Venkatesh B, Tan C H, Lam T J
Department of Zoology, National University of Singapore.
Gen Comp Endocrinol. 1992 Mar;85(3):450-61. doi: 10.1016/0016-6480(92)90090-7.
Production in vitro of estradiol-17 beta, testosterone, 17 alpha-20 beta-dihydroxy-4-pregnen-3-one (17 alpha,20 beta-P), 17 alpha-hydroxyprogesterone, and progesterone by follicles of the guppy at various stages of oocyte growth and gestation was investigated. Basal production of estradiol-17 beta was highest in 0.8- and 1.2-mm follicles, whereas that of testosterone and 17 alpha,20 beta-P was highest in 1.6-mm (postvitellogenic) follicles. Levels of these steroids declined after fertilization and were undetectable in late gestation and postpartum follicles. 17 alpha-Hydroxyprogesterone and progesterone levels were low at all stages. Thus, none of these steroids appears to be involved in maintaining gestation. Regulation of estradiol-17 beta and 17 alpha,20 beta-P secretion by vitellogenic (1.0 mm) and postvitellogenic follicles by precursor substrates, dbcAMP (0.1 to 10 mM) and forskolin (1 to 100 microM), was also investigated. Vitellogenic follicles synthesized increased quantities of estradiol-17 beta in the presence of exogenous testosterone, whereas estradiol-17 beta production by postvitellogenic follicles was not altered by testosterone. These results suggest decreased aromatase activity in the postvitellogenic follicles. Dibutyryl cAMP and/or forskolin stimulated testosterone and estradiol-17 beta production by vitellogenic follicles but did not stimulate conversion of testosterone to estradiol-17 beta, suggesting that the adenylate cyclase system stimulates estradiol-17 beta production by stimulating testosterone production but does not mediate conversion of testosterone to estradiol-17 beta. Postvitellogenic follicles synthesized increased quantities of 17 alpha,20 beta-P in response to 17 alpha-hydroxyprogesterone in a dose-dependent manner. Although 1 microM of forskolin stimulated 17 alpha,20 beta-P production by postvitellogenic follicles in the absence of exogenous 17 alpha-hydroxyprogesterone, 100 microM of forskolin inhibited 17 alpha,20 beta-P production. Dibutyryl cAMP, however, did not affect 17 alpha,20 beta-P production. In the presence of 50 ng of 17 alpha-hydroxyprogesterone, dbcAMP (10 mM) and forskolin (1 to 100 microM) suppressed 17 alpha,20 beta-P production. It is suggested that cAMP mediates 17 alpha,20 beta-P production up to a certain threshold level, beyond which it inhibits 17 alpha,20 beta-P production.
研究了孔雀鱼在卵母细胞生长和妊娠不同阶段卵泡产生雌二醇 - 17β、睾酮、17α - 20β - 二羟基 - 4 - 孕烯 - 3 - 酮（17α,20β - P）、17α - 羟孕酮和孕酮的情况。雌二醇 - 17β的基础产量在0.8毫米和1.2毫米的卵泡中最高，而睾酮和17α,20β - P的基础产量在1.6毫米（卵黄生成后期）的卵泡中最高。受精后这些类固醇的水平下降，在妊娠后期和产后卵泡中无法检测到。17α - 羟孕酮和孕酮水平在所有阶段都很低。因此，这些类固醇似乎都不参与维持妊娠。还研究了卵黄生成期（1.0毫米）和卵黄生成后期卵泡通过前体底物、二丁酰环磷腺苷（dbcAMP，0.1至10 mM）和福斯高林（1至100 μM）对雌二醇 - 17β和17α,20β - P分泌的调节。卵黄生成期卵泡在外源睾酮存在下合成的雌二醇 - 17β量增加，而卵黄生成后期卵泡产生的雌二醇 - 17β不受睾酮影响。这些结果表明卵黄生成后期卵泡中芳香化酶活性降低。二丁酰环磷腺苷和/或福斯高林刺激卵黄生成期卵泡产生睾酮和雌二醇 - 17β，但不刺激睾酮向雌二醇 - 17β的转化，这表明腺苷酸环化酶系统通过刺激睾酮产生来刺激雌二醇 - 17β的产生，但不介导睾酮向雌二醇 - 17β的转化。卵黄生成后期卵泡对17α - 羟孕酮以剂量依赖方式合成增加量的17α,20β - P。虽然在没有外源17α - 羟孕酮的情况下，1 μM福斯高林刺激卵黄生成后期卵泡产生17α,20β - P，但100 μM福斯高林抑制17α,20β - P的产生。然而，二丁酰环磷腺苷不影响17α,20β - P的产生。在存在50 ng 17α - 羟孕酮的情况下，dbcAMP（10 mM）和福斯高林（1至100 μM）抑制17α,20β - P的产生。提示cAMP在一定阈值水平之前介导17α,20β - P的产生，超过该阈值则抑制17α,20β - P的产生。
