Kumar Arun, Biswas Utpal Kumar
Department of Biochemistry, College of Medicine & JNM Hospital, The West Bengal University of Health Sciences, Kalyani, Nadia, West Bengal, India.
Heart Asia. 2011 Jan 1;3(1):115-9. doi: 10.1136/heartasia-2011-010037. eCollection 2011.
Paraoxonase is a high-density lipoprotein (HDL)-associated enzyme that protects lipoproteins from oxidative modifications and from becoming atherogenic in nature. Smoking is a well-known major cardiovascular risk factor that promotes lipid peroxidation (LP). The present study examined the hypothesis that smoking modulates the activity of paraoxonase and depletes antioxidants.
The present study evaluated paraoxonase activity, antioxidant status and LP in smoking and non-smoking normolipidaemic acute myocardial infarct (AMI) patients, and results were compared with controls.
The serum paraoxonase activities, antioxidants and LP were determined in 86 normolipidaemic patients diagnosed of AMI, and 86 age-sex-matched healthy volunteers served as control.
Serum paraoxonase activities were measured by enzymatic kit. The glutathione peroxidase, superoxide dismutase and catalase activity was determined by standard methods. Malondialdehyde was measured by the thiobarbituric acid reaction, and conjugated diene levels by the Recknagel and Glende method. Serum uric acid, total bilirubin, serum albumin and lipid profiles were analysed by standard methods.
The values were expressed as mean±SD, and data from the patients and control were compared using the Student t test.
The total cholesterol/HDL cholesterol ratio, triglycerides, low-density lipoprotein cholesterol, low-density lipoprotein/HDL cholesterol ratio and triglyceride/HDL cholesterol ratio were significantly higher, and HDL cholesterol significantly lower in smokers compared with non-smoking AMI patients. Superoxide dismutase, glutathione peroxidase and catalase were significantly higher in non-smokers compared with smokers. Serum albumin, uric acid and bilirubin were higher in the control compared with smoking AMI patients. The malondialdehyde and conjugated dienes were significantly higher, and paraoxonase activities were significantly lower in smokers compared with non-smokers.
对氧磷酶是一种与高密度脂蛋白（HDL）相关的酶，可保护脂蛋白免受氧化修饰并防止其在本质上变得具有致动脉粥样硬化性。吸烟是一种众所周知的主要心血管危险因素，可促进脂质过氧化（LP）。本研究检验了吸烟会调节对氧磷酶活性并消耗抗氧化剂这一假设。
本研究评估了吸烟和不吸烟的血脂正常的急性心肌梗死（AMI）患者的对氧磷酶活性、抗氧化状态和LP，并将结果与对照组进行比较。
对86例被诊断为AMI的血脂正常患者测定血清对氧磷酶活性、抗氧化剂和LP，86例年龄和性别匹配的健康志愿者作为对照。
用酶试剂盒测定血清对氧磷酶活性。用标准方法测定谷胱甘肽过氧化物酶、超氧化物歧化酶和过氧化氢酶活性。用硫代巴比妥酸反应测定丙二醛，用雷克纳格尔和格伦德方法测定共轭二烯水平。用标准方法分析血清尿酸、总胆红素、血清白蛋白和血脂谱。
数值以均值±标准差表示，患者和对照组的数据用学生t检验进行比较。
与不吸烟的AMI患者相比，吸烟者的总胆固醇/HDL胆固醇比值、甘油三酯、低密度脂蛋白胆固醇、低密度脂蛋白/HDL胆固醇比值和甘油三酯/HDL胆固醇比值显著更高，而HDL胆固醇显著更低。与吸烟者相比，不吸烟者的超氧化物歧化酶、谷胱甘肽过氧化物酶和过氧化氢酶显著更高。与吸烟的AMI患者相比，对照组的血清白蛋白、尿酸和胆红素更高。与不吸烟者相比，吸烟者的丙二醛和共轭二烯显著更高，而对氧磷酶活性显著更低。
