Moslemi A-R, Lindberg C, Toft J, Holme E, Kollberg G, Oldfors A
Department of Pathology, Sahlgrenska University Hospital, 41345 Göteborg, Sweden.
Neuromuscul Disord. 2004 Jan;14(1):46-50. doi: 10.1016/s0960-8966(03)00168-8.
We report a novel heteroplasmic T-->C mutation at nt position 582 within the mitochondrial tRNA(Phe) gene of a 70-year-old woman with mitochondrial myopathy. No other family members were affected, suggesting that our patient was a sporadic case. The muscle showed frequent ragged red fibers and 43% cytochrome c oxidase deficient fibers. The mutation alters a conserved base pairing in the aminoacyl acceptor stem. The mutation load was 70% in muscle homogenate and varied from 0 to 95% in individual muscle fiber segments. Cytochrome c oxidase-negative fibers showed significantly higher levels of mutated mtDNA (>75%) than Cytochrome c oxidase-positive fibers (<55%). This mutation adds to the previously described four pathogenic mutations in the tRNA(Phe) gene.
我们报告了一名70岁线粒体肌病女性患者,其线粒体苯丙氨酸转运RNA(tRNAPhe)基因第582位核苷酸处存在一种新的异质性T→C突变。没有其他家庭成员受影响,提示我们的患者为散发病例。肌肉显示出频繁的破碎红纤维和43%的细胞色素c氧化酶缺陷纤维。该突变改变了氨酰基受体茎中的保守碱基配对。突变负荷在肌肉匀浆中为70%,在单个肌纤维节段中从0%到95%不等。细胞色素c氧化酶阴性纤维显示出比细胞色素c氧化酶阳性纤维(<55%)显著更高水平的突变线粒体DNA(>75%)。该突变补充了先前描述的tRNAPhe基因中的四种致病突变。