PACKER L
J Cell Biol. 1963 Sep;18(3):487-94. doi: 10.1083/jcb.18.3.487.
Two types of swelling-shrinkage change manifested by isolated mammalian heart mitochondria have been studied. One type, designated as phase I or "low amplitude" swelling-shrinkage, is estimated to lead to changes in mitochondrial volume of 20 to 40 per cent, to changes in light scattering of about 30 per cent, and to changes in viscosity. These physical changes in mitochondria are brought about rapidly and reversibly by normal reactants of the respiratory chain. Their speed, specificity, and reversibility indicate that they are closely geared to the normal function of the respiratory chain and are a true reflection of a mechanochemical coupling process characteristic of the physiology of mitochondria. A second type of swelling-shrinkage mechanism, designated as phase II or "high amplitude," leads to changes in light scattering, viscosity, and mitochondrial volume which, frequently but not always, are of higher magnitude than the phase I type. Phase II swelling-shrinkage seems to be only partly under the control of the respiratory chain. Prior to the completion of phase II swelling, a stepwise loss of mitochondrial function can be identified, such as changes in the rate of substrate utilization and loss of respiratory control. Reversal of this type of swelling cannot be effected if the swelling change reaches a steady state. This type of swelling may provide cells with a mechanism for destroying mitochondrial substance.
已经对分离出的哺乳动物心脏线粒体表现出的两种肿胀-收缩变化类型进行了研究。一种类型,称为I期或“低幅度”肿胀-收缩,估计会导致线粒体体积变化20%至40%,光散射变化约30%,以及粘度变化。线粒体的这些物理变化由呼吸链的正常反应物迅速且可逆地引起。它们的速度、特异性和可逆性表明,它们与呼吸链的正常功能紧密相关,是线粒体生理学特征性的机械化学偶联过程的真实反映。第二种肿胀-收缩机制,称为II期或“高幅度”,会导致光散射、粘度和线粒体体积的变化,这些变化通常(但并非总是)比I期类型的幅度更大。II期肿胀-收缩似乎仅部分受呼吸链控制。在II期肿胀完成之前,可以识别出线粒体功能的逐步丧失,例如底物利用速率的变化和呼吸控制的丧失。如果肿胀变化达到稳定状态,则无法逆转这种类型的肿胀。这种类型的肿胀可能为细胞提供一种破坏线粒体物质的机制。