title: Association between serum paraoxonase activity and oxidative stress in acute coronary syndromes.
abstract: OBJECTIVE
  The oxidation of low-density lipoprotein (LDL) is believed to have a central role in atherogenesis. Under oxidative stress not only LDL, but all other serum lipids are exposed to oxidation. High-density lipoprotein (HDL)-associated paraoxonase (PON1) was shown to inhibit LDL and HDL oxidation. We investigated the relationship between PON1 and oxidative stress in acute myocardial infarction and unstable angina in a comparative fashion.
  
  
  RESULTS
  Activities of PON1, concentrations of malondialdehyde (MDA), lipids and lipoproteins were measured in patients (38 subjects with acute myocardial infarction and 33 subjects with unstable angina pectoris) and in age- and sex-matched controls (32 subjects). Serum PONI activity was significantly lower in patients than in controls (p < 0.001). Patients had significantly increased serum MDA concentrations (p < 0.001) and there were strong negative correlations (p < 0.001) between serum PON1 and MDA levels in the acute myocardial infarction group (r = -0.673), in the unstable angina pectoris group (r = -0.868) and in healthy controls (r = -0.778). Serum HDL-cholesterol (HDL-C) concentrations were lower in patients than controls (p < 0.05). No correlation was observed between PON1 and HDL-C levels in patients or controls. Apo A I concentrations were significantly lower in the patient groups (p < 0.01), but were insignificant between patients with AMI and UAP. Apo A-I and PON1 levels did not show any correlation. Apo B concentrations were lowest in the healthy controls, higher in the UAPgroup and highest in the AMI group (p < 0.001). In the acute myocardial infarction group LDL/apo B ratio was lower than in healthy controls and in the UAP group, suggesting smaller LDL particle size.
  
  
  CONCLUSIONS
  Results of this study indicate that lower serum PON1 activity is associated with oxidative stress and the activity of PON1 is not related to HDL-cholesterol.
authors.affiliation: Department of Clinical Biochemistry, Ege University, School of Medicine, Bornova, Izmir, Turkey.
authors.forename: Ceyda
authors.initials: C
authors.lastname: Kabaroglu
authors.forename: Işil
authors.initials: I
authors.lastname: Mutaf
authors.forename: Bahar
authors.initials: B
authors.lastname: Boydak
authors.forename: Dilek
authors.initials: D
authors.lastname: Ozmen
authors.forename: Sara
authors.initials: S
authors.lastname: Habif
authors.forename: Dilek
authors.initials: D
authors.lastname: Erdener
authors.forename: Zuhal
authors.initials: Z
authors.lastname: Parildar
authors.forename: Oya
authors.initials: O
authors.lastname: Bayindir
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000789:Angina, Unstable / Q000097:blood / Q000378:metabolism*; D043303:Aryldialkylphosphatase / Q000097:blood*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000378:metabolism*; D018384:Oxidative Stress; D013577:Syndrome
chemical_list: D043303:Aryldialkylphosphatase