Reactive aldehyde-scavenging enzyme activities in atherosclerotic plaques of cigarette smokers and nonsmokers

Abstract Objective : To investigate enzymatic reactive aldehyde-scavenging enzyme capacity together with lipid peroxidation as expression of oxidative stress in atherosclerotic plaques of cigarette smokers and nonsmokers. Methods : We have assessed specific enzymatic activities of class 1, 2, and 3...

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Veröffentlicht in:Atherosclerosis 2015-02, Vol.238 (2), p.190-194
Hauptverfasser: Lapenna, Domenico, Ciofani, Giuliano, Ucchino, Sante, Giamberardino, Maria Adele, Di Ilio, Carmine, Cuccurullo, Franco
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container_end_page 194
container_issue 2
container_start_page 190
container_title Atherosclerosis
container_volume 238
creator Lapenna, Domenico
Ciofani, Giuliano
Ucchino, Sante
Giamberardino, Maria Adele
Di Ilio, Carmine
Cuccurullo, Franco
description Abstract Objective : To investigate enzymatic reactive aldehyde-scavenging enzyme capacity together with lipid peroxidation as expression of oxidative stress in atherosclerotic plaques of cigarette smokers and nonsmokers. Methods : We have assessed specific enzymatic activities of class 1, 2, and 3 aldehyde dehydrogenase (ALDH1, ALDH2, and ALDH3, respectively), glutathione S -transferase (isozyme A4-4, GSTA4-4), and aldose reductase (AR), namely the major reactive aldehyde-scavenging enzymes, together with lipid peroxidation, i.e., fluorescent damage products of lipid peroxidation (FDPL), in carotid atherosclerotic plaques surgically removed from 17 cigarette smokers and 17 nonsmokers. Results : The enzymatic activities of ALDH1 plus ALDH2, ALDH3, GSTA4-4, and AR were significantly lower in the atherosclerotic plaques of smokers than in those of nonsmokers, while plaque FDPL levels were significantly higher in the smokers than in the nonsmokers. The amount of cigarette smoking was correlated inversely with the aforementioned plaque enzymatic activities and directly with plaque FDPL content. Plaque FDPL levels were inversely correlated with plaque enzymatic activities in smokers and nonsmokers. The degree of carotid atherosclerotic stenosis, as expression of atherosclerosis severity, was correlated inversely with plaque enzymatic activities and directly with plaque FDPL levels in smokers and nonsmokers; moreover, the degree of carotid stenosis was directly correlated with the amount of cigarette smoking. Conclusion : atherosclerotic lesions of cigarette smokers are endowed with a depressed enzymatic reactive aldehyde-scavenging capacity eventually favoring oxidative stress and the severity of atherosclerosis.
doi_str_mv 10.1016/j.atherosclerosis.2014.11.028
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Methods : We have assessed specific enzymatic activities of class 1, 2, and 3 aldehyde dehydrogenase (ALDH1, ALDH2, and ALDH3, respectively), glutathione S -transferase (isozyme A4-4, GSTA4-4), and aldose reductase (AR), namely the major reactive aldehyde-scavenging enzymes, together with lipid peroxidation, i.e., fluorescent damage products of lipid peroxidation (FDPL), in carotid atherosclerotic plaques surgically removed from 17 cigarette smokers and 17 nonsmokers. Results : The enzymatic activities of ALDH1 plus ALDH2, ALDH3, GSTA4-4, and AR were significantly lower in the atherosclerotic plaques of smokers than in those of nonsmokers, while plaque FDPL levels were significantly higher in the smokers than in the nonsmokers. The amount of cigarette smoking was correlated inversely with the aforementioned plaque enzymatic activities and directly with plaque FDPL content. Plaque FDPL levels were inversely correlated with plaque enzymatic activities in smokers and nonsmokers. The degree of carotid atherosclerotic stenosis, as expression of atherosclerosis severity, was correlated inversely with plaque enzymatic activities and directly with plaque FDPL levels in smokers and nonsmokers; moreover, the degree of carotid stenosis was directly correlated with the amount of cigarette smoking. Conclusion : atherosclerotic lesions of cigarette smokers are endowed with a depressed enzymatic reactive aldehyde-scavenging capacity eventually favoring oxidative stress and the severity of atherosclerosis.