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线粒体tRNAleu UUR 基因突变和细胞色素C氧化酶活性降低在妊高征发病中的作用 |
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张广兰 王泽华 林美华
【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。 【关键词】 妊娠并发症,心血管 高血压 线粒体RNA,转移基因 细胞色素C氧化酶聚合酶链反应
Mitochondrial tRNAleu(UUR) Gene Mutation and the Decreased Activity of Cytochrome C Oxidase in Preeclampsia
ZHANG Guanglan, WANG Zehua, LIN Meihua.
Union Hospital Affiliated to the Tongji Medical University,Wuhan 430022
【Abstract】 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). Methods57 cases of PIH and 60 normal pregnancy women were detected of tRNAleu(UUR) nt3243A→G mutation with the method of polymerase chain reaction (PCR) and restriction fragment length polymorphism. Cytochrome C oxidase activity was measured by the rate of cyanide-sensitive 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. 【Key words】 Pregnancy complications,cardiovascular Hypertension Mitochondria RNA, transfer genes Cytochrome-C oxidas[1] [2] 下一页 上一个医学论文: 妊高征孕妇血及其新生儿脐血5 下一个医学论文: 改良筋膜横切口保留腹壁浅静脉的临床意义
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