糖尿病合并冠心病与芳香酯酶基因Q192R多态性分析

目的 :探讨糖尿病 (DM)芳香酯酶 (ArE/PON1)基因Q192R多态性与糖尿病合并冠心病 (DM -CAD)的关系 ,为防治DM -CAD提供理论依据。方法 :调查对象为郑州地区汉族健康人群 6 4例 (对照组 )、2型糖尿病 6 0例 (DM组 )与DM -CAD6 7例 (DM -CAD组 )。测定其血清ArE/PON1活性 ,并用聚合酶链式反应 -单链构型多态性 (PCR -SSCP)分析技术检测ArE/PON1基因Q192R的多态性 ,进行分析研究。结果 :发现对照组、DM组和DM -CAD组均存在ArE/PON1基因 192位点 (Q/R)多态性。对照组基因频率Q为 0 .5 5、R为 0 .4 5 ;DM组为 0 .5 3与 0 .4 7;DM -CAD组为 0 .38与 0 .6 2。DM -CAD组R基因频率明显高于DM组和对照组 (P <0 .0 5 ) ,DM组与对照无显著差异 (P >0 .0 5 ) ,DM与DM -CAD组血清ArE/PON1活性 (分别为 0 .2 2 5± 0 .0 18μ/ml与 0 .2 0 0± 0 .0 19μ/ml)均低于对照组 (0 .2 5 9± 0 .0 18μ/ml) ,DM -CAD组低于DM组 (P <0 .0 5 )。 3组中每组内每种基因型组间酶活性无显著差异。结论 :郑州汉族人群存在ArE/PON1Q192R(GIn/Arg)多态性 ,基因频率分布不同于白种人 ,提示R基因可能是DM合并CAD的危险因素。     

心肌梗死患者对氧磷酶-1 Q/R192基因多态性及活性检测的临床意义

目的探讨心肌梗死(AMI)患者对氧磷酶-1(PON1)Q/R192基因多态性及其活性检测的临床意义。方法分别采用紫外线分光光度法和聚合酶链式反应-限制性片段长度多态性(PCR-RELP)法检测65例AMI患者和70名健康体检者PON1活性及PON1Q/R192基因多态性。结果 AMI组血清PON1活性[(78.56±16.69)U/mL]明显低于健康对照组[(118.65±30.25)U/mL](P<0.01)。AMI组与健康对照组3种基因型及2种等位基因频率分布差异无统计学意义(P>0.05);AMI组与健康对照组间不同PON1 Q/R192基因型间血清PON1活性相比差异有统计学意义(P<0.01);AMI组内及健康对照组内PON1 Q/R192不同基因型间血清PON1活性相比差异无统计学意义(P>0.05)。结论血清PON1活性降低是AMI的危险因素之一;PON1Q/R192基因多态性与AMI的发生无相关性。     

糖尿病并发肾病与对氧磷酶-2基因C311S多态性的关系

目的:研究对氧磷酶-2基因C311S(PON2C311S)多态性和郑州地区汉族人群2型糖尿病(DM)并发肾病的关系.方法:采用聚合酶链反应-限制性片段长度(PCR-RFLP)技术,检测DM(122例)、糖尿病合并微量白蛋白尿(MADM,121例)、糖尿病慢性肾功能衰竭(DN-CRF,123例)患者和健康对照组(125例)的PON2C311S多态性,同时测定其血脂和脂蛋白等的水平.结果:DN-CRF组和MADM组等位基因C的频率均低于DM和对照组,S的频率则高于后2组.等位基因C、S频率在DM组和对照组间的差异无统计学意义.观察4组各组内基因型SS和CC组间血脂、脂蛋白水平均无显著差异.PON2C311S致DM并发肾病的相对危险度(OR)及95%可信限(95%CI):DN-CRF组为2.68(1.48～4.48);MADM组为2.63(1.45～4.74).结论:PON2C311S多态性和DM并发肾病具有密切关系,和3组患者血脂、脂蛋白的异常改变无直接相关性.     

