title: The role of oxidative DNA damage and GSTM1, GSTT1, and hOGG1 gene polymorphisms in coronary artery disease risk.
abstract: Atherosclerotic coronary artery disease (CAD) appears to be a multifactorial process caused by the interaction of environmental risk factors with multiple predisposing genes. Therefore, in this study we aimed to determine the role of oxidative DNA damage and some variations in glutathione S-transferase (GSTM1 and GSTT1) and DNA repair (hOGG1) genes in CAD risk.
  
  
  
  A case-control study was conducted on 59 individuals who had undergone coronary angiographic evaluation. Of these, 29 were patients diagnosed with CAD (mean age =61.5±10.3) and 30 were controls examined for reasons other than suspected CAD and who had angiographically documented normal coronary arteries (mean age =60.4±11.6). Basal DNA damage as well as pyrimidine and purine base damage were evaluated in peripheral blood lymphocytes using the modified comet assay. Polymerase chain reaction-restriction length polymorphism (PCR-RFLP)-based assay was used for genotyping.
  
  
  
  Basal DNA damage levels in patients [9.16 (3.26)] were significantly higher than those in controls [7.59 (3.23); p=0.017], and basal DNA and pyrimidine base damage levels were significantly correlated with disease severity based on Gensini scoring (r=0.352, p=0.006; r=0.318, p=0.014, respectively). However, no significant differences were observed in terms of oxidized DNA bases between patients and controls. The frequencies of studied genotypes (GSTM1, GSTT1, and hOGG1) were similar between groups.
  
  
  
  The results of this study pointed out the role of DNA damage in CAD and its severity. However, GSTM1, GSTT1, and hOGG1 gene polymorphisms seemed to have no effect on individual susceptibility for disease progression.
authors.affiliation: Department of Toxicology, Faculty of Pharmacy, Gazi University, Ankara-Turkey. ela@gazi.edu.tr.
authors.forename: Ela
authors.initials: E
authors.lastname: Kadıoğlu
authors.affiliation: Department of Cardiology, Faculty of Medicine, Gazi University, Ankara-Turkey.
authors.forename: Gülten
authors.initials: G
authors.lastname: Taçoy
authors.affiliation: Department of Toxicology, Faculty of Pharmacy, İstanbul University, İstanbul-Turkey.
authors.forename: Eren
authors.initials: E
authors.lastname: Özçağlı
authors.affiliation: Department of Cardiology, Medical School, Başkent University, Ankara-Turkey.
authors.forename: Kaan
authors.initials: K
authors.lastname: Okyay
authors.affiliation: Department of Cardiology, Türkiye Yüksek İhtisas Training and Research Hospital, Ankara-Turkey.
authors.forename: Mehmet K
authors.initials: MK
authors.lastname: Akboğa
authors.affiliation: Department Cardiology, Faculty of Medicine, Gazi University, Ankara-Turkey.
authors.forename: Atiye
authors.initials: A
authors.lastname: Çengel
authors.affiliation: Department of Toxicology, Faculty of Pharmacy, Marmara University, İstanbul-Turkey.
authors.forename: Semra
authors.initials: S
authors.lastname: Şardaş
mesh_terms: D000328:Adult; D016022:Case-Control Studies; D003324:Coronary Artery Disease / Q000235:genetics*; D004249:DNA Damage; D045647:DNA Glycosylases / Q000235:genetics; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D005982:Glutathione Transferase / Q000235:genetics; D006801:Humans; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress; D011110:Polymorphism, Genetic; D012307:Risk Factors
chemical_list: D045647:DNA Glycosylases; D005982:Glutathione Transferase; C413545:glutathione S-transferase T1; C479058:oxoguanine glycosylase 1, human