Transcriptional and translational control of nafenopin-induced ornithine decarboxylase activity in rat liver.
The induction of liver ornithine decarboxylase activity by nafenopin was studied in rats. The alpha-adrenergic antagonist, phentolamine, injected 0.5 hr before nafenopin, greatly potentiated the response. Actinomycin D, injected before nafenopin, did not affect nafenopin-induced ornithine decarboxylase activity whereas the potentiating effect of phentolamine was inhibited. In contrast, administration of actinomycin D 5.0 hr after nafenopin markedly enhanced nafenopin-induced activity. The induction of ornithine decarboxylase activity by nafenopin, as well as the potentiating effect of phentolamine was inhibited by 1,3-diaminopropane and cycloheximide, implying a requirement for synthesis of new enzyme protein for both effects. These results suggest that nafenopin induced ODC through a posttranscriptional mechanism whereas the potentiating effect of phentolamine requires transcription of new messenger RNA.
D000818:Animals; D002262:Carboxy-Lyases / Q000096:biosynthesis*; D003513:Cycloheximide / Q000494:pharmacology; D003609:Dactinomycin / Q000494:pharmacology; D004790:Enzyme Induction / Q000187:drug effects; D008099:Liver / Q000201:enzymology*; D008297:Male; D009255:Nafenopin / Q000494:pharmacology*; D009955:Ornithine Decarboxylase / Q000096:biosynthesis* / Q000235:genetics; D010646:Phentolamine / Q000494:pharmacology; D011422:Propionates / Q000494:pharmacology*; D014176:Protein Biosynthesis / Q000187:drug effects*; D051381:Rats; D014158:Transcription, Genetic / Q000187:drug effects*
D011422:Propionates; D009255:Nafenopin; D003609:Dactinomycin; D003513:Cycloheximide; D002262:Carboxy-Lyases; D009955:Ornithine Decarboxylase; D010646:Phentolamine