</description><identifier>ISSN: 0021-9150</identifier><identifier>EISSN: 1879-1484</identifier><identifier>DOI: 10.1016/j.atherosclerosis.2014.11.028</identifier><identifier>PMID: 25528427</identifier><language>eng</language><publisher>Ireland: Elsevier Ireland Ltd</publisher><subject>Aged ; Aldehyde dehydrogenase ; Aldehyde Dehydrogenase - analysis ; Aldehyde Dehydrogenase, Mitochondrial ; Aldehyde Reductase - analysis ; Aldose reductase ; Atherosclerosis ; Atherosclerotic plaques ; Biomarkers - analysis ; Cardiovascular ; Carotid Arteries - enzymology ; Carotid Arteries - pathology ; Carotid Arteries - surgery ; Carotid Artery Diseases - diagnosis ; Carotid Artery Diseases - enzymology ; Carotid Artery Diseases - etiology ; Carotid Artery Diseases - surgery ; Cigarette smoke ; Down-Regulation ; Female ; Glutathione S-transferase ; Glutathione Transferase - analysis ; Humans ; Isoenzymes - analysis ; Lipid Peroxidation ; Male ; Middle Aged ; Oxidative Stress ; Plaque, Atherosclerotic ; Prognosis ; Reactive aldehydes ; Retinal Dehydrogenase - analysis ; Severity of Illness Index ; Smoking - adverse effects</subject><ispartof>Atherosclerosis, 2015-02, Vol.238 (2), p.190-194</ispartof><rights>Elsevier Ireland Ltd</rights><rights>2014 Elsevier Ireland Ltd</rights><rights>Copyright © 2014 Elsevier Ireland Ltd. 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Methods : We have assessed specific enzymatic activities of class 1, 2, and 3 aldehyde dehydrogenase (ALDH1, ALDH2, and ALDH3, respectively), glutathione S -transferase (isozyme A4-4, GSTA4-4), and aldose reductase (AR), namely the major reactive aldehyde-scavenging enzymes, together with lipid peroxidation, i.e., fluorescent damage products of lipid peroxidation (FDPL), in carotid atherosclerotic plaques surgically removed from 17 cigarette smokers and 17 nonsmokers. Results : The enzymatic activities of ALDH1 plus ALDH2, ALDH3, GSTA4-4, and AR were significantly lower in the atherosclerotic plaques of smokers than in those of nonsmokers, while plaque FDPL levels were significantly higher in the smokers than in the nonsmokers. The amount of cigarette smoking was correlated inversely with the aforementioned plaque enzymatic activities and directly with plaque FDPL content. Plaque FDPL levels were inversely correlated with plaque enzymatic activities in smokers and nonsmokers. The degree of carotid atherosclerotic stenosis, as expression of atherosclerosis severity, was correlated inversely with plaque enzymatic activities and directly with plaque FDPL levels in smokers and nonsmokers; moreover, the degree of carotid stenosis was directly correlated with the amount of cigarette smoking. 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Ciofani, Giuliano ; Ucchino, Sante ; Giamberardino, Maria Adele ; Di Ilio, Carmine ; Cuccurullo, Franco</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c444t-f9b83f35c4576e3293dd47e97c0fdbc35e3ef5bb06954d5e4831ddc4ed5b0eb13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Aged</topic><topic>Aldehyde dehydrogenase</topic><topic>Aldehyde Dehydrogenase - analysis</topic><topic>Aldehyde Dehydrogenase, Mitochondrial</topic><topic>Aldehyde Reductase - analysis</topic><topic>Aldose reductase</topic><topic>Atherosclerosis</topic><topic>Atherosclerotic plaques</topic><topic>Biomarkers - analysis</topic><topic>Cardiovascular</topic><topic>Carotid