心肌梗死患者对氧磷酶-1 Q/R192基因多态性及活性检测的临床意义

目的探讨心肌梗死（AMI）患者对氧磷酶-1（PON1）Q/R192基因多态性及其活性检测的临床意义。方法分别采用紫外线分光光度法和聚合酶链式反应-限制性片段长度多态性（PCR-RELP）法检测65例AMI患者和70名健康体检者PON1活性及PON1Q/R192基因多态性。结果 AMI组血清PON1活性[（78.56±16.69）U/mL]明显低于健康对照组[（118.65±30.25）U/mL]（P〈0.01）。AMI组与健康对照组3种基因型及2种等位基因频率分布差异无统计学意义（P〉0.05）;AMI组与健康对照组间不同PON1 Q/R192基因型间血清PON1活性相比差异有统计学意义（P〈0.01）;AMI组内及健康对照组内PON1 Q/R192不同基因型间血清PON1活性相比差异无统计学意义（P〉0.05）。结论血清PON1活性降低是AMI的危险因素之一;PON1Q/R192基因多态性与AMI的发生无相关性。     

血清对氧磷酯酶-1活性与肝硬化Child-Pugh分级的关系

目的 探讨血清对氧磷酯酶-1(PON1)酶活性与肝硬化Child-Pugh分级的关系.方法 以对氧磷(paraoxon)为底物测定76例正常、26例急性肝炎、45例慢性肝炎和72例肝硬化患者血清基础PON-1活性和1 mol/L NaC1刺激后PON1活性;PCR扩增PON1基因,Alw I酶切PCR产物,对PON1基因192位多态性进行分型.结果 正常对照组、急性肝炎、慢性肝炎和肝硬化患者血清PON-1基础活性水平分别为403z±145,312±83,201±114,137±99 U/ml;1 m01/L NaC1刺激后PON-1活性分别为673±232,509±139,335±151,233±162 U/ml.与正常对熙比较,急性肝炎、慢性肝炎和肝硬化患者血清PON-1活性基础水平和1 mol/L NaC1刺激后PON1活性均显著下降(P<0.01),肝硬化组下降最明显.肝硬化Child A,Child B和Child C组患者血清PON-1活性基础水平分别为185.5±98.6,141.6±93.6,86.7±51.2 U/ml;1mol/L NaC1刺激后PON-1活性分别为308.9±161.3,227.1±116.3,124.9±78.1 U/ml.Child B组比A组PON1酶活性显著下降(P<0.05),而Child C组又比B组PON1酶活性显著下降(P<0.01).在肝硬化Child A,Child B和Child C组患者PON1的192位R-Q多态性分布频率无显著性差异(P>0.05).结论 血清PONl活性下降与肝硬化Child-Pugh分级相关,可反应肝硬化的严重程度,且PON1基因192位多态性不影响肝硬化各组的PONl酶活性.     

对氧磷酶基因192位点多态性与动脉粥样硬化性脑梗死的关系

目的:研究动脉粥样硬化性脑梗死与血清对氧磷酶(PON1)基因192位点多态性的关系。方法:应用聚合酶链式反应-限制性片段长度多态性(PCR-RFLP)方法,对52例动脉粥样硬化性脑梗死患者,48例正常人的PON1基因192位点多态性进行分析,同时检测血脂水平。结果:脑梗死组及正常组均以QR基因型为主,频率分别为0.50,0.54,QQ,RR基因型频率分别为0.10、0.25,0.40、0.21,两组人群基因型分布处于Hardy-Weinberg平衡。脑梗死组R等位基因频率明显高于正常组,分别为0.65,0.48(χ2=4.18P<0.05)。且脑梗死组血清胆固醇、三酰甘油、载脂蛋白B水平高于正常组,低密度脂蛋白胆固醇有升高趋势,而高密度脂蛋白胆固醇、载脂蛋白A1低于正常组。结论:PON1基因192位点多态性可能与动脉粥样硬化性脑梗死有关。R等位基因可能为动脉粥样硬化性脑梗死的相对危险因素。且血脂异常参与脑梗死的发病。     

对氧磷酶基因192位点多态性与动脉粥样硬化性脑梗死的关系

目的：研究动脉粥样硬化性脑梗死与血清对氧磷酶(PON1)基因192位点多态性的关系。方法：应用聚合酶链式反应-限制性片段长度多态性(PCR-RFLP)方法，对52例动脉粥样硬化性脑梗死患者，48例正常人的PON1基因192位点多态性进行分析，同时检测血脂水平。结果：脑梗死组及正常组均以QR基因型为主，频率分别为O.50，O.54，QQ,RR基因型频率分别为O．10、O．25，O.40、O.21，两组人群基因型分布处于Hardy-Weinberg平衡。脑梗死组R等位基因频率明显高于正常组，分别为O.65，O.48(χ^2=4.18 P&;lt;O.05)。且脑梗死组血清胆固醇、三酰甘油、载脂蛋白B水平高于正常组，低密度脂蛋白胆固醇有升高趋势，而高密度脂蛋白胆固醇、载脂蛋白A1低于正常组。结论：PON1基因192位点多态性可能与动脉粥样硬化性脑梗死有关。R等位基因可能为动脉粥样硬化性脑梗死的相对危险因素。且血脂异常参与脑梗死的发病。     

