Rahman S, Lake B D, Taanman J W, Hanna M G, Cooper J M, Schapira A H, Leonard J V
Metabolic Unit, Institute of Child Health, University College, London, UK.
Brain. 2000 Mar;123 Pt 3:591-600. doi: 10.1093/brain/123.3.591.
Cytochrome c oxidase (COX) is encoded by three mitochondrial and nine nuclear genes. COX deficiency is genetically heterogeneous but current diagnostic methods cannot easily distinguish between mitochondrial and nuclear defects. We hypothesized that there may be differential expression of COX subunits depending on the underlying mutation. COX subunit expression was investigated in five patients with known mtDNA mutations. Severe and selective reduction of mtDNA-encoded COX subunits I and II was consistently observed in all these patients and was restricted to COX-deficient fibres. Immunostaining of nuclear-encoded subunits COX IV and Va was normal, whilst subunit VIc, also nuclear-encoded, was decreased. Twelve of 36 additional patients with histochemically defined COX deficiency also had this pattern of staining, suggesting that they had mtDNA defects. Clinical features in this group were heterogeneous, including infantile encephalopathy, multisystem disease, cardiomyopathy and childhood-onset isolated myopathy. The remaining patients did not have the same pattern of immunostaining. Fourteen had reduced staining of all subunits, whilst 10 had normal staining of all subunits despite reduced enzyme activity. Patients with COX deficiency secondary to mtDNA mutations have a specific pattern of subunit loss, but the majority of children with COX deficiency do not have this pattern of subunit loss and are likely to have nuclear gene defects.
细胞色素c氧化酶(COX)由三个线粒体基因和九个核基因编码。COX缺乏症在遗传上具有异质性,但目前的诊断方法不易区分线粒体缺陷和核缺陷。我们推测,根据潜在的突变情况,COX亚基可能存在差异表达。对五名已知线粒体DNA(mtDNA)突变的患者进行了COX亚基表达研究。在所有这些患者中均一致观察到mtDNA编码的COX亚基I和II严重且选择性降低,且仅限于COX缺陷纤维。核编码亚基COX IV和Va的免疫染色正常,而同样是核编码的亚基VIc减少。另外36名经组织化学确定为COX缺乏症的患者中有12名也有这种染色模式,表明他们存在mtDNA缺陷。该组患者的临床特征具有异质性,包括婴儿期脑病、多系统疾病、心肌病和儿童期起病的孤立性肌病。其余患者没有相同的免疫染色模式。14名患者所有亚基的染色减少,而10名患者尽管酶活性降低,但所有亚基的染色正常。继发于mtDNA突变的COX缺乏症患者具有特定的亚基缺失模式,但大多数COX缺乏症儿童没有这种亚基缺失模式,可能存在核基因缺陷。