Lam D C, Levine W G
Res Commun Chem Pathol Pharmacol. 1980 Apr;28(1):113-22.
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.
研究了萘芬诺平对大鼠肝脏鸟氨酸脱羧酶活性的诱导作用。在给予萘芬诺平前0.5小时注射α-肾上腺素能拮抗剂酚妥拉明,可大大增强该反应。在给予萘芬诺平前注射放线菌素D,并不影响萘芬诺平诱导的鸟氨酸脱羧酶活性,而酚妥拉明的增强作用则受到抑制。相反,在给予萘芬诺平5.0小时后给予放线菌素D,可显著增强萘芬诺平诱导的活性。1,3-二氨基丙烷和环己酰亚胺可抑制萘芬诺平诱导的鸟氨酸脱羧酶活性以及酚妥拉明的增强作用,这意味着这两种效应都需要合成新的酶蛋白。这些结果表明,萘芬诺平通过转录后机制诱导鸟氨酸脱羧酶,而酚妥拉明的增强作用需要新信使核糖核酸的转录。