Ⅰ型对氧磷酯酶基因Gln/Arg192遗传多态性与冠心病相关性的初步研究

目的 探讨中国北方地区I型对氧磷酯酶(paraoxonase l，PON1)基因Gln／Arg192遗传多态性与冠心病发病的关系。方法 应用聚合酶铁反应(polymerase chain reaction，PCR)及限制片段长度多态性(restriction fragment length polymorphisms，RFLP)技术，检测49例老年冠心病患者和38例健康老年对照者的PONl—Gln／Arg192基因多态性，等位基因以A／B表示。结果 冠心病组与健康组比较各基因型分布差异具有显著性意义(χ^2＝6．35，P＝0.042)。B等位基因在冠心病组明显增高(0．56vs0．37)。B等位基因是中国北方地区冠心病发病的危险因素(OR＝2.19，95％CI：1．19～4.05)。结论 PONl基因Gln／Arg192遗传多态性与中国北方地区冠心病发病明显相关。该酶切位点多态性具有明显的种族差异。     

潍坊地区汉族人群PON1(对氧磷酶)Q192R基因多态性与冠心病的相关性研究

目的:测定PON1(对氧磷酶)Q192R基因多态性及在人群中的分布,分析各基因型与冠心病的关系。方法:冠心病患者128例,男80例,女48例,年龄为36~82(65.25±9.83)岁,全部病例有明确心梗病史或经冠状动脉(冠脉)造影确诊。正常对照组110例,男66例,女44例,年龄31~87(63.52±7.91)岁,选自人群健康查体的随机个体。结果:PON1Q192R有QQ、QR、RR三种基因型,正常人的基因型频率分别为0.200 0、0.490 9、0.309 1,冠心病组QQ、QR、RR三种基因频率分别为0.226 6、0.531 3、0.242 1。结论:潍坊地区汉族人群PON1(对氧磷酶)基因多态性和冠心病无关。     

对氧磷酶1基因Q192R和L55M位点多态性与川崎病冠状动脉损伤的相关性

目的探讨对氧磷酶1(paraoxonase 1, PON1)基因Q192R和L55M位点基因多态性与川崎病患儿冠状动脉损伤的关系。方法川崎病患儿73例(川崎病组),其中有冠状动脉损伤34例为损伤组,无冠状动脉损伤39例为未损伤组;同期50例健康儿童为对照组。3组采集空腹静脉血提取全血DNA,采用限制性片段长度多态性PCR技术检测PON1基因Q192R和L55M位点多态性,并进行比较。结果川崎病组Q192R位点RR、QR基因型分布频率(40.0%、44.0%)及Q等位基因频率(38.0%)与对照组(39.7%、45.2%、37.7%)比较差异无统计学意义(P0.05),L55M位点LL基因型分布频率及L等位基因频率(90.0%、95.0%)与对照组(86.3%、92.5%)比较差异无统计学意义(P0.05)。损伤组PON1基因Q192R位点RR基因型分布频率(52.9%)及R等位基因频率(72.1%)均高于未损伤组(28.2%、53.8%)(P0.05)。损伤组PON1基因L55M位点LM+MM基因型分布频率(23.5%)及M等位基因频率(13.2%)均高于未损伤组(5.1%、2.6%)(P0.05)。结论 PON1基因Q192R和L55M位点基因多态性与川崎病发生无明显相关性,与川崎病患儿冠状动脉损伤关系密切。     

Are PON1 Q/R 192 and M/L 55 polymorphisms risk factors for diabetes complications in Turkish population?

