Paraoxonase and arylesterase activities in patients with cardiac syndrome X, and their relationship with oxidative stress markers

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Abstract

Objectives

Paraoxonase-1 is a high-density lipoprotein-associated enzyme with three activities, which are paraoxonase, arylesterase and dyazoxonase. Paraoxonase-1 was shown to decrease in patients with cardiovascular diseases. We aimed to examine serum paraoxonase and arylesterase activities, and their relation with oxidative stress markers such as lipid hydroperoxide and total antioxidant status in patients with cardiac syndrome X.

Methods

Forty-one consecutive patients with cardiac syndrome X (CSX group), 33 consecutive patients without cardiac syndrome X (non-cardiac syndrome X group) and 20 healthy volunteers as control group were taken into the study. Serum paraoxonase and arylesterase activities were measured spectrophotometrically. Lipid hydroperoxide levels were measured by ferrous oxidation with xylenol orange assay. Total antioxidant status was determined using an automated measurement method.

Results

Basal paraoxonase, salt-stimulated paraoxonase and arylesterase activities were significantly lower in patients with cardiac syndrome X than those of the non-cardiac syndrome X and control groups (P<0.001, for both). Moreover, lipid hydroperoxide was found at high level, and total antioxidant status was found at low level in patients with cardiac syndrome X than control and non-cardiac syndrome X groups (P<0.001, for all). In patients with cardiac syndrome X, in multiple linear regression analysis, both paraoxonase and arylesterase activities were independently correlated with lipid hydroperoxide levels (P=0.001, P=0.003, respectively), and also arylesterase activity was independently correlated with magnitude of ST depression (P=0.002).

Conclusion

Reduced paraoxonase and arylesterase activities and total antioxidant status levels and enhanced lipid hydroperoxide levels in patients with cardiac syndrome X might indicate increased oxidative stress that can play a role in pathogenesis of cardiac syndrome X.

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