Sanchez P E, Ryan M A, Kridelka F, Gielen I, Ren S G, Albertson B, Malozowski S, Nieman L, Cassorla F
Developmental Endocrinology Branch, National Institute of Child Health and Human Development, Bethesda, Maryland.
Horm Metab Res. 1989 Jul;21(7):369-71. doi: 10.1055/s-2007-1009240.
RU-486 is a synthetic steroid analogue that can inhibit adrenal steroid synthesis in the rat and rhesus monkey. We measured the activities of five testicular and two ovarian microsomal steroidogenic enzymes to assess the potential effect of RU-486 on rat gonadal steroidogenesis. Hypophysectomized, gonadotropin-replaced rats received RU-486 or a vehicle solution twice daily for seven days. The animals were sacrificed and their gonads were resected, weighed, and microsomal enzyme activities were measured according to RU-486 treatment. Testicular 17-hydroxylase and aromatase activity decreased in RU-486 treated animals whereas 17,20-desmolase, 3 beta-hydroxysteroid dehydrogenase and 17-ketosteroid reductase activities were unaffected. Ovarian 17-hydroxylase but not 3 beta-hydroxysteroid dehydrogenase activity was decreased in the animals receiving the drug. We conclude that RU-486 inhibits both testicular and ovarian steroidogenesis in the rat.
RU-486是一种合成类固醇类似物，它能够抑制大鼠和恒河猴的肾上腺类固醇合成。我们测定了五种睾丸和两种卵巢微粒体类固醇生成酶的活性，以评估RU-486对大鼠性腺类固醇生成的潜在影响。垂体切除、促性腺激素替代的大鼠每天接受两次RU-486或赋形剂溶液，持续七天。处死动物后，切除其性腺，称重，并根据RU-486处理情况测定微粒体酶活性。接受RU-486处理的动物睾丸17-羟化酶和芳香化酶活性降低，而17,20-裂解酶、3β-羟类固醇脱氢酶和17-酮类固醇还原酶活性未受影响。接受药物处理的动物卵巢17-羟化酶活性降低，但3β-羟类固醇脱氢酶活性未降低。我们得出结论，RU-486抑制大鼠睾丸和卵巢的类固醇生成。