ObjectivesWe investigated whether the human serum paraoxonase (PON1) Q/R 192 and M/L 55 polymorphisms are associated with the complications of the type 2 diabetes (T2D).Design and methodsStudy group was consisted of 50 healthy subjects and 100 type 2 diabetes mellitus (DM) patients. Following measuring of serum PON1 activity, isolation of DNA and genotyping analyses were performed.ResultsPON1 activity of the patients with complications was significantly reduced by 23.5% compared to the group of diabetic patients and by 26.3% than the controls. According to multivariate analysis, we observed a three times significant effect of Q/R 192 polymorphism on the susceptibility to the occurrence of complications.ConclusionsProtective effects of paraoxonase against peroxidation of LDL particles are important in T2D complications. Although both of the two polymorphisms are associated, 192 polymorphism seems to be stronger predictor of the risk of diabetic complications.     

The paraoxonase-1 codon 192 polymorphism is associated with fasting total cholesterol and LDL-cholesterol concentrations only in postmenopausal women. The REGICOR study.

Paraoxonase-1 (PON1) is a high-density lipoprotein (HDL)-linked enzyme which appears to protect low-density lipoproteins (LDL) from oxidation. PON1 activity is associated with variation at the PON1 gene locus, specifically the common amino acid polymorphism at codon 192, for which the Q192 allele specifies low activity and the R192 allele specifies high activity. We investigated the association between the PON1 codon 192 polymorphism and fasting concentrations of glucose, lipids, lipoproteins and PON1 activity in 1380 subjects (724 men and 656 women). Several anthropometric and environmental factors were assessed in the present study. The PON1 Q192 allele frequency was 0.70 and 0.68 in men and women, respectively. In women, but not in men, significant associations were found between the PON1 codon 192 genotype and both total and LDL-cholesterol (p=0.004 and p=0.008, respectively), and subgroup analysis indicated that this relationship was predominant in postmenopausal women. Specifically, the Q192 allele was associated with increased total and LDL-cholesterol concentrations. Furthermore, these lipoprotein variables were higher among postmenopausal women with Q192/Q192 and Q192/R192 genotypes than in premenopausal women with the same genotypes (p<0.001). The findings suggest a gender-specific lipoprotein-genotype association with PON1 codon 192 genotypes in this study sample.     

Low paraoxonase activity in type II diabetes mellitus complicated by retinopathy

Human serum paraoxonase 1 (PON1) is located on high-density lipoprotein and has been implicated in the detoxification of organophosphates, and possibly in the prevention of lipid peroxidation of low-density lipoprotein. PON1 has two genetic polymorphisms, both due to amino acid substitutions: one involving glutamine (Q genotype) and arginine (R genotype) at position 192, and the other involving leucine (L genotype) and methionine (M genotype) at position 55. We investigated the effects of these polymorphisms, and of a polymorphism of the PON2 gene at position 310 (Cys/Ser; C and S genotypes respectively), on serum PON1 activity and concentration, plasma lipids and lipoproteins and glycaemic control in 93 individuals with type II diabetes with no complications and in 101 individuals with type II diabetes with retinopathy. Serum PON1 activity in the group with no complications [median 164.1 nmol.min(-1).ml(-1) (range 8.0-467.8)] was significantly higher than in the group with retinopathy [113.4 nmol. min(-1).ml(-1) (3.0-414.6)] (P<0.001), but the serum PON1 concentration was not different between the groups. The gene frequencies of the PON1-55 and PON1-192 polymorphisms and of the PON2-310 polymorphism were not different between the study populations. The PON1-55 and PON1-192 polymorphisms affected PON1 activity in the way described in a previous study of a control group and subjects with type II diabetes. The PON2-310 polymorphism also significantly affected serum PON1. PON1 activity was significantly higher in individuals with the PON2-310 CC genotype in both groups with type II diabetes, and the PON1 concentration was significantly higher in PON2-310 CC homozygotes with no complications than in the group with retinopathy. Neither the PON1-55 nor the PON1-192 polymorphism was correlated with the serum lipid or lipoprotein concentration in either group. In the group with retinopathy (but not the group with no complications), all three PON polymorphisms were correlated with glycaemic control, which was worse for the PON1-55 genotypes in the order MM>LM>LL (P=0.0032), for the PON1-192 genotypes in the order RR>QR>QQ (P=0.011) and for the PON2-310 genotypes in the order CC>CS>SS (P=0.010). Low serum PON1 activity in retinopathy may be related to an increased tendency for lipid peroxidation. Our findings thus raise the possibility that, in retinopathy, the PON2 gene may influence PON1, and that an inter-relationship between the PON1 and PON2 genes may influence glycaemic control in subjects with type II diabetes complicated by retinopathy.     

