Effects of acetaminophen on constitutive and inducible prostanoid biosynthesis in human blood cells
Acetaminophen, an analgesic and antipyretic drug with weak antiinflammatory properties, has been suggested to act as a tissue‐selective inhibitor of prostaglandin H synthases (PGHSs) (e.g. COX‐1 and COX‐2) through its reducing activity, that is influenced by the different cellular levels of peroxide...
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| Veröffentlicht in: | British journal of pharmacology 2003-02, Vol.138 (4), p.634-641 |
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| creator | Sciulli, Maria G Seta, Francesca Tacconelli, Stefania Capone, Marta L Ricciotti, Emanuela Pistritto, Giuseppa Patrignani, Paola |
| description | Acetaminophen, an analgesic and antipyretic drug with weak antiinflammatory properties, has been suggested to act as a tissue‐selective inhibitor of prostaglandin H synthases (PGHSs) (e.g. COX‐1 and COX‐2) through its reducing activity, that is influenced by the different cellular levels of peroxides.
We have studied the effects of acetaminophen on inducible and constitutive prostanoid biosynthesis in monocytes and platelets in vitro. To discriminate between the inhibitory effect of the drug on PGHS‐isozymes vs PGE‐synthases (PGESs), parallel measurements of PGE2 and thromboxane (TX) B2 were carried out. Since antioxidant enzymes and cofactors, present in plasma, may affect acetaminophen‐dependent inhibition of prostanoids, comparative experiments in whole blood vs isolated monocytes were performed.
Acetaminophen inhibited LPS‐induced whole blood PGE2 and TXB2 production, in a concentration‐dependent fashion [IC50 μM (95% confidence intervals): 44 (27–70) and 94 (79–112), respectively]. Therapeutic plasma concentrations (100 and 300 μM) of the drug more profoundly reduced PGE2 than TXB2 (71±3 vs 54±4 and 95±0.8 vs 78±2%, respectively, mean±s.e.mean, n=6, P |
| doi_str_mv | 10.1038/sj.bjp.0705078 |
| format | Article |
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We have studied the effects of acetaminophen on inducible and constitutive prostanoid biosynthesis in monocytes and platelets in vitro. To discriminate between the inhibitory effect of the drug on PGHS‐isozymes vs PGE‐synthases (PGESs), parallel measurements of PGE2 and thromboxane (TX) B2 were carried out. Since antioxidant enzymes and cofactors, present in plasma, may affect acetaminophen‐dependent inhibition of prostanoids, comparative experiments in whole blood vs isolated monocytes were performed.
Acetaminophen inhibited LPS‐induced whole blood PGE2 and TXB2 production, in a concentration‐dependent fashion [IC50 μM (95% confidence intervals): 44 (27–70) and 94 (79–112), respectively]. Therapeutic plasma concentrations (100 and 300 μM) of the drug more profoundly reduced PGE2 than TXB2 (71±3 vs 54±4 and 95±0.8 vs 78±2%, respectively, mean±s.e.mean, n=6, P<0.01).
Differently, in isolated monocytes stimulated with LPS, both PGE2 and TXB2 production was maximally reduced by only 60%.
At 100 and 300 μM, the drug caused a similar and incomplete inhibition of platelet PGE2 and TXB2 production during whole blood clotting (45±4 vs 54±4 and 75±2 vs 75±1%, respectively, mean±s.e.mean, n=4).
In conclusion, therapeutic concentrations of acetaminophen caused an incomplete inhibition of platelet COX‐1 and monocyte COX‐2 but in the presence of plasma, the drug almost completely suppressed inducible PGE2 biosynthesis through its inhibitory effects on both COX‐2 and inducible PGES.
British Journal of Pharmacology (2003) 138, 634–641. doi:10.1038/sj.bjp.0705078</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1038/sj.bjp.0705078</identifier><identifier>PMID: 12598417</identifier><identifier>CODEN: BJPCBM</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Acetaminophen ; Acetaminophen - pharmacology ; Adult ; Analgesics ; Biological and medical sciences ; Blood Cells - drug effects ; Blood Cells - metabolism ; Dose-Response Relationship, Drug ; Female ; Humans ; Male ; Medical sciences ; monocyte COX‐2 ; Neuropharmacology ; PGE‐synthase ; Pharmacology. Drug treatments ; platelet COX‐1 ; Prostaglandins - biosynthesis ; whole blood</subject><ispartof>British journal of pharmacology, 2003-02, Vol.138 (4), p.634-641</ispartof><rights>2003 British Pharmacological Society</rights><rights>2003 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Feb 2003</rights><rights>Copyright 2003, Nature Publishing Group 2003 Nature Publishing Group</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c6091-3816d050994a559b915cfedd2b1495f5a63ca0ad2b88c24bab43b304857aa25b3</citedby><cites>FETCH-LOGICAL-c6091-3816d050994a559b915cfedd2b1495f5a63ca0ad2b88c24bab43b304857aa25b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1573695/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1573695/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,724,777,781,882,1412,1428,27905,27906,45555,45556,46390,46814,53772,53774</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14606681$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12598417$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sciulli, Maria G</creatorcontrib><creatorcontrib>Seta, Francesca</creatorcontrib><creatorcontrib>Tacconelli, Stefania</creatorcontrib><creatorcontrib>Capone, Marta L</creatorcontrib><creatorcontrib>Ricciotti, Emanuela</creatorcontrib><creatorcontrib>Pistritto, Giuseppa</creatorcontrib><creatorcontrib>Patrignani, Paola</creatorcontrib><title>Effects of acetaminophen on constitutive and inducible prostanoid biosynthesis in human blood cells</title><title>British journal of pharmacology</title><addtitle>Br J Pharmacol</addtitle><description>Acetaminophen, an analgesic and antipyretic drug with weak antiinflammatory properties, has been suggested to act as a tissue‐selective inhibitor of prostaglandin H synthases (PGHSs) (e.g. COX‐1 and COX‐2) through its reducing activity, that is influenced by the different cellular levels of peroxides.
