RNA synthesis and number of transcribing polymerase molecules in ischemic liver nuclei.

Nuclei isolated from ischemic liver show a consistent reduction of their RNA synthesis. The reduction persists at high ionic strength and in the presence of heparin, when RNA synthesis in vitro is fully activated and occurs in the presence as well as in the absence of alpha-amanitin. Both the number of transcribing polymerase molecules and the rate of elongation of initiated polynucleotide chains seem to be equally affected

Protein synthesis in liver injury. Soluble factors of protein synthesis in the cytosol from ischemic rat liver.

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