Trijbels F J, Ruitenbeek W, Huizing M, Wendel U, Smeitink J A, Sengers R C
Department of Pediatrics, University Hospital Nijmegen, The Netherlands.
Mol Cell Biochem. 1997 Sep;174(1-2):243-7.
Disturbances in substrate oxidations in muscle mitochondria from patients with a suspicion of a mitochondrial myopathy may arise from a deficiency of one or more of the complexes of the respiratory chain or of the pyruvate dehydrogenase complex. However, we found no clear-cut defect in a substantial part of such patients. In this report we discuss some of the other possibilities which could account for the disturbed substrate oxidation rates. Special attention will be paid to defects which are localized outside the respiratory chain, such as defects in post-respiratory chain enzymes, defects in transport mechanisms of the mitochondrial inner or outer membrane, deficiency of cofactors and deficiency of heat-shock protein.
疑似线粒体肌病患者肌肉线粒体中底物氧化的紊乱可能源于呼吸链中一种或多种复合物或丙酮酸脱氢酶复合物的缺乏。然而,我们发现这类患者的很大一部分并没有明显的缺陷。在本报告中,我们讨论了一些其他可能导致底物氧化速率紊乱的情况。将特别关注位于呼吸链之外的缺陷,例如呼吸链后酶的缺陷、线粒体内膜或外膜转运机制的缺陷、辅助因子的缺乏以及热休克蛋白的缺乏。