Suppr超能文献

[线粒体亮氨酸(UUR)转运RNA基因突变与子痫前期中细胞色素C氧化酶活性降低]

[Mitochondrial tRNA(leu(UUR)) gene mutation and the decreased activity of cytochrome C oxidase in preeclampsia].

作者信息

Zhang G, Wang Z, Lin M

机构信息

Union Hospital, Tongji Medical University, Wuhan 430022.

出版信息

Zhonghua Fu Chan Ke Za Zhi. 1999 Jul;34(7):403-5.

Abstract

OBJECTIVE

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).

METHODS

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.

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.

摘要

目的

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。

方法

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。

结果

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。

结论

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。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验