Potentially reduced exposure cigarettes accelerate atherosclerosis: evidence for the role of nicotine
The tobacco industry markets potentially reduced exposure products (PREPs) as less harmful or addictive alternatives to conventional cigarettes. This study compared the effects of mainstream smoke from Quest, Eclipse, and 2R4F reference cigarettes on the development of atherosclerosis in apolipoprot...
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Veröffentlicht in: | Cardiovascular toxicology 2007-09, Vol.7 (3), p.192-201 |
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creator | Catanzaro, Daniel F Zhou, Ying Chen, Rong Yu, Fangmin Catanzaro, Sarah E De Lorenzo, Mariana S Subbaramaiah, Kotha Zhou, Xi Kathy Pratico, Domenico Dannenberg, Andrew J Weksler, Babette B |
description | The tobacco industry markets potentially reduced exposure products (PREPs) as less harmful or addictive alternatives to conventional cigarettes. This study compared the effects of mainstream smoke from Quest, Eclipse, and 2R4F reference cigarettes on the development of atherosclerosis in apolipoprotein E-deficient (apoE -/-) mice. Mice were exposed to smoke from four cigarette types for 12 weeks beginning at age of 12 weeks, and in a separate study for 8 weeks, beginning at age of 8 weeks. In both studies, mice exposed to smoke from high-nicotine, high-tar Quest 1, and 2R4F cigarettes developed greater areas of lipid-rich aortic lesions than did non-smoking controls. Exposure to smoke from the lower-nicotine products, Eclipse, and Quest 3, was associated with smaller lesion areas, but animals exposed to smoke from all of the tested types of cigarette had larger lesions than did control animals not exposed to smoke. Urinary levels of isoprostane F2 alpha VI, increased proportionally to cigarette nicotine yield, whereas induction of pulmonary cytochrome P4501A1 was proportional to tar yield. Lesion area was associated with both nicotine and tar yields, although in multiple regression analysis only nicotine was a significant predictor of lesion area. Smoke exposure did not alter systolic blood pressure (SBP), heart rate (HR), blood cholesterol, or leukocyte count. Taken together, these observations suggest that smoking may accelerate atherosclerosis by increasing oxidative stress mediated at least in part via the actions of nicotine. |
doi_str_mv | 10.1007/s12012-007-0027-z |
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This study compared the effects of mainstream smoke from Quest, Eclipse, and 2R4F reference cigarettes on the development of atherosclerosis in apolipoprotein E-deficient (apoE -/-) mice. Mice were exposed to smoke from four cigarette types for 12 weeks beginning at age of 12 weeks, and in a separate study for 8 weeks, beginning at age of 8 weeks. In both studies, mice exposed to smoke from high-nicotine, high-tar Quest 1, and 2R4F cigarettes developed greater areas of lipid-rich aortic lesions than did non-smoking controls. Exposure to smoke from the lower-nicotine products, Eclipse, and Quest 3, was associated with smaller lesion areas, but animals exposed to smoke from all of the tested types of cigarette had larger lesions than did control animals not exposed to smoke. Urinary levels of isoprostane F2 alpha VI, increased proportionally to cigarette nicotine yield, whereas induction of pulmonary cytochrome P4501A1 was proportional to tar yield. Lesion area was associated with both nicotine and tar yields, although in multiple regression analysis only nicotine was a significant predictor of lesion area. Smoke exposure did not alter systolic blood pressure (SBP), heart rate (HR), blood cholesterol, or leukocyte count. Taken together, these observations suggest that smoking may accelerate atherosclerosis by increasing oxidative stress mediated at least in part via the actions of nicotine.