{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,26]],"date-time":"2025-10-26T20:35:53Z","timestamp":1761510953717},"reference-count":33,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"9","content-domain":{"domain":["ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[1995,9]]},"abstract":"<jats:p>\n            <jats:italic>Abstract<\/jats:italic>\n            The effects of paracetamol and sodium salicylate on the susceptibility of LDL to oxidative modification were studied. LDL was subjected to Cu\n            <jats:sup>2+<\/jats:sup>\n            -, azo compound\u2013, or peripheral blood mononuclear cell\u2013initiated oxidation in the absence and presence of paracetamol and salicylate. Paracetamol (100 \u03bcmol\/L; 25 \u03bcg LDL\/mL) reduced the rate of formation of conjugated dienes and the amount of conjugated dienes formed during Cu\n            <jats:sup>2+<\/jats:sup>\n            -induced oxidation by 67% and 58%, respectively. Paracetamol (400 \u03bcmol\/L; 100 \u03bcg LDL\/mL) reduced the generation of lipid peroxides during Cu\n            <jats:sup>2+<\/jats:sup>\n            -induced oxidation by 43% (\n            <jats:italic>P<\/jats:italic>\n            &lt;.05), the relative electrophoretic mobility in agarose gels by 16% (\n            <jats:italic>P<\/jats:italic>\n            &lt;.05), and the amount of oxidized LDL taken up by J774 macrophages by 22% (\n            <jats:italic>P<\/jats:italic>\n            &lt;.05). Paracetamol (100 \u03bcmol\/L; 100 \u03bcg LDL\/mL) reduced the 2,2\u2032-azobis-(2-amidinopropane hydrochloride)\u2013initiated lipid peroxidation by 70% (\n            <jats:italic>P<\/jats:italic>\n            &lt;.05) and the relative electrophoretic mobility by 34% (\n            <jats:italic>P<\/jats:italic>\n            &lt;.05). Paracetamol (100 \u03bcmol\/L; 100 \u03bcg LDL\/mL) reduced the amount of lipid peroxides generated in LDL during mononuclear cell\u2013mediated oxidation by 69% (\n            <jats:italic>P<\/jats:italic>\n            &lt;.01) and the relative electrophoretic mobility by 38% (\n            <jats:italic>P<\/jats:italic>\n            &lt;.01). In comparison, 10 \u03bcmol\/L \u03b1-tocopherol reduced the amount of lipid peroxides formed during cellular LDL oxidation and the relative electrophoretic mobility by 52% and 65%, respectively (\n            <jats:italic>P<\/jats:italic>\n            &lt;.05). In the absence of paracetamol, SOD and catalase inhibited the modification of LDL (\n            <jats:italic>P<\/jats:italic>\n            &lt;.05), suggesting that superoxide anions and hydrogen peroxide might be involved in the cell-mediated modification pathway. In the presence of paracetamol, SOD showed no additional inhibitory effect. The 1,1-diphenyl-2-pikrylhydracyl radical\u2013scavenging test showed that paracetamol itself was a free-radical scavenger. In contrast, sodium salicylate (25 to 4000 \u03bcmol\/L) showed no free radical\u2013scavenging property and failed to protect LDL against mononuclear cell\u2013mediated oxidation. In conclusion, the results indicate that paracetamol, but not salicylate, protects LDL against Cu\n            <jats:sup>2+<\/jats:sup>\n            -induced, azo compound\u2013initiated, and mononuclear cell\u2013mediated oxidative modification in vitro and that this may be due to the radical scavenger capacity of paracetamol.\n          <\/jats:p>","DOI":"10.1161\/01.atv.15.9.1338","type":"journal-article","created":{"date-parts":[[2011,6,17]],"date-time":"2011-06-17T19:44:19Z","timestamp":1308339859000},"page":"1338-1344","update-policy":"http:\/\/dx.doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":30,"title":["Paracetamol Inhibits Copper Ion\u2013Induced, Azo Compound\u2013Initiated, and Mononuclear Cell\u2013Mediated Oxidative Modification of LDL"],"prefix":"10.1161","volume":"15","author":[{"given":"Marit S.","family":"Nenseter","sequence":"first","affiliation":[{"name":"From the Institute for Nutrition Research (M.S.N., B.H., C.A.D.) and the Department of Pharmacology, Institute of Pharmacy (\u00d8.R., A.C.R.), University of Oslo, Oslo, Norway."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bente","family":"Halvorsen","sequence":"additional","affiliation":[{"name":"From the Institute for Nutrition Research (M.S.N., B.H., C.A.D.) and the Department of Pharmacology, Institute of Pharmacy (\u00d8.R., A.C.R.), University of Oslo, Oslo, Norway."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"\u00d8yvind","family":"Rosvold","sequence":"additional","affiliation":[{"name":"From the Institute for Nutrition Research (M.S.N., B.H., C.A.D.) and the Department of Pharmacology, Institute of Pharmacy (\u00d8.R., A.C.R.), University of Oslo, Oslo, Norway."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Arild C.","family":"Rustan","sequence":"additional","affiliation":[{"name":"From the Institute for Nutrition Research (M.S.N., B.H., C.A.D.) and the Department of Pharmacology, Institute of Pharmacy (\u00d8.R., A.C.R.), University of Oslo, Oslo, Norway."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Christian A.","family":"Drevon","sequence":"additional","affiliation":[{"name":"From the Institute for Nutrition Research (M.S.N., B.H., C.A.D.) and the Department of Pharmacology, Institute of Pharmacy (\u00d8.R., A.C.R.), University of Oslo, Oslo, Norway."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM198904063201407"},{"key":"e_1_3_2_2_2","doi-asserted-by":"crossref","unstructured":"Witztum JL. 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