title: APE1 and XRCC3 polymorphisms and myocardial infarction.
abstract: BACKGROUND
  In most cells, DNA is regularly damaged by mutagens. Different DNA repair mechanisms operate on specific types of damaged DNA. When DNA damage resulting from free radicals is not repaired, it might lead to deteriorated gene expression, the development of a number of diseases such as cancer, diabetes, vascular diseases, and aging. In the present study, APE1 and XRCC3 gene polymorphisms were investigated in patients with myocardial infarction.
  
  
  METHODS
  Forty-five first time elective coronary artery bypass grafting (CABG) patients with cardiopulmonary bypass (CPB) and 40 healthy individuals were studied. Gene polymorphisms were determined by a polymerase chain reaction-restriction fragment length polymorphism method.
  
  
  RESULTS
  For the APE1 gene, the AG genotype was significantly higher in the patient group than in the control group. The patient group had significantly more G carriers but there was no statistically significant difference between patient and control groups the A allele. The XRCC3 TT genotype was found to be significantly more frequent in the patient group than it was in the control group.
  
  
  CONCLUSIONS
  The results of our study suggested that the XRCC3 gene TT genotype and the APE1 gene AG genotype might increase the risk of myocardial infarcts.
authors: Department of Molecular Medicine, The Institute of Experimental Medicine, Istanbul University, Capa-Istanbul, Turkey.
authors: Atike
authors: A
authors: Tekeli
authors: Selim
authors: S
authors: Isbir
authors: Arzu
authors: A
authors: Ergen
authors: Uzay
authors: U
authors: Görmüş
authors: Nilüfer
authors: N
authors: Bozkurt
authors: Ozlem
authors: O
authors: Timirci
authors: Sinan
authors: S
authors: Arsan
authors: Turgay
authors: T
authors: Isbir
mesh_terms: D000483:Alleles; D016022:Case-Control Studies; D001026:Coronary Artery Bypass; D017931:DNA Primers / Q000737:chemistry; D004260:DNA Repair; D043603:DNA-(Apurinic or Apyrimidinic Site) Lyase / Q000235:genetics* / Q000502:physiology*; D004268:DNA-Binding Proteins / Q000235:genetics* / Q000502:physiology*; D005838:Genotype; D006579:Heterozygote; D006720:Homozygote; D006801:Humans; D009203:Myocardial Infarction / Q000235:genetics* / Q000473:pathology*; D010641:Phenotype; D011110:Polymorphism, Genetic; D012306:Risk
chemical_list: D017931:DNA Primers; D004268:DNA-Binding Proteins; C110901:X-ray repair cross complementing protein 3; C085108:APEX1 protein, human; D043603:DNA-(Apurinic or Apyrimidinic Site) Lyase