A preliminary study of human paraoxonase and PON 1 L/M 55-PON 1 Q/R 192 polymorphisms in Turkish patients with coronary artery disease

dc.contributor.authorKaman, Dilara
dc.contributor.authorIlhan, Necip
dc.contributor.authorMetin, Kerem
dc.contributor.authorAkbulut, Mehmet
dc.contributor.authorUstundag, Bilal
dc.date.accessioned2026-08-12T17:14:04Z
dc.date.issued2009
dc.departmentFırat Üniversitesi
dc.description.abstractParaoxonase 1 (PON 1) is a high-density lipoprotein (HDL)-associated enzyme with antioxidant function protecting low-density lipoprotein (LDL) from oxidation. PON 1 has two amino acid polymorphisms in coding region; L/M 55 and Q/R 192. These polymorphisms modulate paraoxonase activity of the enzyme. PON 1 activity decreases in coronary artery disease (CAD). In the present study, distribution of PON 1 L/M 55 and Q/R 192 polymorphisms and the effect of these polymorphisms on the activities of PON 1, and on the severity of CAD in 277 CAD (+) patient and 92 CAD (-) subjects were examined. PON 1 L/M 55 and Q/R 192 genotypes were determined by PCR, RFLP and agarose gel electrophoresis techniques. Genotype distributions and allele frequencies for PON 1 Q/R 192 polymorphism were not significantly different between controls and CAD (+) patient group (p > 0.05), but in genotype and allele distribution of PON 1 L/M55 polymorphism, there was significantly difference among groups (p < 0.05). Genotype distributions for both polymorphisms were not significantly different between subgroups of single-vessel disease (SVD), double-vessel disease (DVD) and triple-vessel disease (TVD). Serum PON 1 activity was lower in CAD (+) group than in controls and this was also statistically significant (p < 0.001). In both groups, the highest PON activities were detected in LL and RR genotypes. In summary, our results suggest that there is an association between the PON 1 L/M 55 polymorphism of paraoxonase and CAD in Turkish patients but not with PON 1 Q/R 192 polymorphism. However, it is hard to correlate these polymorphisms and severity of CAD. Copyright (C) 2009 John Wiley & Sons, Ltd.
dc.identifier.doi10.1002/cbf.1539
dc.identifier.endpage92
dc.identifier.issn0263-6484
dc.identifier.issue2
dc.identifier.orcid0000-0001-9997-0418
dc.identifier.orcid0000-0001-9629-7002
dc.identifier.orcid0000-0001-6621-2450
dc.identifier.pmid19226538
dc.identifier.scopus2-s2.0-63149105505
dc.identifier.scopusqualityQ3
dc.identifier.startpage88
dc.identifier.urihttps://doi.org/10.1002/cbf.1539
dc.identifier.urihttps://hdl.handle.net/11508/51656
dc.identifier.volume27
dc.identifier.wosWOS:000264118100005
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherJohn Wiley & Sons Ltd
dc.relation.ispartofCell Biochemistry and Function
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_WoS_20260511
dc.subjectparaoxonase
dc.subjectcoronary artery disease
dc.subjectpolymorphism
dc.titleA preliminary study of human paraoxonase and PON 1 L/M 55-PON 1 Q/R 192 polymorphisms in Turkish patients with coronary artery disease
dc.typeArticle

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