Soran Neslihan, Altindag Ozlem, Cakir Hale, Celik Hakim, Demirkol Ahmet, Aksoy Nurten
Department of Physical Medicine and Rehabilitation, Harran University Research Hospital, Sanliurfa, Turkey.
Redox Rep. 2008;13(5):194-8. doi: 10.1179/135100008X308911.
The objective of this study was to investigate serum paraoxonase and arylesterase activities, and lipid hydroperoxide (LOOH) and total thiol (total free sulfhydryl groups, -SH) levels along with lipid parameters in patients with knee osteoarthritis. Thirty-six patients with knee osteoarthritis and 30 healthy individuals were enrolled in the study. Serum paraoxonase and arylesterase activities were measured spectrophotometrically. LOOH levels were measured by ferrous oxidation with xylenol orange assay (FOX-2). Serum high-density lipoprotein-cholesterol (HDL-C), -SH levels, paraoxonase and arylesterase activities were significantly lower in the patient group than those in the controls (P < 0.05, for all), while LOOH and low-density lipoprotein (LDL) levels were significantly higher. In conclusion, paraoxonase and arylesterase activities were decreased significantly in patients with knee osteoarthritis. Lower serum paraoxonase-1 activity and lower level of HDL-C seem to be related to increased oxidative stress and inflammatory condition in these patients. It is known that paraoxonases reduce oxidative stress in serum and tissues thereby protecting against cardiovascular disease, particularly atherosclerosis. Thus, decreased paraoxonase and arylesterase activities play a role in the pathogenesis of atherosclerosis through increased susceptibility to lipid peroxidation in patients with osteoarthritis.
本研究的目的是调查膝骨关节炎患者的血清对氧磷酶和芳基酯酶活性、脂质过氧化氢(LOOH)和总硫醇(总游离巯基,-SH)水平以及脂质参数。36例膝骨关节炎患者和30名健康个体纳入本研究。采用分光光度法测定血清对氧磷酶和芳基酯酶活性。通过二甲酚橙亚铁氧化法(FOX-2)测定LOOH水平。患者组血清高密度脂蛋白胆固醇(HDL-C)、-SH水平、对氧磷酶和芳基酯酶活性显著低于对照组(均P<0.05),而LOOH和低密度脂蛋白(LDL)水平显著更高。总之,膝骨关节炎患者的对氧磷酶和芳基酯酶活性显著降低。血清对氧磷酶-1活性降低和HDL-C水平降低似乎与这些患者氧化应激增加和炎症状态有关。已知对氧磷酶可降低血清和组织中的氧化应激,从而预防心血管疾病,尤其是动脉粥样硬化。因此,对氧磷酶和芳基酯酶活性降低通过增加骨关节炎患者脂质过氧化易感性在动脉粥样硬化发病机制中起作用。