</description><identifier>ISSN: 1530-7905</identifier><identifier>EISSN: 1559-0259</identifier><identifier>DOI: 10.1007/s12012-007-0027-z</identifier><identifier>PMID: 17901562</identifier><language>eng</language><publisher>United States: Springer Nature B.V</publisher><subject>Administration, Inhalation ; Animals ; Aorta - drug effects ; Aorta - pathology ; Apolipoproteins E - deficiency ; Apolipoproteins E - genetics ; Atherosclerosis ; Azo Compounds - chemistry ; Cigarettes ; Coloring Agents - chemistry ; Coronary Artery Disease - etiology ; Coronary Artery Disease - metabolism ; Coronary Artery Disease - pathology ; Cotinine - urine ; Cytochrome P-450 CYP1A1 - metabolism ; Gene Silencing ; Lung - drug effects ; Lung - enzymology ; Male ; Medical research ; Mice ; Mice, Knockout ; Nicotine ; Nicotine - toxicity ; Nicotine - urine ; Oxidative Stress ; Regression analysis ; Smoking - adverse effects ; Tars - analysis ; Tobacco Products</subject><ispartof>Cardiovascular toxicology, 2007-09, Vol.7 (3), p.192-201</ispartof><rights>Humana Press, Inc. 2007</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c357t-6f7de142ce476f16c2db96537668719364044c11f7a4c822a80befbe621714403</citedby><cites>FETCH-LOGICAL-c357t-6f7de142ce476f16c2db96537668719364044c11f7a4c822a80befbe621714403</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17901562$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Catanzaro, Daniel F</creatorcontrib><creatorcontrib>Zhou, Ying</creatorcontrib><creatorcontrib>Chen, Rong</creatorcontrib><creatorcontrib>Yu, Fangmin</creatorcontrib><creatorcontrib>Catanzaro, Sarah E</creatorcontrib><creatorcontrib>De Lorenzo, Mariana S</creatorcontrib><creatorcontrib>Subbaramaiah, Kotha</creatorcontrib><creatorcontrib>Zhou, Xi Kathy</creatorcontrib><creatorcontrib>Pratico, Domenico</creatorcontrib><creatorcontrib>Dannenberg, Andrew J</creatorcontrib><creatorcontrib>Weksler, Babette B</creatorcontrib><title>Potentially reduced exposure cigarettes accelerate atherosclerosis: evidence for the role of nicotine</title><title>Cardiovascular toxicology</title><addtitle>Cardiovasc Toxicol</addtitle><description>The tobacco industry markets potentially reduced exposure products (PREPs) as less harmful or addictive alternatives to conventional cigarettes. This study compared the effects of mainstream smoke from Quest, Eclipse, and 2R4F reference cigarettes on the development of atherosclerosis in apolipoprotein E-deficient (apoE -/-) mice. Mice were exposed to smoke from four cigarette types for 12 weeks beginning at age of 12 weeks, and in a separate study for 8 weeks, beginning at age of 8 weeks. In both studies, mice exposed to smoke from high-nicotine, high-tar Quest 1, and 2R4F cigarettes developed greater areas of lipid-rich aortic lesions than did non-smoking controls. Exposure to smoke from the lower-nicotine products, Eclipse, and Quest 3, was associated with smaller lesion areas, but animals exposed to smoke from all of the tested types of cigarette had larger lesions than did control animals not exposed to smoke. Urinary levels of isoprostane F2 alpha VI, increased proportionally to cigarette nicotine yield, whereas induction of pulmonary cytochrome P4501A1 was proportional to tar yield. Lesion area was associated with both nicotine and tar yields, although in multiple regression analysis only nicotine was a significant predictor of lesion area. Smoke exposure did not alter systolic blood pressure (SBP), heart rate (HR), blood cholesterol, or leukocyte count. Taken together, these observations suggest that smoking may accelerate atherosclerosis by increasing oxidative stress mediated at least in part via the actions of nicotine.</description><subject>Administration, Inhalation</subject><subject>Animals</subject><subject>Aorta - drug effects</subject><subject>Aorta - pathology</subject><subject>Apolipoproteins E - deficiency</subject><subject>Apolipoproteins E - genetics</subject><subject>Atherosclerosis</subject><subject>Azo Compounds - chemistry</subject><subject>Cigarettes</subject><subject>Coloring Agents - chemistry</subject><subject>Coronary Artery Disease - etiology</subject><subject>Coronary Artery Disease - metabolism</subject><subject>Coronary Artery Disease - pathology</subject><subject>Cotinine - urine</subject><subject>Cytochrome P-450 CYP1A1 - metabolism</subject><subject>Gene Silencing</subject><subject>Lung - drug effects</subject><subject>Lung - enzymology</subject><subject>Male</subject><subject>Medical