Johnson D C
Department of Gynecology and Obstetrics, Ralph L. Smith Research Center, University of Kansas Medical Center, Kansas City 66103.
J Steroid Biochem. 1988 May;29(5):545-51. doi: 10.1016/0022-4731(88)90191-4.
Administration of human chorionic gonadotropin (hCG) to hypophysectomized immature rats caused a rapid reduction in ovarian microsomal 17 alpha-hydroxylase/C17,20-lyase activity (cytochrome P450(17 alpha] with a concomitant large increase in serum progesterone (P4) level. Pretreatment with cycloheximide (Cyclo) or aminoglutethimide (Ag) prevented these effects of hCG, while Actinomycin D (Act-D) or Azastene, an inhibitor of 3-hydroxysteroid dehydrogenase, were ineffective. In ovaries with enzyme activity increased by 48 h exposure to pregnant mare's serum gonadotropin, hCG also caused a large decrease in enzyme activity but only after a lag period of about 2 h: P4 levels were increased simultaneously. Administration of Cyclo. or puromycin (Puro) caused a loss of enzyme activity without changing P4 levels, but both inhibitors prevented some of the loss of activity and rise in P4 induced by hCG. AG and Act D completely inhibited the enzyme reducing action of hCG, as well as the increase in P4 synthesis, in these animals. P4 applied directly onto one ovary of an animal given hCG plus AG reduced enzyme activity by 69%. The results are consistent with the interpretation that increased substrate concentration is one of but not the only important factor in loss of hydroxylase/lyase activity induced by a sudden large increase in luteinizing hormone activity.
给垂体切除的未成熟大鼠注射人绒毛膜促性腺激素（hCG），可导致卵巢微粒体17α-羟化酶/C17,20-裂解酶活性（细胞色素P450(17α)）迅速降低，同时血清孕酮（P4）水平大幅升高。用环己酰亚胺（Cyclo）或氨鲁米特（Ag）预处理可阻止hCG的这些作用，而放线菌素D（Act-D）或3-羟基类固醇脱氢酶抑制剂阿扎司特则无效。在经48小时孕马血清促性腺激素暴露后酶活性增加的卵巢中，hCG也会导致酶活性大幅下降，但有大约2小时的延迟期：同时P4水平升高。注射Cyclo或嘌呤霉素（Puro）会导致酶活性丧失，而P4水平不变，但这两种抑制剂都能阻止hCG诱导的部分酶活性丧失和P4升高。在这些动物中，AG和Act D完全抑制了hCG的酶还原作用以及P4合成的增加。将P4直接施加到给予hCG加AG的动物的一侧卵巢上，可使酶活性降低69%。这些结果符合这样的解释，即底物浓度增加是促黄体生成素活性突然大幅增加诱导羟化酶/裂解酶活性丧失的重要因素之一，但不是唯一重要因素。
