Fassati A, Bordoni A, Amboni P, Fortunato F, Fagiolari G, Bresolin N, Prelle A, Comi G, Scarlato G
Department of Experimental Pathology, UMDS Guy's Hospital, London, UK.
J Neurol Sci. 1994 May;123(1-2):140-6. doi: 10.1016/0022-510x(94)90216-x.
We studied muscle biopsies of 5 patients with Kearns-Sayre syndrome and 3 patients with chronic progressive external ophthalmoplegia all with the common deletion. Steady state levels of normal and deleted mitochondrial DNA (mtDNA) measured in each patient by quantitative PCR were correlated with histochemical and biochemical features. We found that (1) normal mtDNA levels were higher in many patients than in controls; (2) as levels of deleted mtDNA increased, so did levels of normal mtDNA; (3) cytochrome c oxidase (COX) activity and the percentage of COX negative fibers were both related to the levels of deleted mtDNA; and (4) as percentage of ragged red fibers increased, so did levels of total, deleted and normal mtDNA. The quantity of deleted mtDNA plays a key role in determining the severity of COX deficiency, which is responsible for the overaccumulation of mitochondria in muscle.
我们研究了5例患有卡恩斯-塞尔综合征(Kearns-Sayre syndrome)和3例患有慢性进行性外眼肌麻痹(chronic progressive external ophthalmoplegia)且均存在共同缺失的患者的肌肉活检样本。通过定量PCR测定的每位患者中正常和缺失线粒体DNA(mtDNA)的稳态水平与组织化学和生化特征相关。我们发现:(1)许多患者的正常mtDNA水平高于对照组;(2)随着缺失mtDNA水平的增加,正常mtDNA水平也增加;(3)细胞色素c氧化酶(COX)活性和COX阴性纤维的百分比均与缺失mtDNA的水平相关;(4)随着破碎红纤维百分比的增加,总mtDNA、缺失mtDNA和正常mtDNA的水平也增加。缺失mtDNA的数量在决定COX缺乏的严重程度方面起关键作用,而COX缺乏是导致肌肉中线粒体过度积累的原因。