Evidence that androgens and oestrogens, as well as follicle-stimulating hormone, can alter Sertoli cell number in the neonatal rat
Evidence that androgens and oestrogens, as well as follicle-stimulating hormone, can alter Sertoli cell number in the neonatal rat
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DOI：
10.1677/joe.1.05884
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发表时间：
2005-01-01
影响因子：
4
通讯作者：
Sharpe, RM
中科院分区：
文献类型：
--
作者：
Atanassova, NN;Walker, M;Sharpe, RM
用己烯雌酚（DES）或促性腺激素释放激素拮抗剂（GnRHa）对雄性大鼠进行新生儿期处理会减少最终的支持细胞数量，这种效应被认为是通过抑制卵泡刺激素（FSH）而发生的。由于这两种处理也会抑制雄激素的作用，我们使用对FSH、睾酮和雌激素（DES）水平有不同影响的单一或联合处理方法，研究了雄激素和雌激素是否可能影响大鼠支持细胞核体积/数量。新生儿期用氟他胺（50mg/kg）处理在第18天显著降低了每个睾丸的支持细胞核体积/数量以及血液中抑制素 - B的水平，尽管FSH水平升高；这种处理还加剧了由0.1μg DES处理引起的每个睾丸支持细胞核体积的减少，且不影响FSH水平。单独用0.1μg DES处理也降低了每个睾丸的支持细胞核体积，且不影响FSH/睾酮水平，但联合使用0.1μg DES + GnR - Ha（抑制FSH和睾酮水平）会导致更显著的效果。单独用GnRHa或10μg DES处理会大幅抑制FSH和睾酮水平，并使每个睾丸的支持细胞核体积/数量减少约60%，但两种处理联合使用的效果并不比单独使用任何一种更强。睾酮酯与10μg DES联合使用部分阻止了10μg DES引起的每个睾丸支持细胞核体积的减少，并使FSH水平正常化。在所有处理组中，血浆抑制素 - B水平与每个睾丸支持细胞核体积/数量的变化平行，但抑制FSH水平的处理（GnRHa，10μg DES）导致抑制素 - B水平的降低比例（约90%）比支持细胞核体积/数量的降低比例（50 - 60%）更大。在单独用10μg DES处理或用0.1μg DES加上氟他胺或GnRHa处理的动物中，单位支持细胞的生殖细胞体积减少，但在其他处理组之间相对保持不变。结论是，在新生大鼠中，（1）内源性雄激素以及FSH在增加支持细胞数量方面具有生理作用，（2）外源性雌激素暴露可在不改变FSH水平的情况下减少支持细胞数量，（3）这些效应可能有一个共同的途径，（4）血液抑制素 - B为支持细胞数量的变化提供了一个可靠的指标。
Neonatal treatment of male rats with diethylstilboestrol (DES) or a gonadotrophin-releasing hormone antagonist (GnRHa) reduces final Sertoli cell number, an effect presumed to occur via suppression of follicle-stimulating hormone (FSH). As both treatments also suppress androgen action, we investigated whether androgens and oestrogens might affect Sertoli cell nuclear volume/number in the rat using single or combined treatments that differentially affected FSH, testosterone and oestrogen (DES) levels. Neonatal treatment with flutamide (50 mg/kg) significantly reduced Sertoli cell nuclear volume/ number per testis and blood inhibin-B levels at day 18, despite elevating FSH levels; this treatment also exacerbated the reduction in Sertoli cell nuclear volume per testis induced by treatment with 0.1 mug DES without affecting FSH levels. Treatment with 0.1 mug DES on its own also reduced Sertoli cell unclear volume per testis without affecting FSH/testosterone levels, but co-administration of 0.1 mug DES+GnR-Ha, which suppressed FSH and testosterone levels, resulted in a markedly greater effect. Treatment with GnRHa alone or 10 lug DES alone grossly suppressed FSH and testosterone levels and reduced Sertoli cell nuclear volume/number per testis by approximately 60%, but co-administration of the two treatments had no greater effect than either alone. Co-administration of testosterone esters with 10 mug DES partially prevented the 10 mug DES-induced reduction in Sertoli cell nuclear volume per testis, and normalized FSH levels. In all treatment groups, plasma levels of inhibin-B paralleled changes in Sertoli cell nuclear volume/number per testis, but treatments that suppressed FSH levels (GnRHa, 10 lug DES) caused a proportionately greater reduction (approximately 90%) in inhibin-B levels than in Sertoli cell nuclear volume/number (50-60%). Germ cell volume per unit Sertoli cell was reduced in animals treated with 10 mug DES alone or in those treated with 0.1 mug DES plus either flutmaide or GnRHa, but other-wise remained relatively constant between treatment groups. It is concluded that, in the neonatal rat, (1) endogenous androgens, as well as FSH, play a physiological role in increasing Sertoli cell number, (2) exogenous oestrogen exposure can decrease Sertoli cell number without altering FSH levels, (3) these effects probably share a common pathway and (4) blood inhibin-B provides a robust indicator of change in Sertoli cell number.