Relationship between paraoxonase 1 55 Met/Leu, paraoxonase 2 148 Ala/Gly genetic polymorphisms and coronary artery disease / 中华医学遗传学杂志

<p><b>OBJECTIVE</b>To study the relationships between paraoxonase 1 55 Met/Leu (PON1 55Met/Leu), paraoxonase 2 148 Ala/Gly(PON2 148Ala/Gly) genetic polymorphisms and coronary artery disease(CAD), plasma activities of paraoxonase (PON), total superoxide dismutase (T-SOD), as well as plasma concentration of maleic dialdehyde (MDA).</p><p><b>METHODS</b>The PCR-RFLP method was applied to identify the genetic polymorphisms of PON1 55Met/Leu and PON2 148Ala/Gly, and the colorimetry way was used to detect plasma activities of PON, T-SOD and plasma MDA concentration of 262 CAD patients and 100 controls.</p><p><b>RESULTS</b>Comparing with control, the CAD patient had the obviously lower activities of enzymes PON (349.27+/- 138.36 nmol/min.mL vs 454.75+/- 166.00 nmol/min.mL, P< 0.001) and T-SOD (23.61+/- 16.51 U/mL vs 44.01+/- 22.68 U/mL, P< 0.001) while getting the plasma MDA concentration increased markedly(2.47+/- 0.73 nmol/mL vs2.15+/- 0.55 nmol/mL, P< 0.01). The CAD patient had more LM genotype and M allele of PON1 55Met/Leu(24.8% vs 1.4%, P< 0.001 and 12.4% vs 0.5%, P was 0.001 respectively), GG and AG genotype and G allele of PON2 148 Ala/Gly(11.8% vs 5.0%, P< 0.001; 48.1% vs 24.0%, P< 0.001 and 36.0% vs 17.0%, P< 0.001 respectively) than control did. The activities of plasma PON and T-SOD were lower in individuals with PON??1 55 LM genotype than those with LL genotype(304.73+/- 125.04 vs 394.84+/- 154.87 nmol/min.mL and 24.89+/- 16.14 vs 30.22+/- 21.29 U/mL, P< 0.001 and P< 0.05 respectively). The activity of plasma PON was also lower in individuals with PON2 148 GG/AG genotype than that with AA genotype(281.47+/- 84.70 vs 356.00+/- 145.95 vs 417.34+/- 159.00 nmol/min.mL, P< 0.001). Logistic regression analysis showed that PON1 55 LM genotype (OR 29.08, 95%CI 2.88-294.04, P was 0.004) and M allele(OR 15.17, 95%CI 1.32-174.29, P was 0.029), PON2 148 GG/AG genotype (OR 2.32, 95%CI 1.52-3.54, P< 0. 001) and G allele (OR 3.24, 95%CI 1.38-7.61, P was 0.007) were independent risk factors for CAD.</p><p><b>CONCLUSION</b>The CAD patient has the obviously low activities of plasma PON and T-SOD but on the contrary, get the plasma MDA concentration increased markedly. PON1 55 LM genotype and M allele, PON2 148 GG/AG genotype and G allele are the risk factors for coronary artery disease, and the activity of plasma PON is also markedly reduced in individuals with above genotypes.</p>

Study of the association between paraoxonase1 55 Met/Leu, paraoxonase2 148 Ala/Gly and manganese superoxide dismutase (MnSOD) 9 Ala/Val genetic polymorphisms and coronary heart disease / 中华流行病学杂志

<p><b>OBJECTIVE</b>To study the associations between paraoxonase, 55 Met/Leu (PON1 55 Met/ Leu), paraoxonase2 148 Ala/Gly (PON2 148 Ala/Gly) and manganese superoxide dismutase 9 Ala/Val (MnSOD 9 Ala/Val) genetic polymorphisms and coronary heart disease (CHD), plasma activities of paraoxonase (PON), total superoxide dismutase (T-SOD), MnSOD, as well as plasma concentration of maleic dialdehyde (MDA).</p><p><b>METHODS</b>Using PCR-RFLP method to identify genotype of PON1 55 Met/Leu, PON2 148 Ala/Gly and MnSOD 9 Ala/Val genetic polymorphisms, and using colorimetry to detect plasma activities of PON, T-SOD, MnSOD and plasma concentration of MDA in 262 CHD patients and 100 controls.</p><p><b>RESULTS</b>Compared with controls, the plasma activities of PON [(349.27 +/- 138.36 vs. 454.75 +/- 166.00) nmol x min(-1) x ml(-1), P < 0.001], T-SOD [(23.61 +/- 16.51 vs. 44.01 +/- 22.68) U/ml, P < 0.001] and MnSOD [(21.56 +/- 13.11 vs. 28.79 +/- 8.65) U/ml, P < 0.001] reduced obviously,while plasma MDA concentration increased markedly [(2.47 +/- 0.73 vs. 2.15 +/- 0.55)nmol/ml, P < 0.01] in CHD patients. There were more LM genotype and Met allele of PON, 55 Met/Leu (24.8% vs. 1.4%, P < 0.001 and 12.4% vs. 0.5%, P = 0.001, respectively), GG and AG genotype and G allele of PON2 148 Ala/Gly (11.8% vs. 5.0%, P < 0.001, 48.1% vs. 24.0%, P < 0.001 and 36.0% vs. 17.0%, P < 0.001, respectively) and AA genotype, A allele of MnSOD 9 Ala/Val genetic polymorphisms (64.2% vs. 43.0%, P = 0.001 and 80.0% vs. 67.0%, P = 0.014, respectively) in CHD patients than in controls. The activities of plasma PON and T-SOD were lower in individuals with PON1 55 LM genotype than those with LL genotype. The activity of plasma PON was also lower in individuals with PON2 148 GG/AG genotype than those with AA genotype. The activities of plasma PON and MnSOD depressed in individuals with MnSOD AA genotype compared with those with VV genotype. Logistic regression analysis demonstrated that PON1 55 LM genotype, PON2 148 GG/AG genotype and G allele were independent risk factors for CHD.</p><p><b>CONCLUSION</b>The antioxidative ability decreased, while lipid superoxide increased in CHD patients. Gene polymorphisms of PON1 55 Met/Leu, PON2 148 Ala/Gly and MnSOD 9 Ala/Val seemed to involve in the morbidity of CHD by influencing the plasma activities of PON and MnSOD.</p>