Effect of inhibitors of RNA and protein synthesis on the prostatic response to testosterone

Abstract

Testosterone stimulated the in vitro incorporation of 14C-labeled amino acids into protein, [U- 14C]glucose into CO 2 and [ 3H]uridine into RNA in the ventral prostate of the rat. The bulk of the testosterone-stimulated RNA synthesis was blocked by a low dose of actinomycin D (25 μg per 100 g) while the two other responses remained unaffected. Experiments involving an inhibitor of protein synthesis (cycloheximide) indicated that the expression of the prostatic response to testosterone (including increased RNA synthesis and incorporation of [ 14C]glucose into CO 2) is dependent upon the continuous synthesis of proteins. It was thus concluded that the effect of testosterone on RNA synthesis represents predominantly a growth response (an amplification step in the hormone action?) superimposed upon, and perhaps emanating from, an effect of the hormone on the protein synthesis. However, an activation of the synthesis of a few selected species of RNA as the primary response to testosterone could not be excluded.