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机构地区:[1]同济医科大学附属协和医院妇产科
出 处:《中华妇产科杂志》1999年第7期403-405,共3页Chinese Journal of Obstetrics and Gynecology
摘 要:目的探讨细胞色素C氧化酶活性及线粒体tRNAleu(UUR)基因3243位点A→G突变在妊高征发病中的作用。方法应用聚合酶链反应(PCR)结合限制性核酸内切酶酶切反应,对57例妊高征患者(妊高征组)和60例正常妊娠妇女(对照组)进行线粒体tRNAleu(UUR)基因3243位点A→G突变的检测,并应用紫外分光光度法对两组部分病例的胎盘细胞色素C氧化酶的活性进行测定。结果妊高征组细胞色素C氧化速率为(0.30±0.39)/分,明显低于对照组(0.73±0.54)/分,两组均未检测到线粒体tRNAleu(UUR)基因3243位点A→G突变,仅见294bp片段。结论细胞色素C氧化酶活性降低,可能导致妊高征发病及胎盘功能障碍;线粒体tRNAleu(UUR)基因3243位点A→G突变可能不是引起妊高征的常见原因。Objective To study the effect of mitochondrial tRNAleu(UUR) gene mutation at nuecleotide 3243 and the activity of cytochrome C oxidase on the pathogenesis of pregnancy induced hypertension(PIH). Methods 57 cases of PIH and 60 normal pregnancy women were detected of tRNAleu(UUR) nt3243AG mutation with the method of polymerase chain reaction (PCR) and restriction fragment length polymorphism. Cytochrome C oxidase activity was measured by the rate of cyanidesensitive oxidation of reduced cytochrome C using luminosity photographer. Results Cytochrome C oxidase activity was significantly lower in the PIH group than that of controls. The mitochondrial DNA mutation at position 3243 was not found in any of the cases. Conclusion These results suggested that the decreased activity of cytochrome C oxidase might impair the energy production, leading to the mitochondrial dysfunction and placental dysfunction in PIH patients. Mitochondrial dysfunction may be involved in the pathogenesis of preeclampsia. The particular mutation of mitochondrial DNA may not be the common contributor of PIH.
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