Ciprofibrate treatment in patients with atherogenic lipoprotein phenotype : effects on HDL quality, LDL susceptibility to oxidation and DNA damage
This study was conducted to examine a complex effect of ciprofibrate therapy in patients with atherogenic lipoprotein phenotype. Effects of ciprofibrate were studied on HDL subpopulations, HDL ability to esterify cholesterol (FER(HDL)), susceptibility of LDL to oxidation as well as on in vivo oxidat...
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| Veröffentlicht in: | European journal of clinical pharmacology 1998-11, Vol.54 (9-10), p.697-699 |
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| creator | RASLOVA, K DOBIASOVA, M NAGYOVA, A FABRY, R RAUCHOVA, H DUSINSKA, M |
| description | This study was conducted to examine a complex effect of ciprofibrate therapy in patients with atherogenic lipoprotein phenotype.
Effects of ciprofibrate were studied on HDL subpopulations, HDL ability to esterify cholesterol (FER(HDL)), susceptibility of LDL to oxidation as well as on in vivo oxidative DNA damage in peripheral lymphocytes, measured as strand breaks (SBs) by the comet assay.
Ciprofibrate treatment significantly decreased total cholesterol, and triglycerides, and increased HDL-cholesterol. The FER(HDL) showed a significant reduction (29.5+/-7.4 to 23+/-7.5% x h(-1), P=0.0001). The relative concentrations of HDL subclasses did not differ between baseline and after treatment. Ciprofibrate induced a significant increase in LDL oxidation lag time (93+/-7 to 102=11 min, P=0.02) and a decrease in DNA strand breaks (34.0+/-16.2 to 17.8+/-7.5, P=0.02). A significant correlation between maximal rate of diene production and strand breaks was found (r=0.55, P=0.01). These findings may be explained by an improvement of LDL resistance to oxidation, resulting in a decrease in oxidatively modified LDL's cytotoxic effect.
Ciprofibrate treatment favourably affected the quality of plasma HDL, probably by the improvement of triglyceride rich lipoprotein metabolism and/or LDL subpopulation profile, increased LDL resistance to oxidation, and decreased the level of DNA damage in peripheral lymphocytes. |
| doi_str_mv | 10.1007/s002280050537 |
| format | Article |
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Effects of ciprofibrate were studied on HDL subpopulations, HDL ability to esterify cholesterol (FER(HDL)), susceptibility of LDL to oxidation as well as on in vivo oxidative DNA damage in peripheral lymphocytes, measured as strand breaks (SBs) by the comet assay.
Ciprofibrate treatment significantly decreased total cholesterol, and triglycerides, and increased HDL-cholesterol. The FER(HDL) showed a significant reduction (29.5+/-7.4 to 23+/-7.5% x h(-1), P=0.0001). The relative concentrations of HDL subclasses did not differ between baseline and after treatment. Ciprofibrate induced a significant increase in LDL oxidation lag time (93+/-7 to 102=11 min, P=0.02) and a decrease in DNA strand breaks (34.0+/-16.2 to 17.8+/-7.5, P=0.02). A significant correlation between maximal rate of diene production and strand breaks was found (r=0.55, P=0.01). These findings may be explained by an improvement of LDL resistance to oxidation, resulting in a decrease in oxidatively modified LDL's cytotoxic effect.
