Chinnery P F, Taylor D J, Manners D, Styles P, Lodi R
Department of Neurology, the University of Newcastle upon Tyne, UK.
Neurology. 2001 Apr 24;56(8):1101-4. doi: 10.1212/wnl.56.8.1101.
The authors studied the relationship between the percentage level of A3243G mitochondrial DNA mutation and the degree of mitochondrial dysfunction in vivo in nine individuals from four pedigrees using phosphorus MRS in muscle. There was no significant correlation between mutation load and maximum rate of adenosine triphosphate production (V(max)). V(max) was normal in a subject with 32% A3243G in muscle, which is in contrast with a previous observation of markedly reduced V(max) in a patient with only 6% A3243G in muscle. Factors besides mutation load, such as nuclear genes, influence expression of the A3243G mutation in vivo.
作者使用肌肉磷磁共振波谱技术,研究了来自四个家系的九名个体体内A3243G线粒体DNA突变的百分比水平与线粒体功能障碍程度之间的关系。突变负荷与三磷酸腺苷产生的最大速率(V(max))之间没有显著相关性。在一名肌肉中A3243G含量为32%的受试者中,V(max)正常,这与之前观察到的一名肌肉中A3243G仅为6%的患者V(max)明显降低的情况形成对比。除了突变负荷外,诸如核基因等因素也会影响体内A3243G突变的表达。