title: Paraoxonase gene Q192R & L55M polymorphisms in Indians with acute myocardial infarction & association with oxidized low density lipoprotein.
abstract: OBJECTIVE
  Paraoxonase (PON) is an HDL associated ester hydrolase with an ability to retard LDL oxidation in vitro by preventing lipid peroxide generation. The population variability in enzyme activity is attributed to polymorphisms in paraoxonase gene. For example, polymorphism at codon 192 and 55 of the paraoxonase gene has been reported to be associated with coronary heart disease (CAD) and diabetes among different ethnic groups. The present study looks at PON192 and 55 polymorphism among hospitalized Asian Indian patients with myocardial infarction (MI) and their association with circulating oxidized LDL and antioxidant status.
  
  
  METHODS
  One hundred and twenty four consecutive patients of acute myocardial infarction and 221 age-matched controls were recruited for the study. Oxidized LDL was measured in serum by ELISA and total antioxidant levels by the 2,2'-azino-bis-(3 ethyl benzothiozoline-6-sulfonate) (ABTS) method. Other known cardiovascular risk factors, apolipoprotein B, apolipoproteinA1, lipoprotein(a), hsCRP and homocysteine were also measured. Paraoxonase gene polymorphism at codon 192 and 55 were analyzed by PCR-RFLP.
  
  
  RESULTS
  Patients with MI had significantly higher oxidized LDL (P<0.05) and lower total antioxidant capacity (P<0.001) as compared to controls. Oxidized LDL correlated with total cholesterol, LDL and Apo B in patients. B allele frequency of the codon 192 polymorphism in paraoxonase gene was higher in cases as compared to controls and odds ratio of developing the MI with BB genotype versus AA genotype was 2.37, (P=0.044). Codon 55 polymorphism in paraoxonase gene was not associated with CAD. There was no difference in oxidized LDL between the different genotypes of PON192 and PON55.
  
  
  CONCLUSIONS
  Although PON192 polymorphism was associated with CAD, no correlation of PON192 or 55 polymorphism was found with oxidized LDL suggesting that presence of other antioxidant factors may be of equal importance in preventing LDL oxidation.
authors.affiliation: Departments of Cardiac Biochemistry , All India Institute of Medical Sciences, New Delhi, India. lakshmy_ram@yahoo.com
authors.forename: Ramakrishnan
authors.initials: R
authors.lastname: Lakshmy
authors.forename: Dilawar
authors.initials: D
authors.lastname: Ahmad
authors.forename: Rani Ann
authors.initials: RA
authors.lastname: Abraham
authors.forename: Mukta
authors.initials: M
authors.lastname: Sharma
authors.forename: Kranthi
authors.initials: K
authors.lastname: Vemparala
authors.forename: Siuli
authors.initials: S
authors.lastname: Das
authors.forename: K Srinath
authors.initials: KS
authors.lastname: Reddy
authors.forename: Dorairaj
authors.initials: D
authors.lastname: Prabhakaran
mesh_terms: D043303:Aryldialkylphosphatase / Q000235:genetics*; D001483:Base Sequence; D017931:DNA Primers; D006801:Humans; D008077:Lipoproteins, LDL / Q000097:blood*; D009203:Myocardial Infarction / Q000097:blood / Q000235:genetics*; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D012150:Polymorphism, Restriction Fragment Length
chemical_list: D017931:DNA Primers; D008077:Lipoproteins, LDL; C099252:oxidized low density lipoprotein; D043303:Aryldialkylphosphatase