Alexandrová M
Institute of Experimental Endocrinology, Slovak Academy of Sciences, Bratislava, Czechoslovakia.
J Steroid Biochem Mol Biol. 1992 Mar;41(3-8):723-5. doi: 10.1016/0960-0760(92)90412-c.
The duration of the antagonizing activity of RU486 on tyrosine aminotransferase (TAT) induction and the glucocorticoid receptor in rat liver was studied. A single dose of RU486 (10 mg/kg) caused occupation of the cytosol glucocorticoid receptor in rat liver at 1 h. During this time no nuclear binding of [3H]dexamethasone ([3H]Dex) receptor complex was recorded, and TAT induction was completely blocked. TAT inducibility recovery parallelled receptor binding in both the cytosol and the nuclei, reaching maximum at 12 h. In contrast, nuclear binding recovered in 24 h, and [3H]Dex receptor binding in cytosol 48 h after RU486 application. It is concluded that the inhibitory effect of a single dose of RU486 on TAT induction is of rather short duration. At concomitant presence of agonist and antagonist in vivo, no direct correlation between agonist receptor occupancy and TAT induction could be observed.
研究了RU486对大鼠肝脏酪氨酸转氨酶（TAT）诱导及糖皮质激素受体的拮抗活性持续时间。单剂量的RU486（10毫克/千克）在1小时时导致大鼠肝脏胞质溶胶糖皮质激素受体被占据。在此期间，未记录到[3H]地塞米松（[3H]Dex）受体复合物的核结合，并且TAT诱导被完全阻断。TAT诱导恢复在胞质溶胶和细胞核中均与受体结合平行，在12小时时达到最大值。相比之下，核结合在24小时恢复，RU486应用后48小时胞质溶胶中[3H]Dex受体结合恢复。得出结论，单剂量RU486对TAT诱导的抑制作用持续时间相当短。在体内激动剂和拮抗剂同时存在时，未观察到激动剂受体占据与TAT诱导之间的直接相关性。
