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目的探讨对氧磷酶1 55 Met／Leu(PON1 55 Met／Leu)、对氧磷酶2 148 Ala／Gly(PON2 148 Ala／Gly)和锰超氧化物歧化酶9 Ala／Val(MnSOD 9 Ala／Val)基因多态性与冠心病(CHD)、血浆对氧磷酶(PON)、总超氧化物歧化酶(T-SOD)和锰超氧化物歧化酶(MnSOD)活性以及丙二醛(MDA)浓度的关系。方法采用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)方法检测262例CHD患者和100名对照组的PON1 55 Met／Leu、PON2 148 Ala／Gly和MnSOD 9 Ala／Val基因多态性的基因型,采用比色法测定血浆PON、T-SOD和MnSOD活性以及MDA浓度。结果与对照组比较,CHD患者的血浆PON[(349．27±138．36 vs. 454．75±166．00)nmol·min-1·ml-1,P<0．001]、T-SOD[(23．61±16．51 vs．44．01±22．68)U／ml,P<0．001]和MnSOD活性[(21．56±13．11 vs．28.79±8．65)U／ml,P<0．001]明显降低,MDA浓度显著增高[(2．47±0．73 vs．2．15±0．55)nmol／ml,P<0．01];CHD患者的PON1 55 LM杂合子基因型、M等位基因频率,PON2 148 GG纯合子基因型和AG杂合子基因型、G等位基因频率和MnSOD 9 AA基因型、A等位基因频率较对照组明显增多;PON1 55 LM杂合子基因型的PON和T-SOD活性较LL纯合子基因型明显降低;PON2 148 GG基因型和AG基因型的PON活性较AA基因型明显降低;MnSODAA基因型的PON和MnSOD活性较VV基因型明显降低;logistic回归分析显示PON1 55 LM杂合子基因型、M等位基因、PON2 148 GG／AG基因型、G等位基因是CHD的危险因子。结论CHD患者的抗氧化能力明显降低,脂质过氧化物显著增高;PON1 55 Met／Leu、PON2 148 Ala／Gly和MnSOD 9 Ala／Val基因多态性通过影响血浆PON和MnSOD活性而参与CHD的发病。
Objective To investigate the effects of paraoxonase 1 55 Met / Leu (PON1 55 Met / Leu), paraoxonase 2 148 Ala / Gly (PON2 148 Ala / Gly) and manganese superoxide dismutase 9 Ala / Val / Val) gene polymorphisms and coronary heart disease (CHD), plasma paraoxonase (PON), total superoxide dismutase (T-SOD) and manganese superoxide dismutase (MnSOD) MDA) concentration relationship. Methods PON1 55 Met / Leu, PON2 148 Ala / Gly and MnSOD 9 Ala / Val genes were detected by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) in 262 CHD patients and 100 control subjects The genotypes of plasma, PON, T-SOD and MnSOD were measured by colorimetric method and MDA concentration. Results Compared with the control group, the plasma levels of PON in patients with CHD (349.27 ± 138.36 vs. 454.75 ± 166.00 nmol · min-1 · ml-1, P <0.001) [(23.61 ± 16.51 vs.44.01 ± 22.68) U / ml, P <0.001] and MnSOD activity [(21.56 ± 13.11 vs.28.79 ± 8.65) U / Ml, P <0.001], and the concentration of MDA significantly increased (2.47 ± 0.73 vs.2.15 ± 0.55 nmol / ml, P <0.01). The PON1 55 LM heterozygous genotype, M allele frequency, PON2 148 GG homozygous genotype and AG heterozygous genotype, G allele frequency and MnSOD 9 AA genotype, A allele frequency increased significantly compared with the control group; PON and T-SOD activities of PON1 55 LM heterozygous genotypes were significantly lower than those of LL homozygous genotypes; PON activity of PON2 148 GG genotype and AG genotype was significantly lower than AA genotypes; PON and MnSOD activities of MnSODAA genotype Logistic regression analysis showed that PON1 55 LM heterozygote, M allele, PON2 148 GG / AG genotype and G allele were risk factors for CHD. Conclusions The antioxidant capacity of CHD patients was significantly lower and the level of lipid peroxides was significantly higher. The genetic polymorphisms of PON1 55 Met / Leu, PON2 148 Ala / Gly and MnSOD 9 Ala / Val were involved in CHD by affecting plasma PON and MnSOD activity Disease.