Cihak A
Eur J Biochem. 1975 Oct 1;58(1):3-7. doi: 10.1111/j.1432-1033.1975.tb02341.x.
Administration of cycloheximde to adult rats resulted in the enhancement of uridine kinase activity in the liver. The increase of enzyme activity was not affected by adrenal secretion or uptake of food. Actinomycin D, hydroxyurea and puromycin injected simultaneously with cycloheximide depressed the increase of enzyme activity. On the contrary, administration of 5-azacytidine following cycloheximide resulted in further enhancement of uridine kinase. While the half-time of template RNA for uridine kinase in control rat livers was 24 h, for cycloheximide-stimulated enzyme it was about 11 h. At higher dose levels cycloheximide leads to an increased incorporation of both uridine and orotic acid into liver RNA; however, this effect was not observed in the starved animals. The mechanism of action of cycloheximide is briefly mentioned.
给成年大鼠注射放线菌酮会导致肝脏中尿苷激酶活性增强。酶活性的增加不受肾上腺分泌或食物摄取的影响。与放线菌酮同时注射的放线菌素D、羟基脲和嘌呤霉素会抑制酶活性的增加。相反，在放线菌酮之后给予5-氮杂胞苷会导致尿苷激酶进一步增强。对照大鼠肝脏中尿苷激酶模板RNA的半衰期为24小时，而放线菌酮刺激的酶的半衰期约为11小时。在较高剂量水平下，放线菌酮会导致尿苷和乳清酸掺入肝脏RNA的量增加；然而，在饥饿动物中未观察到这种效应。文中简要提及了放线菌酮的作用机制。