We have studied the effects of acetaminophen on inducible and constitutive prostanoid biosynthesis in monocytes and platelets in vitro. To discriminate between the inhibitory effect of the drug on PGHS‐isozymes vs PGE‐synthases (PGESs), parallel measurements of PGE2 and thromboxane (TX) B2 were carried out. Since antioxidant enzymes and cofactors, present in plasma, may affect acetaminophen‐dependent inhibition of prostanoids, comparative experiments in whole blood vs isolated monocytes were performed.
Acetaminophen inhibited LPS‐induced whole blood PGE2 and TXB2 production, in a concentration‐dependent fashion [IC50 μM (95% confidence intervals): 44 (27–70) and 94 (79–112), respectively]. Therapeutic plasma concentrations (100 and 300 μM) of the drug more profoundly reduced PGE2 than TXB2 (71±3 vs 54±4 and 95±0.8 vs 78±2%, respectively, mean±s.e.mean, n=6, P<0.01).
Differently, in isolated monocytes stimulated with LPS, both PGE2 and TXB2 production was maximally reduced by only 60%.
At 100 and 300 μM, the drug caused a similar and incomplete inhibition of platelet PGE2 and TXB2 production during whole blood clotting (45±4 vs 54±4 and 75±2 vs 75±1%, respectively, mean±s.e.mean, n=4).
In conclusion, therapeutic concentrations of acetaminophen caused an incomplete inhibition of platelet COX‐1 and monocyte COX‐2 but in the presence of plasma, the drug almost completely suppressed inducible PGE2 biosynthesis through its inhibitory effects on both COX‐2 and inducible PGES.
British Journal of Pharmacology (2003) 138, 634–641. doi:10.1038/sj.bjp.0705078</description><subject>Acetaminophen</subject><subject>Acetaminophen - pharmacology</subject><subject>Adult</subject><subject>Analgesics</subject><subject>Biological and medical sciences</subject><subject>Blood Cells - drug effects</subject><subject>Blood Cells - metabolism</subject><subject>Dose-Response Relationship, Drug</subject><subject>Female</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>monocyte COX‐2</subject><subject>Neuropharmacology</subject><subject>PGE‐synthase</subject><subject>Pharmacology. Drug treatments</subject><subject>platelet COX‐1</subject><subject>Prostaglandins - biosynthesis</subject><subject>whole blood</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFkc2L1TAUxYMoznN061KCoLs-c5vmayOMw-gIA7rQdUjS1JfSJrVpR95_b4ZXHHUzqxDu736ccxB6CWQPhMp3ud_bftoTQRgR8hHaQSN4xaiEx2hHCBEVgJRn6FnOPSGlKNhTdAY1U7IBsUPuquu8WzJOHTbOL2YMMU0HH3GK2KWYl7CsS7j12MQWh9iuLtjB42lOeTExhRbbkPIxLgefQy4EPqyjidgOKbXY-WHIz9GTzgzZv9jec_T949W3y-vq5sunz5cXN5XjREFVbuZtkaFUYxhTVgFznW_b2kKjWMcMp84QU_5SurqxxjbUUtJIJoypmaXn6P1p7rTa0bfOx2U2g57mMJr5qJMJ-t9KDAf9I91qYIJyxcqAt9uAOf1cfV70GPKdBBN9WrMWZZuC4vtDYLFcQs1pAV__B_ZpnWNxQdcgQHEBvED7E-SKqXn23Z-Tgei7lHXudUlZbymXhld_C73Ht1gL8GYDTHZm6GYTXcj3XMMJ5xIKR0_crzD44wNr9Yev103NgP4GF2DCzg</recordid><startdate>200302</startdate><enddate>200302</enddate><creator>Sciulli, Maria G</creator><creator>Seta, Francesca</creator><creator>Tacconelli, Stefania</creator><creator>Capone, Marta L</creator><creator>Ricciotti, Emanuela</creator><creator>Pistritto, Giuseppa</creator><creator>Patrignani, Paola</creator><general>Blackwell Publishing Ltd</general><general>Nature Publishing</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7U7</scope><scope>C1K</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>200302</creationdate><title>Effects of acetaminophen on constitutive and inducible prostanoid biosynthesis in human blood cells</title><author>Sciulli, Maria G ; Seta, Francesca ; Tacconelli, Stefania ; Capone, Marta L ; Ricciotti, Emanuela ; Pistritto, Giuseppa ; Patrignani, Paola</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6091-3816d050994a559b915cfedd2b1495f5a63ca0ad2b88c24bab43b304857aa25b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Acetaminophen</topic><topic>Acetaminophen - pharmacology</topic><topic>Adult</topic><topic>Analgesics</topic><topic>Biological and medical sciences</topic><topic>Blood Cells - drug effects</topic><topic>Blood Cells - metabolism</topic><topic>Dose-Response Relationship, Drug</topic><topic>Female</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>monocyte COX‐2</topic><topic>Neuropharmacology</topic><topic>PGE‐synthase</topic><topic>Pharmacology. Drug treatments</topic><topic>platelet COX‐1</topic><topic>Prostaglandins - biosynthesis</topic><topic>whole blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sciulli, Maria G</creatorcontrib><creatorcontrib>Seta, Francesca</creatorcontrib><creatorcontrib>Tacconelli, Stefania</creatorcontrib><creatorcontrib>Capone, Marta L</creatorcontrib><creatorcontrib>Ricciotti, Emanuela</creatorcontrib><creatorcontrib>Pistritto, Giuseppa</creatorcontrib><creatorcontrib>Patrignani, Paola</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>British journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sciulli, Maria G</au><au>Seta, Francesca</au><au>Tacconelli, Stefania</au><au>Capone, Marta L</au><au>Ricciotti, Emanuela</au><au>Pistritto, Giuseppa</au><au>Patrignani, Paola</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of acetaminophen on constitutive and inducible prostanoid biosynthesis in human blood cells</atitle><jtitle>British journal of pharmacology</jtitle><addtitle>Br J Pharmacol</addtitle><date>2003-02</date><risdate>2003</risdate><volume>138</volume><issue>4</issue><spage>634</spage><epage>641</epage><pages>634-641</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><coden>BJPCBM</coden><abstract>Acetaminophen, an analgesic and antipyretic drug with weak antiinflammatory properties, has been suggested to act as a tissue‐selective inhibitor of prostaglandin H synthases (PGHSs) (e.g. COX‐1 and COX‐2) through its reducing activity, that is influenced by the different cellular levels of peroxides.
We have studied the effects of acetaminophen on inducible and constitutive prostanoid biosynthesis in monocytes and platelets in vitro. To discriminate between the inhibitory effect of the drug on PGHS‐isozymes vs PGE‐synthases (PGESs), parallel measurements of PGE2 and thromboxane (TX) B2 were carried out. Since antioxidant enzymes and cofactors, present in plasma, may affect acetaminophen‐dependent inhibition of prostanoids, comparative experiments in whole blood vs isolated monocytes were performed.
Acetaminophen inhibited LPS‐induced whole blood PGE2 and TXB2 production, in a concentration‐dependent fashion [IC50 μM (95% confidence intervals): 44 (27–70) and 94 (79–112), respectively]. Therapeutic plasma concentrations (100 and 300 μM) of the drug more profoundly reduced PGE2 than TXB2 (71±3 vs 54±4 and 95±0.8 vs 78±2%, respectively, mean±s.e.mean, n=6, P<0.01).
Differently, in isolated monocytes stimulated with LPS, both PGE2 and TXB2 production was maximally reduced by only 60%.
At 100 and 300 μM, the drug caused a similar and incomplete inhibition of platelet PGE2 and TXB2 production during whole blood clotting (45±4 vs 54±4 and 75±2 vs 75±1%, respectively, mean±s.e.mean, n=4).
In conclusion, therapeutic concentrations of acetaminophen caused an incomplete inhibition of platelet COX‐1 and monocyte COX‐2 but in the presence of plasma, the drug almost completely suppressed inducible PGE2 biosynthesis through its inhibitory effects on both COX‐2 and inducible PGES.
British Journal of Pharmacology (2003) 138, 634–641. doi:10.1038/sj.bjp.0705078</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>12598417</pmid><doi>10.1038/sj.bjp.0705078</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Acetaminophen Acetaminophen - pharmacology Adult Analgesics Biological and medical sciences Blood Cells - drug effects Blood Cells - metabolism Dose-Response Relationship, Drug Female Humans Male Medical sciences monocyte COX‐2 Neuropharmacology PGE‐synthase Pharmacology. Drug treatments platelet COX‐1 Prostaglandins - biosynthesis whole blood |
| title | Effects of acetaminophen on constitutive and inducible prostanoid biosynthesis in human blood cells |
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