EFFECT OF ESTRADIOL ON TESTICULAR TESTOSTERONE BIOSYNTHESIS
EFFECT OF ESTRADIOL ON TESTICULAR TESTOSTERONE BIOSYNTHESIS
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DOI：
10.1210/endo-106-1-35
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发表时间：
1980-01-01
期刊：
影响因子：
4.8
通讯作者：
LORIAUX, DL
中科院分区：
文献类型：
--
作者：
KALLA, NR;NISULA, BC;LORIAUX, DL
间质细胞胞浆中雌激素受体的存在提示雌激素可能对间质细胞功能有直接作用。用400IU人绒毛膜促性腺激素(HCG)和1IU人卵泡刺激素(Pergonal)，研究了雌二醇(E_2)对睾丸间质细胞睾酮(T)生物合成的直接影响。雌二醇组在S.C.硅橡胶胶囊。将胶囊中含有E2的大鼠与胶囊为空的大鼠进行比较。E_2处理使血浆E_2浓度从380.+-升高。56至670。+-Pg/ml(平均值+-)。SD；P<；0.01)，并将血浆T水平从999.0+-降低。167至461。+-。156 ng/100ml(P<；0.01)。这些血浆类固醇激素的变化与睾丸重量从1167.+-下降有关。170至870+-72 mg(P<；0.01)。前列腺和精囊重量无明显变化。探讨了雌二醇降低血浆T的三种可能机制，即血浆T清除量的改变、睾丸hCG结合的改变和间质细胞T生物合成的改变。E2治疗对血浆T清除率无明显影响。睾丸组织匀浆的HCG结合量从4.70±-下降。0.63至3.12+-0.26 ng hCG/睾丸(P<；0.05)。E_2处理使睾丸T含量从347.+-降低。70至226。+-。15 ng/睾丸(P<；0.05)。睾丸雄烯二酮和脱氢表雄酮也降低。睾丸孕酮含量从13.7。+-升高。2.9至80.2。+-。10.7 ng/睾丸(P<；0.01)，睾丸17-羟孕酮由14.6±-增加。3.2至53.4+-5.7 ng/睾丸(P<；0.01)。雌激素治疗不改变睾丸孕烯醇酮含量(13.78±-)。5.8比21.26。+-。10.5 ng/睾丸)。睾丸类固醇含量的这些变化与微粒体细胞色素P-450(1.38+-)的减少有关。0.08至0.71。+-。0.13nmol/睾丸；P<；0.01)，17.α-羟基酶活性(1.197.+-。0.386至0.157+-0.029毫微克分子/睾丸。17.β-脱氢酶(0.990.+-。0.171至0.443+-0.164毫微克分子/睾丸。最小；P<；0.02)。体内的E2可直接干扰间质细胞的功能。E_2对T生物合成的抑制作用主要表现为17-20脱解酶活性明显降低。
The presence of an estrogen receptor in Leydig cell cytosol suggests that estrogen could have a direct action on Leydig cell function. The direct effects of estradiol (E2) on Leydig cell testosterone (T) biosynthesis were studied using hypophysectomized rats treated daily for 4 days with 400 IU hCG (human chorionic gonadotropin, Pregnyl) and 1 IU human FSH (follitropin, Pergonal), a model that eliminates the possibility of feedback effects of E2 on gonadotropin secretion. E2 was administered in s.c. silastic capsules. Rats having capsules that contained E2 were compared to rats having capsules that were empty. E2 treatment increased plasma E2 concentration from 380 .+-. 56 to 670 .+-. 64 pg/ml (mean .+-. SD; P < 0.01) and decreased plasma T levels from 999 .+-. 167 to 461 .+-. 156 ng/100 ml (P < 0.01). These plasma steroid changes were associated with a decrease in testis weight from 1167 .+-. 170 to 870 .+-. 72 mg (P < 0.01). No change was seen in prostate or seminal vesicle weight. Three possible mechanisms by which E2 treatment could decrease plasma T were investigated, i.e. changes in clearance of plasma T, changes in testicular hCG binding, and altered Leydig cell T biosynthesis. Plasma T clearance was not significantly changed by E2 treatment. hCG binding by testis homogenates was decreased from 4.70 .+-. 0.63 to 3.12 .+-. 0.26 ng hCG/testis (P < 0.05), in E2-treated animals. E2 treatment decreased testicular T content from 347 .+-. 70 to 226 .+-. 15 ng/testis (P < 0.05). Testicular androstenedione and dehydroepiandrosterone were also decreased. Testicular progesterone content increased from 13.7 .+-. 2.9 to 80.2 .+-. 10.7 ng/testis (P < 0.01), and testicular 17-hydroxyprogesterone increased from 14.6 .+-. 3.2 to 53.4 .+-. 5.7 ng/testis (P < 0.01). The pregnenolone content of the testis was not changed by estrogen therapy (13.78 .+-. 5.8 vs. 21.26 .+-. 10.5 ng/testis). These changes in testicular steroid content were associated with a decrease in microsomal cytochrome P-450 (1.38 .+-. 0.08 to 0.71 .+-. 0.13 nmol/testis; P < 0.01), 17.alpha.-hydroxylase activity (1.197 .+-. 0.386 to 0.157 .+-. 0.029 nmol/testis .cntdot. min; P < 0.05), and 17.beta.-dehydrogenase (0.990 .+-. 0.171 to 0.443 .+-. 0.164 nmol/testis .cntdot. min; P < 0.02). E2 in vivo can directly interfere with Leydig cell function. The principal manifestation of the inhibitory effect of E2 on T biosynthesis is an apparent reduction in 17-20 desmolase activity.