Miyahara M, Enzan H, Shiraishi N, Kawase M, Yamamoto M, Hara H, Utsumi K
Biochim Biophys Acta. 1982 Feb 25;714(3):505-15. doi: 10.1016/0304-4165(82)90161-1.
Mitochondria isolated from livers of rats which received D-galactosamine (375 mg/kg body wt., four times) demonstrated a marked decrease in respiratory control ratios, the ADP/O ratios, and state 3 respiration rates and an increase in state 4 respiration rates. The aberration was profound with site I being altered prior to sites II and III. Quantitation of phospholipids revealed a reduction of total phospholipids per mg protein with decreases in phosphatidylcholine and phosphatidylethanolamine contents. Caldiolipin was the only phospholipid which remained unaltered. Fatty acid composition was altered in these phospholipids; caldiolipin was altered most severely, showing reductions in linoleic and arachidonic acids, and an elevation in saturated fatty acids and in some other small components of fatty acids. In phosphatidylethanolamine, palmitic acid decreased, whereas stearic and docosahexenoic acids increased. These changes were smaller in phosphatidylcholine fatty acids. These mitochondria were also characterized by an altered composition in high molecular weight polypeptide components. By experiments with normal mitochondria in vitro, galactosamine, but not other aminohexoses, was proved to be an uncoupling agent of the oxidative phosphorylation system. Electron microscopic observation demonstrated that both in vivo and in vitro treatments with galactosamine induced marked disorganization of mitochondrial structures. These results suggest that mitochondrial damage is also included in galactosamine-induced hepatic lesion.
从接受D-半乳糖胺（375毫克/千克体重，共四次）的大鼠肝脏中分离出的线粒体，其呼吸控制率、ADP/O比率和状态3呼吸速率显著降低，状态4呼吸速率增加。这种异常很严重，位点I比位点II和III更早发生改变。磷脂定量显示，每毫克蛋白质的总磷脂减少，磷脂酰胆碱和磷脂酰乙醇胺含量降低。心磷脂是唯一未发生变化的磷脂。这些磷脂的脂肪酸组成发生了改变；心磷脂改变最为严重，亚油酸和花生四烯酸减少，饱和脂肪酸及其他一些脂肪酸小成分增加。在磷脂酰乙醇胺中，棕榈酸减少，而硬脂酸和二十二碳六烯酸增加。这些变化在磷脂酰胆碱脂肪酸中较小。这些线粒体还具有高分子量多肽成分组成改变的特征。通过体外对正常线粒体进行实验，证明半乳糖胺而非其他氨基己糖是氧化磷酸化系统的解偶联剂。电子显微镜观察表明，体内和体外使用半乳糖胺处理均会导致线粒体结构明显紊乱。这些结果表明，线粒体损伤也包含在半乳糖胺诱导的肝脏病变中。
