Zhang G, Wang Z, Lin M
Union Hospital, Tongji Medical University, Wuhan 430022.
Zhonghua Fu Chan Ke Za Zhi. 1999 Jul;34(7):403-5.
To study the effect of mitochondrial tRNA(leu(UUR)) gene mutation at nuecleotide 3243 and the activity of cytochrome C oxidase on the pathogenesis of pregnancy induced hypertension(PIH).
57 cases of PIH and 60 normal pregnancy women were detected of tRNA(leu(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.
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.
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.
研究线粒体tRNA(亮氨酸(UUR))基因3243位点突变及细胞色素C氧化酶活性在妊娠高血压综合征(PIH)发病机制中的作用。
采用聚合酶链反应(PCR)及限制性片段长度多态性方法检测57例PIH患者和60例正常孕妇tRNA(亮氨酸(UUR))3243位点A→G突变。采用光度摄影法通过还原型细胞色素C的氰化物敏感氧化速率测定细胞色素C氧化酶活性。
PIH组细胞色素C氧化酶活性显著低于对照组。所有病例均未发现3243位点的线粒体DNA突变。
这些结果提示细胞色素C氧化酶活性降低可能损害能量产生,导致PIH患者线粒体功能障碍和胎盘功能障碍。线粒体功能障碍可能参与子痫前期的发病机制。线粒体DNA的特定突变可能不是PIH的常见病因。