Pedroso F C, Campello A P, Werneck L C, Klüppel M L
Departamento de Bioquímica, Universidade Federal do Paraná (UFPR), Curitiba, Brasil.
Arq Neuropsiquiatr. 1997 Jun;55(2):249-57. doi: 10.1590/s0004-282x1997000200013.
The activities of the enzymes NADH dehydrogenase, NADH cytochrome e reductase, succinate dehydrogenase, succinate cytochrome e reductase, cytochrome c oxidase and citrate synthase in normal and sick human skeletal muscle mitochondria were determined. A control group was formed by 13 normal people and without using continuous medication. The patient group was formed by 10 people whose pathological diagnosis indicated suspicion of mitochondrial myopathy. A decrease in the activity of the enzymes in all patient was observed: 7 with abnormality in all the tested enzymes; 2 with deficiencies in all the enzymes except cytochrome e oxidase; and 1 with dysfunction only in the activities of succinate dehydrogenase and succinate cytochrome e reductase. The results indicate multiple or combined deficiencies in the respiratory chain, besides dysfunction of citrate synthase in 9 patients. In one exceptional case, the enzymatic deficiency was restricted to complex II. It is possible to conclude that the methodology used herein is adequate and easily applicable to clinical objectives, and that the results obtained allow characterization of the deficient mitochondrial enzymatic complexes, thus showing that the origin of the diseases is an energetic metabolic dysfunction.
测定了正常人和患病人类骨骼肌线粒体中NADH脱氢酶、NADH细胞色素e还原酶、琥珀酸脱氢酶、琥珀酸细胞色素e还原酶、细胞色素c氧化酶和柠檬酸合酶的活性。对照组由13名未使用持续药物治疗的正常人组成。患者组由10名病理诊断怀疑有线粒体肌病的人组成。观察到所有患者的酶活性均降低:7名患者所有测试酶均异常;2名患者除细胞色素e氧化酶外所有酶均缺乏;1名患者仅琥珀酸脱氢酶和琥珀酸细胞色素e还原酶活性异常。结果表明,除9名患者柠檬酸合酶功能异常外,呼吸链存在多种或联合缺陷。在一个特殊病例中,酶缺乏仅限于复合体II。可以得出结论,本文所用方法是适当的,易于应用于临床目的,并且所获得的结果能够对缺陷的线粒体酶复合体进行表征,从而表明疾病的起源是能量代谢功能障碍。