Kobayashi M, Morishita H, Sugiyama N, Yokochi K, Nakano M, Wada Y, Hotta Y, Terauchi A, Nonaka I
J Pediatr. 1987 Feb;110(2):223-7. doi: 10.1016/s0022-3476(87)80158-0.
Muscle biopsy specimens from two patients with MELAS syndrome (mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes) were studied biochemically. 14CO2 production rates from (1-14C)pyruvate, (U-14C)malate, and (1-14C)2-ketoglutarate were all decreased in intact mitochondria in both patients. Rotenone-sensitive NADH cytochrome c reductase activities were decreased to 8% (patient 1) and 6% (patient 2) of control values; succinate cytochrome c reductase and cytochrome c oxidase values were within normal limits. These results indicate that both patients have a defect of NADH-CoQ reductase of the respiratory chain and that MELAS can be brought about by a defect of NADH-CoQ reductase.
对两名患有线粒体肌病、脑病、乳酸酸中毒和卒中样发作综合征(MELAS)的患者的肌肉活检标本进行了生化研究。两名患者完整线粒体中,(1-14C)丙酮酸、(U-14C)苹果酸和(1-14C)2-酮戊二酸的14CO2生成率均降低。鱼藤酮敏感的NADH细胞色素c还原酶活性分别降至对照值的8%(患者1)和6%(患者2);琥珀酸细胞色素c还原酶和细胞色素c氧化酶值在正常范围内。这些结果表明,两名患者均存在呼吸链NADH-CoQ还原酶缺陷,且MELAS可能由NADH-CoQ还原酶缺陷引起。