Renouf S, Fairand A, Husson A
Groupe de Biochimie, Physiopathologie Digestive et Nutritionnelle, UFR Médecine-Pharmacie de Rouen, St-Etienne-du-Rouvray, France.
Biol Neonate. 1995;68(3):221-8. doi: 10.1159/000244240.
Dexamethasone increased both argininosuccinate lyase (ASL) activity and specific mRNA level in cultured fetal hepatocytes. Addition of various inhibitors of RNA synthesis showed that the increase in ASL mRNA may be related to an enhancement of ASL gene transcription, but not to a specific messenger stabilization. An apparent half-life of about 12 h for ASL mRNA was found in both untreated and dexamethasone-treated hepatocytes. About 30 h were necessary to observe the maximal effect of dexamethasone, and, in addition, both puromycin and cycloheximide (two inhibitors of protein synthesis) blocked the inducing effect of the steroid. These results suggested the involvement of intermediary protein(s) in the mechanism of induction of ASL mRNA by glucocorticoids.
地塞米松可提高培养的胎儿肝细胞中精氨琥珀酸裂解酶（ASL）的活性和特异性mRNA水平。添加各种RNA合成抑制剂表明，ASL mRNA的增加可能与ASL基因转录增强有关，而非特定信使的稳定化。在未处理和地塞米松处理的肝细胞中，ASL mRNA的表观半衰期约为12小时。观察地塞米松的最大作用约需30小时，此外，嘌呤霉素和环己酰亚胺（两种蛋白质合成抑制剂）均能阻断该类固醇的诱导作用。这些结果提示中间蛋白参与了糖皮质激素诱导ASL mRNA的机制。
