title: [The relationship between paraoxanase gene Leu-Met (55) and Gln-Arg (192) polymorphisms and coronary artery disease].
abstract: OBJECTIVE
  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.
  
  
  METHODS
  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).
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Medical Biology and Genetics, Medicine Faculty of Celal Bayar University, Manisa, Turkey.
authors.forename: Pinar
authors.initials: P
authors.lastname: Taşkiran
authors.forename: Sirri F
authors.initials: SF
authors.lastname: Cam
authors.forename: Cevat
authors.initials: C
authors.lastname: Sekuri
authors.forename: Nurullah
authors.initials: N
authors.lastname: Tüzün
authors.forename: Emin
authors.initials: E
authors.lastname: Alioğlu
authors.forename: Nuray
authors.initials: N
authors.lastname: Altintaş
authors.forename: Afig
authors.initials: A
authors.lastname: Berdeli
mesh_terms: D000328:Adult; D019943:Amino Acid Substitution; D001120:Arginine / Q000235:genetics; D043303:Aryldialkylphosphatase / Q000235:genetics*; D003062:Codon / Q000235:genetics; D003327:Coronary Disease / Q000201:enzymology / Q000235:genetics*; D017931:DNA Primers; D005260:Female; D005787:Gene Frequency; D005838:Genotype; D005973:Glutamine / Q000235:genetics; D006801:Humans; D007930:Leucine / Q000235:genetics; D008297:Male; D008715:Methionine / Q000235:genetics; D008875:Middle Aged; D011110:Polymorphism, Genetic
chemical_list: D003062:Codon; D017931:DNA Primers; D005973:Glutamine; D001120:Arginine; D008715:Methionine; D043303:Aryldialkylphosphatase; D007930:Leucine