Kang E S, Capaci M T, Kang E H, Law P K, Crosby G
Comp Biochem Physiol B. 1986;83(3):545-50. doi: 10.1016/0305-0491(86)90294-4.
Measurements of [1-14C]oleoyl CoA oxidation in homogenates and isolated mitochondria of skeletal muscles, hearts and livers from dystrophic C57BL/6J mice and unaffected litter-mates indicate that rates are lower in dystrophic mitochondria, but are comparable in whole homogenates. These findings are not due to differences in the endogenous concentrations of the fatty CoA esters. Qualitative and quantitative differences in the molecular weight distribution of the proteins in the mitochondria and post-mitochondrial supernatants are found in the skeletal muscles with increases in the post-mitochondrial supernatant and decreases in the mitochondria in dystrophic samples. We suggest that these results are due to increased leakiness of the mitochondrial membranes in dystrophic muscles. Such differences were not observed in preparations from normal animals.
对营养不良的C57BL/6J小鼠以及未受影响的同窝小鼠的骨骼肌、心脏和肝脏匀浆及分离的线粒体中[1-14C]油酰辅酶A氧化的测量表明，营养不良的线粒体中氧化速率较低，但在整个匀浆中氧化速率相当。这些发现并非由于脂肪酰辅酶A酯的内源性浓度差异所致。在营养不良的样本中，骨骼肌的线粒体和线粒体后上清液中的蛋白质分子量分布存在定性和定量差异，表现为线粒体后上清液增加而线粒体减少。我们认为这些结果是由于营养不良肌肉中线粒体膜的通透性增加所致。在正常动物的制剂中未观察到此类差异。