Ciprofibrate treatment favourably affected the quality of plasma HDL, probably by the improvement of triglyceride rich lipoprotein metabolism and/or LDL subpopulation profile, increased LDL resistance to oxidation, and decreased the level of DNA damage in peripheral lymphocytes.</description><identifier>ISSN: 0031-6970</identifier><identifier>EISSN: 1432-1041</identifier><identifier>DOI: 10.1007/s002280050537</identifier><identifier>PMID: 9923570</identifier><language>eng</language><publisher>Heidelberg: Springer</publisher><subject>Arteriosclerosis - genetics ; Biological and medical sciences ; Cholesterol ; Ciprofibrate ; Clofibric Acid - analogs & derivatives ; Clofibric Acid - therapeutic use ; Comet assay ; Cytotoxicity ; Deoxyribonucleic acid ; DNA ; DNA Damage ; Female ; Fibric Acids ; General and cellular metabolism. Vitamins ; Genotype & phenotype ; Humans ; Hypolipidemic Agents - therapeutic use ; Kinetics ; Lipid metabolism ; Lipoproteins ; Lipoproteins (high density) ; Lipoproteins (low density) ; Lipoproteins - genetics ; Lipoproteins, HDL - blood ; Lipoproteins, HDL - genetics ; Lipoproteins, LDL - blood ; Lipoproteins, LDL - genetics ; Lymphocytes ; Lymphocytes - drug effects ; Lymphocytes - metabolism ; Male ; Medical sciences ; Middle Aged ; Oxidation ; Oxidation-Reduction ; Pharmacology. Drug treatments ; Phenotype ; Triglycerides</subject><ispartof>European journal of clinical pharmacology, 1998-11, Vol.54 (9-10), p.697-699</ispartof><rights>1999 INIST-CNRS</rights><rights>Springer-Verlag Berlin Heidelberg 1998</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c378t-ef93a2a89828eb8f749f8d0801fda813d9ac5a8347dbb978ae515c6f95dd5e523</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1655973$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9923570$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>RASLOVA, K</creatorcontrib><creatorcontrib>DOBIASOVA, M</creatorcontrib><creatorcontrib>NAGYOVA, A</creatorcontrib><creatorcontrib>FABRY, R</creatorcontrib><creatorcontrib>RAUCHOVA, H</creatorcontrib><creatorcontrib>DUSINSKA, M</creatorcontrib><title>Ciprofibrate treatment in patients with atherogenic lipoprotein phenotype : effects on HDL quality, LDL susceptibility to oxidation and DNA damage</title><title>European journal of clinical pharmacology</title><addtitle>Eur J Clin Pharmacol</addtitle><description>This study was conducted to examine a complex effect of ciprofibrate therapy in patients with atherogenic lipoprotein phenotype.
Effects of ciprofibrate were studied on HDL subpopulations, HDL ability to esterify cholesterol (FER(HDL)), susceptibility of LDL to oxidation as well as on in vivo oxidative DNA damage in peripheral lymphocytes, measured as strand breaks (SBs) by the comet assay.
Ciprofibrate treatment significantly decreased total cholesterol, and triglycerides, and increased HDL-cholesterol. The FER(HDL) showed a significant reduction (29.5+/-7.4 to 23+/-7.5% x h(-1), P=0.0001). The relative concentrations of HDL subclasses did not differ between baseline and after treatment. Ciprofibrate induced a significant increase in LDL oxidation lag time (93+/-7 to 102=11 min, P=0.02) and a decrease in DNA strand breaks (34.0+/-16.2 to 17.8+/-7.5, P=0.02). A significant correlation between maximal rate of diene production and strand breaks was found (r=0.55, P=0.01). These findings may be explained by an improvement of LDL resistance to oxidation, resulting in a decrease in oxidatively modified LDL's cytotoxic effect.