Arteries - enzymology</topic><topic>Carotid Arteries - pathology</topic><topic>Carotid Arteries - surgery</topic><topic>Carotid Artery Diseases - diagnosis</topic><topic>Carotid Artery Diseases - enzymology</topic><topic>Carotid Artery Diseases - etiology</topic><topic>Carotid Artery Diseases - surgery</topic><topic>Cigarette smoke</topic><topic>Down-Regulation</topic><topic>Female</topic><topic>Glutathione S-transferase</topic><topic>Glutathione Transferase - analysis</topic><topic>Humans</topic><topic>Isoenzymes - analysis</topic><topic>Lipid Peroxidation</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Oxidative Stress</topic><topic>Plaque, Atherosclerotic</topic><topic>Prognosis</topic><topic>Reactive aldehydes</topic><topic>Retinal Dehydrogenase - analysis</topic><topic>Severity of Illness Index</topic><topic>Smoking - adverse effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lapenna, Domenico</creatorcontrib><creatorcontrib>Ciofani, Giuliano</creatorcontrib><creatorcontrib>Ucchino, Sante</creatorcontrib><creatorcontrib>Giamberardino, Maria Adele</creatorcontrib><creatorcontrib>Di Ilio, Carmine</creatorcontrib><creatorcontrib>Cuccurullo, Franco</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Atherosclerosis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lapenna, Domenico</au><au>Ciofani, Giuliano</au><au>Ucchino, Sante</au><au>Giamberardino, Maria Adele</au><au>Di Ilio, Carmine</au><au>Cuccurullo, Franco</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Reactive aldehyde-scavenging enzyme activities in atherosclerotic plaques of cigarette smokers and nonsmokers</atitle><jtitle>Atherosclerosis</jtitle><addtitle>Atherosclerosis</addtitle><date>2015-02-01</date><risdate>2015</risdate><volume>238</volume><issue>2</issue><spage>190</spage><epage>194</epage><pages>190-194</pages><issn>0021-9150</issn><eissn>1879-1484</eissn><abstract>Abstract Objective : To investigate enzymatic reactive aldehyde-scavenging enzyme capacity together with lipid peroxidation as expression of oxidative stress in atherosclerotic plaques of cigarette smokers and nonsmokers. 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The degree of carotid atherosclerotic stenosis, as expression of atherosclerosis severity, was correlated inversely with plaque enzymatic activities and directly with plaque FDPL levels in smokers and nonsmokers; moreover, the degree of carotid stenosis was directly correlated with the amount of cigarette smoking. Conclusion : atherosclerotic lesions of cigarette smokers are endowed with a depressed enzymatic reactive aldehyde-scavenging capacity eventually favoring oxidative stress and the severity of atherosclerosis.</abstract><cop>Ireland</cop><pub>Elsevier Ireland Ltd</pub><pmid>25528427</pmid><doi>10.1016/j.atherosclerosis.2014.11.028</doi><tpages>5</tpages></addata></record>
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subjects Aged
Aldehyde dehydrogenase
Aldehyde Dehydrogenase - analysis
Aldehyde Dehydrogenase, Mitochondrial
Aldehyde Reductase - analysis
Aldose reductase
Atherosclerosis
Atherosclerotic plaques
Biomarkers - analysis
Cardiovascular
Carotid Arteries - enzymology
Carotid Arteries - pathology
Carotid Arteries - surgery
Carotid Artery Diseases - diagnosis
Carotid Artery Diseases - enzymology
Carotid Artery Diseases - etiology
Carotid Artery Diseases - surgery
Cigarette smoke
Down-Regulation
Female
Glutathione S-transferase
Glutathione Transferase - analysis
Humans
Isoenzymes - analysis
Lipid Peroxidation
Male
Middle Aged
Oxidative Stress
Plaque, Atherosclerotic
Prognosis
Reactive aldehydes
Retinal Dehydrogenase - analysis
Severity of Illness Index
Smoking - adverse effects
title Reactive aldehyde-scavenging enzyme activities in atherosclerotic plaques of cigarette smokers and nonsmokers
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