The relationship between paraoxanase gene Leu-Met (55) and Gln-Arg (192) polymorphisms and coronary artery disease.]

Yazan: admin Tarih: Şub 3rd, 2010 | Kategori:: Paraoxanase gene

Turk Kardiyol Dern Ars. 2009;37(7):473-478.

Taşkıran P, Cam SF, Sekuri C, Tüzün N, Alioğlu E, Altıntaş N, Berdeli A.

Department of Medical Biology and Genetics, Medicine Faculty of Celal Bayar University, Manisa, Turkey.

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 were 6.7% and 4.9% for MM, 46.7% and 29.4% for LM, 46.7% and 65.7% for LL, respectively. The frequency 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 (p>0.05). 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.


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Association of Serotonin 2A Receptor and Lack of Association of CYP1A2 Gene Polymorphism with Tardive Dyskinesia in a Turkish Population

Yazan: admin Tarih: Nis 22nd, 2009 | Kategori:: Tardive Dyskinesia
To cite this paper:
Omer Boke, Sezgin Gunes, Nurten Kara, Servet Aker, Ahmet Rifat Sahin, Yildiz Basar, Hasan Bagci. DNA and Cell Biology. August 2007, 26(8): 527-531. doi:10.1089/dna.2007.0605.

Full Text: • PDF for printing (73.7 KB) • PDF w/ links (114.4 KB)

Omer Boke

Department of Psychiatry, Faculty of Medicine, Ondokuz Mayis University, Samsun, Turkey.
Sezgin Gunes

Department of Medical Biology and Genetics, Faculty of Medicine, Ondokuz Mayis University, Samsun, Turkey.
Nurten Kara

Department of Medical Biology and Genetics, Faculty of Medicine, Ondokuz Mayis University, Samsun, Turkey.
Servet Aker

Department of Public Health, Faculty of Medicine, Ondokuz Mayis University, Samsun, Turkey.
Ahmet Rifat Sahin

Department of Psychiatry, Faculty of Medicine, Ondokuz Mayis University, Samsun, Turkey.
Yildiz Basar

Psikotem Private Psychiatry Center, Samsun, Turkey.
Hasan Bagci

Department of Medical Biology and Genetics, Faculty of Medicine, Ondokuz Mayis University, Samsun, Turkey.

The aim of this study was to investigate the possible association of serotonin 2A receptor gene (HTR2A) −1438 G/A polymorphism and CYP1A2 gene 163C/A polymorphism with tardive dyskinesia (TD) in a Turkish population. A total of 47 patients with persistent TD, 80 patients who were consistently without TD, and 100 healthy controls were included in this study. The polymorphic regions of −1438 G/A polymorphism of HTR2A receptor gene (rs6311) and 163C/A of CYP1A2 (rs762551) gene were amplified using polymerase chain reaction (PCR), followed by digestion with restriction enzymes MspI and Bsp1201. Genotype and allele frequencies were calculated by the χ2-test. Crude and adjusted odds ratios (ORs) were estimated, and 95% confidence intervals (CIs) were computed by multivariate logistic regression analysis. The genotype and allele frequencies of HTR2A and CYP1A2 gene were similar in schizophrenia with TD, schizophrenia without TD, and healthy controls. The logistic regression analysis showed that cumulative exposure to antipsychotic drugs for every year (p = 0.003; OR = 1.15; CI = 1.07–1.23), and AA genotype of HTR2A gene (p = 0.0258; OR = 4.34; CI = 1.19–15.81) are risk factors for TD. The same logistic regression model showed no association between CYP1A2 polymorphism and TD. The results of the present study seem to indicate that HTR2A gene polymorphism influences the tendency to express TD following prolonged antipsychotic drug exposure in Turkish schizophrenia patients.


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