SULM – Schweizerische Union für Labormedizin | Union Suisse de Médecine de Laboratoire | Swiss Union of Laboratory Medicine

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Z FLEGAR-MESTRIC1 , D VRHOVSKI-HEBRANG1 , D JURETIC2 , S PERKOV1 , V PREDEN-KEREKOVIC1 , A HEBRANG3 , A VIDJAK3 , D ODAK3 , A GRGA4

1Clinical Hospital Merkur, Institute of Clinical Chemistry, Zagreb, Croatia, 2Faculty of Pharmacy and Biochemistry, Department of Medical Biochemistry and Hematology, Zagreb, Croatia, 3Clinical Hospital Merkur, Clinical Department for Diagnostic and Clinical Radiology, Zagreb, Croatia, 4Clinical Hospital Merkur, Department of Surgery, Division of Vascular Surgery, Zagreb, Croatia

Objective. Human serum paraoxonase [(PON1); (aryldialkylphosphatase (EC 3.1.8.1)] is a serum esterase which is associated with high density lipoprotein particles (HDL). The decreased PON1 activity has been found associated with an increased risk of coronary artery disease. The aim of this study was to examine the human serum PON1 activities in relation to angiographically established stenosis of cerebral arteries in comparison to the control group.
Methods. A total of 119 patients, mean age of 66 years (range 31-83 years), with stenosis of extracranial cerebral arteries of more than 50%, established angiographically was studied. The control group consisted of 87 apparently healthy individuals, mean age of 64 years (range 44-82 years), with normal cerebral arteries on ultrasound examination. Serum total cholesterol and triacylglycerol were measured by enzymatic PAP-method. HDL-cholesterol was measured directly based on selective inhibition of the non-HDL fractions by means of polyanions. A homogeneous assay for the selective measurement of LDL-cholesterol in serum was used. Basal and NaCl-stimulated paraoxonase activities were determined by measuring the rate of paraoxon hydrolysis at 37 °C, based on the change of absorbance at 410 nm. All measurements were performed on the Olympus AU 600 automatic analyser.
Results. Our results showed that basal and stimulated PON1 activities were significantly decreased in patient’s group with cerebrovascular stenosis versus controls (p < 0.05). The median values for lipid parameters were not in accordance with the recommended values for the prevention of atherosclerosis and there concentrations did not show statistically significant relationships with PON1 activity (p>0.05).
Conclusion. The decreased PON1 activities in patients with cerebrovascular stenosis may cause decreased HDL antioxidant capacity and therefore contribute to the increase risk of the development of cerebrovascular atherosclerosis.

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