Verity M A, Brown W J, Cheung M
Am J Pathol. 1974 Feb;74(2):241-62.
Studies of mitochondrial respiratory control and swelling contraction activity during early cell regeneration after partial hepatectomy have revealed a selective defect in the rate of substrate-supported, phosphate-induced mitochondrial swelling. Swelling profiles induced by Fe(2-) or Cu(2-) revealed no differences between sham-operated and partially hepatectomized mice, which suggests no defects in -SH group composition or ability to form lipid peroxides. The specific activity of mitochondrial cytochrome c oxidase was unchanged. There was no significant mitochondrial swelling in situ as determined from mitocrit and mitochondrial protein ratios. A significant decline in respiratory control and efficiency of oxidative phosphorylation was found in mitochondria from animals 8 and 24 hours after partial hepatectomy, partially reversed by bovine serum albumin. No significant change in ADP:O ratio was noted and the decrease in RCI was due primarily to a significant decline in state 3 respiration rate. In situ electron microscopic studies of mitochondria failed to reveal significant abnormalities during early cell regeneration apart from decrease in numbers of matrix granules, focal matrix rarefaction and predominance of round forms. Electron microscopic studies of mitochondria after in vitro phosphate-induced swelling experiments showed no differences between sham and partially hepatectomized animals, but revealed two distinct populations of mitochondria, the predominant form (type III) showing distortion, matrix lucency and outer membrane rupture. ATP induced a diminished reversal in light scattering in partially hepatectomized mitochondria even when examined at 20 minutes, manifested as an increase in numbers of orthodox mitochondrial forms at the expense of the swollen type III forms. The pathogenesis of the impaired respiratory control and phosphate-induced swelling is unknown, but analogous observations have been found in mitochondria harvested from cells in which abnormal accumulations of free fatty acids have been demonstrated.
对部分肝切除术后早期细胞再生过程中线粒体呼吸控制及肿胀收缩活性的研究表明，在底物支持的、磷酸盐诱导的线粒体肿胀速率方面存在选择性缺陷。由Fe(2-)或Cu(2-)诱导的肿胀曲线显示，假手术组和部分肝切除组小鼠之间没有差异，这表明在-SH基团组成或形成脂质过氧化物的能力方面没有缺陷。线粒体细胞色素c氧化酶的比活性没有变化。根据红细胞压积和线粒体蛋白比率确定，原位线粒体没有明显肿胀。在部分肝切除术后8小时和24小时的动物线粒体中，发现呼吸控制和氧化磷酸化效率显著下降，牛血清白蛋白可部分逆转这种下降。ADP:O比率没有显著变化，呼吸控制率（RCI）的降低主要是由于状态3呼吸速率显著下降。线粒体的原位电子显微镜研究未能揭示早期细胞再生过程中的显著异常，只是基质颗粒数量减少、局部基质稀疏和圆形形态占优势。体外磷酸盐诱导肿胀实验后的线粒体电子显微镜研究表明，假手术组和部分肝切除组动物之间没有差异，但揭示了两种不同的线粒体群体，主要形式（III型）表现出变形、基质透亮和外膜破裂。即使在20分钟时进行检查，ATP也会使部分肝切除的线粒体中光散射的逆转减弱，表现为正常线粒体形态数量增加，以肿胀的III型形态为代价。呼吸控制受损和磷酸盐诱导肿胀的发病机制尚不清楚，但在从已证明存在游离脂肪酸异常积累的细胞中收获的线粒体中也发现了类似的观察结果。
