Metabolic adaptations in rat hepatomas. IV. Regulation of threonine and serine dehydrase.

Abstract

The failure of induction of tryptophan pyrrolase (TP) in the majority of hepatomas after the administration of substrate or hormone was shown probably to be the result of a basic defect in the tumor cell itself, and not of the lowered blood flow or the lack of portal blood supply to the tumor. Two exceptions, Hepatomas H-35 and 7793, were shown to have a significant substrate induction in the intact but not in the adrenalectomized host. The absence of “pure” substrate induction in these heptomas was interpreted in the light of modern concepts of protein synthesis and the control of enzyme synthesis. The interpretation suggested that hepatomas may have lost the capacity to maintain a stable RNA template for tryptophan pyrrolase synthesis, so that the substrate induction in the hepatomas no longer occurs unless the RNA template is renewed by corticosteroid stimulation.