The Role of Polymorphisms Within Paraoxonases (192 Gln/Arg in PON1 and 311Ser/Cys in PON2) in the Modulation of Cardiovascular Risk: A Pilot Study

被引:42
作者
Gluba, Anna [2 ]
Pietrucha, Tadeusz
Banach, Maciej [1 ]
Piotrowski, Grzegorz [3 ]
Rysz, Jacek [2 ]
机构
[1] Med Univ Lodz, Dept Hypertens, PL-90549 Lodz, Poland
[2] Med Univ Lodz, Dept Nephrol Hypertens & Family Med, PL-90549 Lodz, Poland
[3] M Kopernik Prov Specialist Hosp Lodz, Dept Cardiol, Lodz, Poland
关键词
cardiovascular disease; cholesterol profile; paraoxonase; polymorphisms; gene; HIGH-DENSITY-LIPOPROTEIN; CORONARY-ARTERY-DISEASE; LECITHIN-CHOLESTEROL ACYLTRANSFERASE; MYOCARDIAL-INFARCTION RISK; APOLIPOPROTEIN-A-I; HEART-DISEASE; FAMILIAL HYPERCHOLESTEROLEMIA; GLN-ARG192; POLYMORPHISM; GENE POLYMORPHISMS; PARENTAL HISTORY;
D O I
10.1177/0003319709351258
中图分类号
R6 [外科学];
学科分类号
1002 ; 100210 ;
摘要
Paraoxonases (PONs) may exert anti-atherogenic action by reducing lipid peroxidation. We evaluated the influence of 2 polymorphisms within PON1 (192 Gln/Arg) and PON2 (311 Ser/Cys) genes in 407 young Poles: 273 patients who experienced a first myocardial infarction (MI) under the age of 45 (study group) and 134 healthy volunteers (control group) with a HEART Score <= 2 (low risk). Paraoxonase 1 polymorphism 192Gln/Arg influenced the risk of premature MI (P=.0054). A positive family history of coronary artery disease (CAD) was associated with the 192Arg allele (P=.0107). The association between PON1 genotype 192 Gln/Arg) and low-density lipoprotein cholesterol (LDL-C) (P=.036) levels was also observed. However, we did not find any relationship between polymorphism 311Ser/Cys and CAD risk (P=.418). PON1 polymorphism 192Gln/Arg influenced the risk of premature MI. The association between PON1 genotype ( 192 Gln/Arg) and serum LDL-C levels may be explained by PON participation in reverse cholesterol transport.
引用
收藏
页码:157 / 165
页数:9
相关论文
共 67 条
[1]  
[Anonymous], [No title captured], DOI 10.1053/eurj.2000.2305
[2]  
[Anonymous], 1989, Molecular Cloning: A Laboratory
[3]   The Gln-Arg191 polymorphism of the human paraoxonase gene (HUMPONA) is not associated with the risk of coronary artery disease in Finns [J].
Antikainen, M ;
Murtomaki, S ;
Syvanne, M ;
Pahlman, R ;
Tahvanainen, E ;
Jauhiainen, M ;
Frick, MH ;
Ehnholm, C .
JOURNAL OF CLINICAL INVESTIGATION, 1996, 98 (04) :883-885
[4]   Human serum paraoxonases (PON1) Q and R selectively decrease lipid peroxides in human coronary and carotid atherosclerotic lesions - PON1 esterase and peroxidase-like activities [J].
Aviram, M ;
Hardak, E ;
Vaya, J ;
Mahmood, S ;
Milo, S ;
Hoffman, A ;
Billicke, S ;
Draganov, D ;
Rosenblat, M .
CIRCULATION, 2000, 101 (21) :2510-2517
[5]   Paraoxonase active site required for protection against LDL oxidation involves its free sulfhydryl group and is different from that required for its arylesterase/paraoxonase activities - Selective action of human paraoxonase allozymes Q and R [J].
Aviram, M ;
Billecke, S ;
Sorenson, R ;
Bisgaier, C ;
Newton, R ;
Rosenblat, M ;
Erogul, J ;
Hsu, C ;
Dunlop, C ;
La Du, B .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 1998, 18 (10) :1617-1624
[6]   Paraoxonase inhibits high-density lipoprotein oxidation and preserves its functions - A possible peroxidative role for paraoxonase [J].
Aviram, M ;
Rosenblat, M ;
Bisgaier, CL ;
Newton, RS ;
Primo-Parmo, SL ;
La Du, BN .
JOURNAL OF CLINICAL INVESTIGATION, 1998, 101 (08) :1581-1590
[7]  
Bielecka-Dabrowa A, 2009, EXPERT OPIN THER TAR, V13, P307, DOI [10.1517/14728220902725149, 10.1517/14728220902725149 ]
[8]  
Bielicki JK, 1999, J LIPID RES, V40, P948
[9]   IDENTIFICATION OF A DISTINCT HUMAN HIGH-DENSITY-LIPOPROTEIN SUBSPECIES DEFINED BY A LIPOPROTEIN-ASSOCIATED PROTEIN, K-45 - IDENTITY OF K-45 WITH PARAOXONASE [J].
BLATTER, MC ;
JAMES, RW ;
MESSMER, S ;
BARJA, F ;
POMETTA, D .
EUROPEAN JOURNAL OF BIOCHEMISTRY, 1993, 211 (03) :871-879
[10]   Parental history of myocardial infarction: lipid traits, gene polymorphisms and lifestyle [J].
Boer, JMA ;
Feskens, EJM ;
Kuivenhoven, JA ;
Schouten, EG ;
Havekes, LM ;
Kastelein, JJP ;
Seidell, JC ;
Kromhout, D .
ATHEROSCLEROSIS, 2001, 155 (01) :149-156