research</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Nicotine</subject><subject>Nicotine - toxicity</subject><subject>Nicotine - urine</subject><subject>Oxidative Stress</subject><subject>Regression analysis</subject><subject>Smoking - adverse effects</subject><subject>Tars - analysis</subject><subject>Tobacco Products</subject><issn>1530-7905</issn><issn>1559-0259</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqFkU1r3DAQhkVIyFf7A3opIofe3GjGsiT3Fpa2KQSSQ3oWWnncOnitrSSHJL--MrsQyCWH0bxonhmkeRn7BOIrCKEvE6AArIosgbp6OWCn0DRtJbBpDxddi0q3ojlhZyk9FAZRNcfsBMolNApPGd2FTFMe3Dg-80jd7Knj9LQNaY7E_fDHRcqZEnfe00jRZeIu_6UYkh-Xc0jfOD0OHU2eeB8iL0Uew0g89HwafMjDRB_YUe_GRB_3-Zz9_vH9fnVd3dz-_LW6uql83ehcqV53BBI9Sa16UB67dauaWitlNLS1kkJKD9BrJ71BdEasqV-TQtAgpajP2Zfd3G0M_2ZK2W6GVN49uonCnKwyNUqB8C6IwhgFYAp48QZ8CHOcyies0a3SWBssEOwgXxaSIvV2G4eNi88WhF2csjun7CIXp-xL6fm8HzyvN9S9duytqf8DxFyO7w</recordid><startdate>200709</startdate><enddate>200709</enddate><creator>Catanzaro, Daniel F</creator><creator>Zhou, Ying</creator><creator>Chen, Rong</creator><creator>Yu, Fangmin</creator><creator>Catanzaro, Sarah E</creator><creator>De Lorenzo, Mariana S</creator><creator>Subbaramaiah, Kotha</creator><creator>Zhou, Xi Kathy</creator><creator>Pratico, Domenico</creator><creator>Dannenberg, Andrew J</creator><creator>Weksler, Babette B</creator><general>Springer Nature B.V</general><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>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7U7</scope><scope>C1K</scope><scope>7X8</scope></search><sort><creationdate>200709</creationdate><title>Potentially reduced exposure cigarettes accelerate atherosclerosis: evidence for the role of nicotine</title><author>Catanzaro, Daniel F ; 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This study compared the effects of mainstream smoke from Quest, Eclipse, and 2R4F reference cigarettes on the development of atherosclerosis in apolipoprotein E-deficient (apoE -/-) mice. Mice were exposed to smoke from four cigarette types for 12 weeks beginning at age of 12 weeks, and in a separate study for 8 weeks, beginning at age of 8 weeks. In both studies, mice exposed to smoke from high-nicotine, high-tar Quest 1, and 2R4F cigarettes developed greater areas of lipid-rich aortic lesions than did non-smoking controls. Exposure to smoke from the lower-nicotine products, Eclipse, and Quest 3, was associated with smaller lesion areas, but animals exposed to smoke from all of the tested types of cigarette had larger lesions than did control animals not exposed to smoke. Urinary levels of isoprostane F2 alpha VI, increased proportionally to cigarette nicotine yield, whereas induction of pulmonary cytochrome P4501A1 was proportional to tar yield. Lesion area was associated with both nicotine and tar yields, although in multiple regression analysis only nicotine was a significant predictor of lesion area. Smoke exposure did not alter systolic blood pressure (SBP), heart rate (HR), blood cholesterol, or leukocyte count. Taken together, these observations suggest that smoking may accelerate atherosclerosis by increasing oxidative stress mediated at least in part via the actions of nicotine.</abstract><cop>United States</cop><pub>Springer Nature B.V</pub><pmid>17901562</pmid><doi>10.1007/s12012-007-0027-z</doi><tpages>10</tpages></addata></record> |
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subjects | Administration, Inhalation Animals Aorta - drug effects Aorta - pathology Apolipoproteins E - deficiency Apolipoproteins E - genetics Atherosclerosis Azo Compounds - chemistry Cigarettes Coloring Agents - chemistry Coronary Artery Disease - etiology Coronary Artery Disease - metabolism Coronary Artery Disease - pathology Cotinine - urine Cytochrome P-450 CYP1A1 - metabolism Gene Silencing Lung - drug effects Lung - enzymology Male Medical research Mice Mice, Knockout Nicotine Nicotine - toxicity Nicotine - urine Oxidative Stress Regression analysis Smoking - adverse effects Tars - analysis Tobacco Products |
title | Potentially reduced exposure cigarettes accelerate atherosclerosis: evidence for the role of nicotine |
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