动脉粥样硬化性脑梗塞患者血脂与对氧磷酶基因多态性的关系

目的:研究动脉粥样硬化性脑梗塞患者血脂水平与对氧磷酶(PON_1)基因192位点多态性的关系。方法:应用聚合酶链式反应-限制性片段长度多态性(PCR-RFLP)方法,对动脉粥样硬化性脑梗塞52例,正常人48例的PON_1基因192位点多态性进行分析,并同时检测血脂水平。结果:与正常组相比脑梗塞组存在明显的血脂异常(P<0.05),两组人群PON_1基因192位点基因型分布处于Hardy-Weinberg平衡,且脑梗塞组R等位基因频率明显高于正常组,分别为0.65、0.48(P<0.05)。但血脂水平与各基因型之间比较无显著差异(P>0.05)。结论:PON_1基因192位点多态性可能与动脉粥样硬化性脑梗塞有关,但未发现其与血脂水平有关。     

PON1 L55M polymorphism is not a predictor of coronary atherosclerosis either alone or in combination with Q192R polymorphism in an Italian population

BACKGROUND: The present study evaluated the role of the PON1 L55M polymorphism independently and in conjunction with the Q192R polymorphism on the risk of coronary atherosclerosis in an Italian population. MATERIALS AND METHODS: Three hundred and ninety-one subjects with significant coronary stenosis (> 50%) (coronary artery disease-positive; CAD+), 196 subjects with normal coronary arteries (< 10% stenosis) (CAD-) and 178 healthy controls were screened using a combination of polymerase chain reaction and restriction enzyme digestion. RESULTS: In the pooled population, the frequencies of L and M alleles were 0.63 and 0.37, respectively; the most common haplotypes were QQ/LM (24.2%) and QR/LL (21.8%) and a strong linkage disequilibrium between L/55 and R/192 alleles was observed (D' = -0.91; P < 0.0001). CAD+ subjects did not show any significant differences in the distribution of PON1-55 genotypes as compared to CAD- subjects and population controls (chi2 = 1.5, P = 0.8). After controlling for other risk factors, the low-concentration M allele was not associated with a significant change of CAD risk (OR 1.02; 95% CI 0.80-1.29; P = 0.87). Moreover, the L55M polymorphism did not show any interaction with other risk factors such as smoking, diabetes, hypertension, low levels of high-density lipoprotein (HDL) or high ratios of low-density to high-density lipoproteins. The combination of L55M with the Q192R polymorphism did not show any effect on CAD risk. However, a marginal decrease in myocardial infarction risk was detected when QQ/MM carriers (OR 0.51; 95% CI 0.26-0.99; P = 0.048), but not LL/RR carriers, were compared with subjects not homozygous for an L or R allele. CONCLUSIONS: These findings did not indicate a major effect of the PON1 L55M polymorphism, either alone or in combination with the Q192R polymorphism, on CAD risk. Additional studies are needed for a better evaluation of the role of the 55/192 PON1 genotypes in combination on myocardial infarction risk.     

Paraoxonase 1-192Q allele is a risk factor for idiopathic chronic pancreatitis.

BACKGROUND: The cause of chronic pancreatitis (CP) remains unknown. However, oxidative stress might play a role since recent animal studies have demonstrated that oxygen-free radicals contribute to the pathogenesis of experimental pancreatitis. Human serum paraoxonase (PON1) is an antioxidant enzyme that protects against cellular damage from oxidative stress. Genetic variations resulting in variable activity rates of this enzyme, are of toxicological and physiological importance. AIM: We investigated whether genetic polymorphisms of the PON1 gene modify the risk for CP. MATERIALS AND METHODS: DNA samples were obtained from 236 adult CP patients of hereditary (n = 23), alcoholic (n = 137), or idiopathic (n = 76) origin. DNA from 113 healthy controls and from 93 alcoholic controls were analyzed for comparison. Patients and controls were all of Caucasian origin. Genetic polymorphisms (L55M and Q192R) in PON1 were determined by PCR, followed by restriction fragment length polymorphism analyses in all subjects. RESULTS: The frequencies of the PON1-55 alleles did not differ between CP patients and healthy controls. However, the PON1-192Q allele was significantly more common in idiopathic CP patients (OR : 1.5, 95% CI 1.02, 2.5) compared with healthy controls. CONCLUSIONS: These data suggest that the PON1-192Q allele, resulting in partly deficient antioxidant and detoxification activity of this enzyme, might be a risk factor for idiopathic CP in Caucasians.     

