Lucas-Heron B, Schmitt N, Ollivier B
Laboratoire de Physiologie, Faculté de Médecine, Nantes, France.
Neurosci Lett. 1994 Mar 14;169(1-2):97-100. doi: 10.1016/0304-3940(94)90365-4.
We compared the myotoxic effect of chlorpromazine on mitochondria of gastrocnemius muscle in X-related muscular dystrophy (mdx) and control mice relative to changes in calmitine and calcium concentrations before and 3 and 6 days after a single injection of the drug. The results indicate that mdx mouse mitochondria are less sensitive to the myotoxic effect of chlorpromazine; calmitine and calcium binding were only slightly reduced compared to controls. Our observations indicate that the calmitine structure could differ in mdx and control mice with respect to calcium binding structures, and that the presence of calmitine in the mitochondria of mdx mouse skeletal muscle could explain why muscle degeneration does not occur in these animals. However, the muscles of patients with Duchenne muscular dystrophy (DMD) are lacking in calmitine and are subject to extensive progressive degeneration.
我们比较了氯丙嗪对X连锁型肌营养不良（mdx）小鼠和对照小鼠腓肠肌线粒体的肌毒性作用，以及单次注射该药物前、注射后3天和6天钙调素和钙浓度的变化。结果表明，mdx小鼠线粒体对氯丙嗪的肌毒性作用较不敏感；与对照组相比，钙调素和钙结合仅略有减少。我们的观察结果表明，mdx小鼠和对照小鼠的钙调素结构在钙结合结构方面可能有所不同，并且mdx小鼠骨骼肌线粒体中钙调素的存在可以解释为什么这些动物不会发生肌肉退化。然而，杜氏肌营养不良（DMD）患者的肌肉缺乏钙调素，并会发生广泛的进行性退化。
