Dufy B, Dufy-Barbe L, Vincent J D
Horm Res. 1978;9(5):279-91. doi: 10.1159/000178923.
Ovariectomized female rabbits were pretreated with actinomycin D (80 microgram/100 g body weight) cycloheximide (300 microgram/100 g body weight) or chloramphenicol (300 microgram/100 g body weight) 4 h before an intravenous injection of 25 microgram of estradiol benzoate. Actinomycin D, cycloheximide and chloramphenicol decreased basal gonadotropin levels, but actinomycin D was less active than chloramphenicol and cycloheximide. Despite this effect on basal levels, such treatment did not prevent the effect of estradiol benzoate on LH release. Moreover, no significant impairment of the LH response to LH-RH was found. The interpretation of experiments using drugs such actinomycin D, cycloheximide or chloramphenicol requires caution; however, one cannot disregard the possibility that the negative feed-back effect of estrogen, in contrast to the positive effect, may not be mediated by RNA-dependent DNA and the protein-synthesizing systems.
去卵巢的雌性兔子在静脉注射25微克苯甲酸雌二醇前4小时,用放线菌素D(80微克/100克体重)、放线菌酮(300微克/100克体重)或氯霉素(300微克/100克体重)进行预处理。放线菌素D、放线菌酮和氯霉素降低了基础促性腺激素水平,但放线菌素D的活性低于氯霉素和放线菌酮。尽管对基础水平有这种影响,但这种处理并不能阻止苯甲酸雌二醇对促黄体生成素释放的作用。此外,未发现促黄体生成素对促黄体生成素释放激素反应有明显损害。使用放线菌素D、放线菌酮或氯霉素等药物进行实验的解释需要谨慎;然而,人们不能忽视这样一种可能性,即与雌激素的正性作用相反,其负反馈作用可能不是由RNA依赖性DNA和蛋白质合成系统介导的。