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.
Methods and 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.