Cahill A, Baio D L, Ivester P, Cunningham C C
Department of Biochemistry, Wake Forest University Medical Center, Winston-Salem, North Carolina 27157-1016, USA.
Alcohol Clin Exp Res. 1996 Nov;20(8):1362-7. doi: 10.1111/j.1530-0277.1996.tb01135.x.
The effects of chronic ethanol consumption on the properties of mitochondrial and cytoplasmic ribosomes were investigated in rat liver. Sedimentation properties of purified mitochondrial (55S) and cytoplasmic (80S) ribosomes were determined by analyses on sucrose density gradients. Mitochondrial ribosomes from control animals moved further in the gradients than did those isolated from ethanol-fed rats, which suggests that ethanol ribosomes have a lower molecular weight. In addition, mitochondrial from ethanol-fed animals contained a lower percentage of ribosomes present as the intact monosome, suggesting that ethanol may have an effect on the stability of the functional mitochondrial ribosomes. This was confirmed by the presence of the larger 39S subunit in preparations from ethanol-fed animals. No such ethanol-related alterations were seen with cytoplasmic ribosomes. The protein composition of mitochondrial cytoplasmic ribosomes was investigated using two-dimensional gel electrophoresis, followed by two-dimensional densitometry. As indicated by differences in protein staining intensity, ethanol consumption seemed to alter the concentration of seven mitochondrial ribosomal proteins. In contrast, no such changes were observed in the protein pattern from cytoplasmic ribosomes. Observations in this study provide for the possibility that alterations in the amounts of selected proteins in the mitochondrial ribosome lead to impaired assembly of the ribosome. These ethanol-related structural changes may be responsible for the decreased activity of mitochondrial ribosomes that results in impaired hepatic mitochondrial protein synthesis (W.B. Coleman and C.C. Cunningham, Biochim. Biophys, Acta 1058:178-186, 1991). Furthermore, this study reemphasizes the increased susceptibility of the hepatic mitochondrial translation system, compared with the cytoplasmic system to chronic ethanol consumption.
研究了长期摄入乙醇对大鼠肝脏线粒体和细胞质核糖体性质的影响。通过在蔗糖密度梯度上进行分析，确定了纯化的线粒体（55S）和细胞质（80S）核糖体的沉降特性。来自对照动物的线粒体核糖体在梯度中的移动比从乙醇喂养大鼠分离的核糖体更远，这表明乙醇处理的核糖体分子量较低。此外，乙醇喂养动物的线粒体中完整单核糖体形式的核糖体百分比更低，这表明乙醇可能对功能性线粒体核糖体的稳定性有影响。乙醇喂养动物的制剂中存在较大的39S亚基证实了这一点。细胞质核糖体未观察到这种与乙醇相关的改变。使用二维凝胶电泳，随后进行二维光密度测定，研究了线粒体和细胞质核糖体的蛋白质组成。如蛋白质染色强度的差异所示，摄入乙醇似乎改变了七种线粒体核糖体蛋白的浓度。相比之下，细胞质核糖体的蛋白质模式未观察到此类变化。本研究中的观察结果表明，线粒体核糖体中特定蛋白质数量的改变可能导致核糖体组装受损。这些与乙醇相关的结构变化可能是线粒体核糖体活性降低的原因，而这会导致肝脏线粒体蛋白质合成受损（W.B.科尔曼和C.C.坎宁安，《生物化学与生物物理学学报》1058:178 - 186，1991）。此外，本研究再次强调，与细胞质系统相比，肝脏线粒体翻译系统对长期摄入乙醇更敏感。