Ciprofibrate treatment favourably affected the quality of plasma HDL, probably by the improvement of triglyceride rich lipoprotein metabolism and/or LDL subpopulation profile, increased LDL resistance to oxidation, and decreased the level of DNA damage in peripheral lymphocytes.</description><subject>Arteriosclerosis - genetics</subject><subject>Biological and medical sciences</subject><subject>Cholesterol</subject><subject>Ciprofibrate</subject><subject>Clofibric Acid - analogs & derivatives</subject><subject>Clofibric Acid - therapeutic use</subject><subject>Comet assay</subject><subject>Cytotoxicity</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA Damage</subject><subject>Female</subject><subject>Fibric Acids</subject><subject>General and cellular metabolism. Vitamins</subject><subject>Genotype & phenotype</subject><subject>Humans</subject><subject>Hypolipidemic Agents - therapeutic use</subject><subject>Kinetics</subject><subject>Lipid metabolism</subject><subject>Lipoproteins</subject><subject>Lipoproteins (high density)</subject><subject>Lipoproteins (low density)</subject><subject>Lipoproteins - genetics</subject><subject>Lipoproteins, HDL - blood</subject><subject>Lipoproteins, HDL - genetics</subject><subject>Lipoproteins, LDL - blood</subject><subject>Lipoproteins, LDL - genetics</subject><subject>Lymphocytes</subject><subject>Lymphocytes - drug effects</subject><subject>Lymphocytes - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Oxidation</subject><subject>Oxidation-Reduction</subject><subject>Pharmacology. Drug treatments</subject><subject>Phenotype</subject><subject>Triglycerides</subject><issn>0031-6970</issn><issn>1432-1041</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNpdkcFu1DAQhiMEKtvCkSOSJThwIDCO47XNrdoWirSCC5yjSTzuusrGqe0I9jV4YrzqCgSn8cx8889Yf1W94PCOA6j3CaBpNIAEKdSjasVb0dQcWv64WgEIXq-NgqfVeUp3AFwaEGfVmTGNkApW1a-Nn2Nwvo-YieVImPc0ZeYnNmP25ZnYD593DPOOYrilyQ9s9HMoU5mO1I6mkA8zsQ-MnKOhDISJ3Vxt2f2Co8-Ht2xbkrSkgebse3-ssRxY-OltWVFgnCy7-nLJLO7xlp5VTxyOiZ6f4kX1_eP1t81Nvf366fPmclsPQulckzMCG9RGN5p67VRrnLaggTuLmgtrcJCoRats3xulkSSXw9oZaa0k2YiL6s2DbvnK_UIpd3tfbhxHnCgsqeONlmDKLlnQV_-hd2GJU7nuSK1V27aNLlT9QA0xpBTJdXP0e4yHjkN39Kr7x6vCvzypLv2e7B_6ZE7pvz71MQ04uojT4NNf0bWURgnxG6bhnMk</recordid><startdate>19981101</startdate><enddate>19981101</enddate><creator>RASLOVA, K</creator><creator>DOBIASOVA, M</creator><creator>NAGYOVA, A</creator><creator>FABRY, R</creator><creator>RAUCHOVA, H</creator><creator>DUSINSKA, M</creator><general>Springer</general><general>Springer Nature B.V</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>7RV</scope><scope>7TK</scope><scope>7U9</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>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7TM</scope></search><sort><creationdate>19981101</creationdate><title>Ciprofibrate treatment in patients with atherogenic lipoprotein phenotype : effects on HDL quality, LDL susceptibility to oxidation and DNA damage</title><author>RASLOVA, K ; DOBIASOVA, M ; NAGYOVA, A ; FABRY, R ; RAUCHOVA, H ; DUSINSKA, M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c378t-ef93a2a89828eb8f749f8d0801fda813d9ac5a8347dbb978ae515c6f95dd5e523</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Arteriosclerosis - genetics</topic><topic>Biological and medical sciences</topic><topic>Cholesterol</topic><topic>Ciprofibrate</topic><topic>Clofibric Acid - analogs & derivatives</topic><topic>Clofibric Acid - therapeutic use</topic><topic>Comet assay</topic><topic>Cytotoxicity</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA Damage</topic><topic>Female</topic><topic>Fibric Acids</topic><topic>General and cellular metabolism. Vitamins</topic><topic>Genotype & phenotype</topic><topic>Humans</topic><topic>Hypolipidemic Agents - therapeutic use</topic><topic>Kinetics</topic><topic>Lipid metabolism</topic><topic>Lipoproteins</topic><topic>Lipoproteins (high density)</topic><topic>Lipoproteins (low density)</topic><topic>Lipoproteins - genetics</topic><topic>Lipoproteins, HDL - blood</topic><topic>Lipoproteins, HDL - genetics</topic><topic>Lipoproteins, LDL - blood</topic><topic>Lipoproteins, LDL - genetics</topic><topic>Lymphocytes</topic><topic>Lymphocytes - drug effects</topic><topic>Lymphocytes - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Oxidation</topic><topic>Oxidation-Reduction</topic><topic>Pharmacology. Drug treatments</topic><topic>Phenotype</topic><topic>Triglycerides</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>RASLOVA, K</creatorcontrib><creatorcontrib>DOBIASOVA, M</creatorcontrib><creatorcontrib>NAGYOVA, A</creatorcontrib><creatorcontrib>FABRY, R</creatorcontrib><creatorcontrib>RAUCHOVA, H</creatorcontrib><creatorcontrib>DUSINSKA, M</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>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS 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>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</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical 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>Nucleic Acids Abstracts</collection><jtitle>European journal of clinical pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>RASLOVA, K</au><au>DOBIASOVA, M</au><au>NAGYOVA, A</au><au>FABRY, R</au><au>RAUCHOVA, H</au><au>DUSINSKA, M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ciprofibrate treatment in patients with atherogenic lipoprotein phenotype : effects on HDL quality, LDL susceptibility to oxidation and DNA damage</atitle><jtitle>European journal of clinical pharmacology</jtitle><addtitle>Eur J Clin Pharmacol</addtitle><date>1998-11-01</date><risdate>1998</risdate><volume>54</volume><issue>9-10</issue><spage>697</spage><epage>699</epage><pages>697-699</pages><issn>0031-6970</issn><eissn>1432-1041</eissn><abstract>This study was conducted to examine a complex effect of ciprofibrate therapy in patients with atherogenic lipoprotein phenotype.
Effects of ciprofibrate were studied on HDL subpopulations, HDL ability to esterify cholesterol (FER(HDL)), susceptibility of LDL to oxidation as well as on in vivo oxidative DNA damage in peripheral lymphocytes, measured as strand breaks (SBs) by the comet assay.
Ciprofibrate treatment significantly decreased total cholesterol, and triglycerides, and increased HDL-cholesterol. The FER(HDL) showed a significant reduction (29.5+/-7.4 to 23+/-7.5% x h(-1), P=0.0001). The relative concentrations of HDL subclasses did not differ between baseline and after treatment. Ciprofibrate induced a significant increase in LDL oxidation lag time (93+/-7 to 102=11 min, P=0.02) and a decrease in DNA strand breaks (34.0+/-16.2 to 17.8+/-7.5, P=0.02). A significant correlation between maximal rate of diene production and strand breaks was found (r=0.55, P=0.01). These findings may be explained by an improvement of LDL resistance to oxidation, resulting in a decrease in oxidatively modified LDL's cytotoxic effect.
Ciprofibrate treatment favourably affected the quality of plasma HDL, probably by the improvement of triglyceride rich lipoprotein metabolism and/or LDL subpopulation profile, increased LDL resistance to oxidation, and decreased the level of DNA damage in peripheral lymphocytes.</abstract><cop>Heidelberg</cop><cop>Berlin</cop><pub>Springer</pub><pmid>9923570</pmid><doi>10.1007/s002280050537</doi><tpages>3</tpages></addata></record> |
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| ispartof | European journal of clinical pharmacology, 1998-11, Vol.54 (9-10), p.697-699 |
| issn | 0031-6970 1432-1041 |
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| subjects | Arteriosclerosis - genetics Biological and medical sciences Cholesterol Ciprofibrate Clofibric Acid - analogs & derivatives Clofibric Acid - therapeutic use Comet assay Cytotoxicity Deoxyribonucleic acid DNA DNA Damage Female Fibric Acids General and cellular metabolism. Vitamins Genotype & phenotype Humans Hypolipidemic Agents - therapeutic use Kinetics Lipid metabolism Lipoproteins Lipoproteins (high density) Lipoproteins (low density) Lipoproteins - genetics Lipoproteins, HDL - blood Lipoproteins, HDL - genetics Lipoproteins, LDL - blood Lipoproteins, LDL - genetics Lymphocytes Lymphocytes - drug effects Lymphocytes - metabolism Male Medical sciences Middle Aged Oxidation Oxidation-Reduction Pharmacology. Drug treatments Phenotype Triglycerides |
| title | Ciprofibrate treatment in patients with atherogenic lipoprotein phenotype : effects on HDL quality, LDL susceptibility to oxidation and DNA damage |
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