Zanssen S, Molnar M, Buse G, Schröder J M
Institut für Biochemie, Universitätsklinikum, RWTH, Aachen, Germany.
Clin Neuropathol. 1998 Nov-Dec;17(6):291-6.
Kearns-Sayre syndrome (KSS) is a progressive neuromuscular disease characterized by ophthalmoplegia, cardiac conduction block, and pigmentary retinopathy associated with abnormal mitochondrial structure and function. Usually mitochondrial DNA (mtDNA) deletions have been associated with Kearns-Sayre syndrome and chronic progressive external ophthalmoplegia. Size and position of the deletions differ markedly among these patients. The present study confirms this observation for a patient with KSS by a muscle and nerve biopsy in which we detected a 1.2 kb mtDNA deletion. The location of the deletion, however, is unusual in this case: its position comprises nucleotides 14952 to 15739. The defect is heteroplasmic and concerns the cytochrome b and tRNA genes. Complex I and IV of the respiratory chain were intact in this case, indicating that below a threshold of tRNA formation, the impaired biosynthesis and membrane integration of one respiratory complex may cause the phenotypical appearance of the KSS syndrome associated with a subclinical neuropathy.
卡恩斯-塞尔综合征(KSS)是一种进行性神经肌肉疾病,其特征为眼肌麻痹、心脏传导阻滞以及与线粒体结构和功能异常相关的色素性视网膜病变。通常,线粒体DNA(mtDNA)缺失与卡恩斯-塞尔综合征及慢性进行性外眼肌麻痹有关。这些患者中缺失的大小和位置差异显著。本研究通过肌肉和神经活检对一名KSS患者证实了这一观察结果,我们在该活检中检测到一个1.2 kb的mtDNA缺失。然而,在这种情况下缺失的位置并不寻常:其位置包括核苷酸14952至15739。该缺陷是异质性的,涉及细胞色素b和tRNA基因。在这种情况下呼吸链的复合体I和IV是完整的,这表明在tRNA形成阈值以下,一个呼吸复合体生物合成和膜整合受损可能导致与亚临床神经病变相关的KSS综合征的表型出现。