Browsing by Author "Cam, SF"

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    The G894T polymorphism on endothelial nitric oxide synthase gene is associated with premature coronary artery disease in a Turkish population
    Cam, SF; Sekuri, C; Tengiz, I; Ercan, E; Sagcan, A; Akin, M; Berdeli, A
    Introduction: The aim of the present study was to investigate the association between premature coronary artery disease and Glu298Asp polymorphism of the endothelial nitric oxide synthase gene. Materials and methods: The eNOS gene polymorphism was analysed in 115 (mean age, 48.1 +/- 7.9 years) Turkish patients with a diagnosis of premature coronary artery disease and 83 (mean age, 44.6 +/- 1.4 years) control subjects. The Glu298Asp polymorphism of the endothelial nitric oxide synthase gene was determined by polymerase chain reaction and restriction fragment length polymorphism. Results: The patients group showed an increase in the frequency of the T allele compared to controls (0.456 versus 0.169, p=0.0001). There was a significant association between the TT genotype and premature coronary artery disease [eNOS TT vs. TG and GG; OR=17.000 (CI 95% 3.952-73.125, p=0.0001)]. The eNOS T/G genotypes were not associated with the number of affected vessels (p > 0.05). In addition, the family history of premature coronary artery disease, smoking, diabetes, obesity, dyslipidemia and eNOS TT genotype were independent risk factors of coronary artery disease. The patients with eNOS TT genotype had 15 fold risk of coronary artery disease compared with the control group [OR= I 5,356(Cl 95%3.262-77.289, p=0.001)]. Conclusions: These results suggest that premature coronary artery disease is associated with the Glu298Asp polymorphism of the endothelial nitric oxide synthase gene in our population. (c) 2004 Elsevier Ltd. All rights reserved.
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    The relationship between paraoxanase gene Leu-Met (55) and Gln-Arg (192) polymorphisms and coronary artery disease
    Taskiran, P; Cam, SF; Sekuri, C; Tuzun, N; Alioglu, E; Altintas, N; Berdeli, A
    Objectives: Paraoxonase (PON1) is a high-density lipoprotein (HDL)-associated esterase that hydrolyses lipoperoxides. PON1 serves as a protective factor against oxidative modification of LDL, suggesting that it may play an important role in the prevention of atherosclerotic process. Research has focused on two polymorphisms: leucine (L allele) to methionine (M allele) substitution at codon 55, and glutamine (A allele) to arginine (B allele) substitution at codon 192. Study design: We examined amino acid changes at codon 55 and 192 in the PON1 gene by polymerase chain reaction and using restriction enzymes in 120 patients (92 men, 28 women; mean age 48.2 +/- 4.3 years) with premature coronary artery disease (CAD) and in 102 healthy subjects (80 men, 22 women; mean age 46.8 +/- 5.2 years) with no history of CAD and a normal electrocardiogram. Results: Distribution of genotypes in the patient and control groups at codon 55 was 6.7% and 4.9% for MM, 46.7% and 29.4% for LM, 46.7% and 65.7% for LL, respectively. The frequencies of genotypes at codon 192 were as follows: 4.2% and 2% for RR, 40% and 35.3% for QR, and 55.8% and 62.8% for QQ, respectively. While the frequency of PON1 55M allele was higher in the CAD group (0.3 vs. 0.2), PON1 192R allele frequency did not differ (0.2). There was a significant relationship between the PON1 M/L55 polymorphism and CAD (p=0.017), whereas the R/Q192 polymorphism was not associated with CAD (p=0.445). Conclusion: These data suggest that the PON1 M/L55 polymorphism shows a significant relationship with CAD and the Q/R192 polymorphism is not a major risk factor causing susceptibility to CAD in our population.