d6acd2e790cff32c06ba1e68906afb3a63544a"}
    experimental_model
    High pressure liquid chromatography of plasma acetylsalicylate and salicylate with radiometric platelet cyclooxygenase assay
    exposure
    650 milligrams of aspirin as compressed or enteric-coated tablets
    limitations
    Measures the parent drug and the metabolite separately alongside the enzyme effect, which is exactly the distinction this chapter turns on. Healthy subjects and a single dose.
    nutrient_topic
    Aspirin research collection; topical membership is not evidence of a direct clinical effect, and aspirin is recorded separately from salicylate, the metabolite it becomes. · Aspirin / acetylsalicylic acid
    organism
    Human
    plain_language
    The drug catches the platelets that are in the blood at the time, and nothing else.
    primary_references
    [asa-p7355437] Plasma acetylsalicylate and salicylate and platelet cyclooxygenase activity following plain and enteric-coated aspirin. (1980). https://pubmed.ncbi.nlm.nih.gov/7355437/ DOI: 10.1161/01.str.11.1.9
    tissue_or_cell_type
    Plasma and platelets

    Aspirin: the serine it acetylates, the enzyme that acetylation creates, the dose that separates platelet from vessel wall, and the metabolite that is a different drug (2026-09-22) · lines 403–414

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · High pressure liquid chromatography of plasma acetylsalicylate and salicylate with radiometric platelet cyclooxygenase assay · source_derived_draft · unverified_draft

    ### asa-only-circulating-platelets Following ingestion of 650 milligrams of acetylsalicylate as compressed tablets, platelet cyclooxygenase activity was inhibited 95% within 45 minutes, enzyme activity was observed to increase within 8 hours and reached 10% of control level by 24 hours, a pattern suggesting that only circulating platelets are affected by ingestion; enteric-coated tablets gave comparable inhibition with a delayed onset reflecting delayed appearance of acetylsalicylate in plasma, and returned to control along a similar pattern. Condition category: normal nutrient_topic: Aspirin research collection; topical membership is not evidence of a direct clinical effect, and aspirin is recorded separately from salicylate, the metabolite it becomes. plain_language: The drug catches the platelets that are in the blood at the time, and nothing else. organism: Human tissue_or_cell_type: Plasma and platelets experimental_model: High pressure liquid chromatography of plasma acetylsalicylate and salicylate with radiometric platelet cyclooxygenase assay limitations: Measures the parent drug and the metabolite separately alongside the enzyme effect, which is exactly the distinction this chapter turns on. Healthy subjects and a single dose. exposure: 650 milligrams of aspirin as compressed or enteric-coated tablets evidence_span: {"source_cache": "artifacts/aspirin-research/7355437.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "01e0a159576fdabca8185271b0d6acd2e790cff32c06ba1e68906afb3a63544a", "start_char": 0, "end_char": 909, "text_sha256": "01e0a159576fdabca8185271b0d6acd2e790cff32c06ba1e68906afb3a63544a"} [asa-p7355437] Plasma acetylsalicylate and salicylate and platelet cyclooxygenase activity following plain and enteric-coated aspirin. (1980). https://pubmed.ncbi.nlm.nih.gov/7355437/ DOI: 10.1161/01.str.11.1.9
    Complete structured claim and evidence

In the sources

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