Cajone F, Schiaffonati L, Bernelli-Zazzera A
Lab Invest. 1976 Apr;34(4):387-93.
The high speed supernatant (cell sap) obtained from ischemic livers is less efficient than normal in supporting protein synthesis in cell-free systems. Cell saps from ischemic livers contain a reduced amount of transfer-RNA; the transfer of leucine to the specific tRNA is impaired; the incorporation of leucyl-tRNA into protein is reduced, although less than the incorporation of the corresponding amino acid. The binding of aminoacyl-tRNA to ribosomal subunits and exogenous messengers (polyuridylic acid and uridyl-3'-5'-uridyl-3'-5'-guanosine), is less efficient with ischemic than with normal cells sap, thus indicating a defective activity of elongation factor 1. The total amount-and possibly the intracellular distribution-of elongation factor 2 is also altered in ischemic livers. These changes, which are the expression of a multifunctional deficit of ischemic cell sap, are in general correlated with the duration of ischemia and do not seem to appear around the "point of no return" of the ischemic liver cells.
从缺血肝脏获得的高速上清液（细胞液）在无细胞系统中支持蛋白质合成的效率低于正常情况。缺血肝脏的细胞液中转移RNA的含量减少；亮氨酸向特定转运RNA的转移受损；亮氨酰转运RNA掺入蛋白质的过程减少，尽管比相应氨基酸的掺入减少程度要小。与正常细胞液相比，缺血细胞液中氨酰转运RNA与核糖体亚基和外源性信使（聚尿苷酸和尿苷-3'-5'-尿苷-3'-5'-鸟苷）的结合效率较低，这表明延伸因子1的活性存在缺陷。延伸因子2的总量以及可能的细胞内分布在缺血肝脏中也发生了改变。这些变化是缺血细胞液多功能缺陷的表现，总体上与缺血持续时间相关，似乎在缺血肝细胞的“不可逆点”附近并未出现。
