It has been demonstrated that administration of prednisolone to rats causes loss of RNA and protein in the gastrocnemius muscle and increases in RNA and protein levels in the liver. These changes have been shown to involve alterations in RNA turnover in the two tissues. In liver, rate of synthesis of ribosomal RNA was shown to be increased and its rate of breakdown decreased following administration of prednisolone. In muscle, the steroid caused net decreases in rates of synthesis and breakdown of ribosomal RNA. These prednisolone-induced alterations in RNA turnover were not the result of changes in the RNA precursor pool in the tissues. Prednisolone treatment was shown to cause an increase in the activity of the RNA polymerase believed to be responsible for ribosomal RNA synthesis in the liver. This enzyme activity in the muscle was decreased following administration of prednisolone. Ribonuclease activity was decreased in the liver and muscle of prednisolone-treated animals. These alterations of enzymic activities could explain the observed changes in RNA turnover in prednisolone-treated animals. More prednisolone binding occurred in the liver cytosol than occurred in the muscle cytosol. Prednisolone receptors in the muscle appeared to be of a smaller molecular size than receptors in the liver. The prednisolone-receptor complexes from muscle were less stable in a low ionic environment than complexes from the liver. These quantitative and qualitative differences may have dictated the response of each tissue to prednisolone. In the course of this work conditions have been established for isolating cytoplasmic RNA from rat gastrocnemius muscle in an essentially undegraded form and in good yield.
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RNA metabolism in the muscle and liver of prednisolone-treated rats