High-density lipoprotein cholesterol and paraoxonase 1 (PON1) genetics and serum PON1 activity in prepubertal children in Spain

BACKGROUND: Oxidative stress plays an important role in atherosclerosis. Paraoxonase 1 (PON1) is a high-density lipoprotein (HDL)-associated enzyme that inhibits low-density lipoprotein (LDL) oxidation and may play a protective role against coronary heart disease. The aim of this study was to analyze the relationship between HDL-cholesterol (HDL-C) and PON1 in a Spanish prepubertal population with high plasma HDL-C levels. METHODS: The study population included 1,266 children between the ages of 6 and 8 years. Serum PON1 activity was measured by the hydrolysis of paraoxon. PON1 192Q/R and PON1 55L/M polymorphisms were analyzed by PCR and restriction analysis. RESULTS: The prevalence of the less common PON1 192R and PON 55M alleles in this population was 30% and 38%, respectively. No significant correlations between serum PON1 activity and lipid profile were observed. Multiple linear regression analysis showed that the PON1 192Q/R polymorphism accounts for 69% of PON1 activity in the children in the study, with the PON1 55L/M polymorphism accounting for an additional 5% of this variation in boys, and for an additional 3% together with HDL-C concentration in girls. CONCLUSIONS: PON1 192Q/R polymorphism is the main determinant of PON1 activity in the prepubertal population in this study, accounting for around 70% of serum PON1 activity. HDL-C concentration has a small contribution to serum PON1 activity in girls.     

The relationship between paraoxonase1-192 polymorphism and activity with coronary artery disease

ObjectiveWe tested the association between PON1 polymorphism, PON1 activity, oxidative susceptibility of LDL and coronary artery disease in Egyptians.MethodsPON1 polymorphism, serum PON1 activity, lipoprotein oxidation susceptibility and lipid profile were measured.ResultsLevels of HDL and paraoxonase activity were significantly decreased in CAD patients compared to control group, and in patients with three vessels compared to those of single or two vessels disease. High-activity allele (R) has a more atherogenic lipid profile than for the low activity allele (Q). PON1 RR genotype has nine fold risks to develop CAD in Egyptians while those with PON1 QR genotype have four fold risks.ConclusionThe PON1 activity is lower in subject with CAD and there is a significant relationship between activity of PON1 and the severity of coronary atherosclerosis. Also, we provide evidence of a significant association between R allele of the PON1 polymorphism and the development of coronary artery disease.     

Paraoxonase-1 (PON1) activity, but not PON1(Q192R) phenotype, is a predictor of coronary artery disease in a middle-aged Serbian population.

BACKGROUND: Paraoxonase-1 (PON1) is a high-density lipoprotein (HDL)-associated serum enzyme that protects lipoproteins from oxidative modifications. Polymorphisms in the gene, including PON1Q192R, have been studied. However, inconsistencies regarding the above-mentioned polymorphism obscure its association with vascular disease. METHODS: Using a two-substrate (paraoxon/diazoxon) activity method, we investigated the frequencies of PON1Q192R phenotypes in 261 middle-aged subjects: 156 patients with angiographically assessed coronary heart disease (CHD) and 105 CHD-free subjects as the control group. The PON1(192) phenotype was predicted from examination of the two-dimensional plot of hydrolysis rates of diazoxon vs. paraoxon and by using the antimode of the histogram of the ratio of diazoxonase/paraoxonase activity. RESULTS: The PON1Q192R phenotype frequencies in 113 patients with occlusion >50% (coronary artery disease-positive, CAD+ group) vs. control population were as follows: QQ (0.552 vs. 0.510), QR (0.382 vs. 0.408) and RR (0.066 vs. 0.082); chi2=0.414, p=0.813. We found lower paraoxonase (POase) and diazoxonase (DZOase) activities in the CAD+ patients when compared to the control population. According to logistic regression analysis, POase activity was a better predictor of coronary disease onset compared with DZOase activity measurements and PON1Q192R phenotyping. CONCLUSIONS: We conclude that enzyme activity (within a particular phenotypic group) is more important than phenotype alone in predicting susceptibility to coronary artery disease.