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Leydig cell desensitization from HCG has been shown to be blocked/minimized by Nolvadex. This occurs by supressing HCG's ability to inhibit the conversion of 17 alpha hydroxyprogesterone to testosterone.
Modulation of Leydig Cell Androgen Biosynthesis and Cytochrome P-450 Levels during Estrogen Treatment and Human Chorionic Gonadotropin induced Desensitization
The similarity of estrogen dependent lesions to those produced by hCG treatment further indicates the involvement of endogenous estrogen in the development of the microsomal enzymatic lesions in gonadotropin-induced desensitization of testicular androgen production.
Tamoxifen suppresses gonadotropin-induced 17 alpha-hydroxyprogesterone accumulation in normal men.
Simultaneous administration of hCG and the estrogen antagonist tamoxifen (20 mg twice daily) almost completely abolished the hCG-induced steroidogenic block localized between 17 OHP and T (17 OHP to T ratio at 24 h, 1.1 +/- 0.1 times baseline; P < 0.01 vs. hCG alone). These data indirectly suggest that, in man, the hCG-induced steroidogenic lesion might be mediated through its estrogen-stimulating effect.
Effect of an antiestrogen on the testicular response to acute and chronic administration of hCG in normal and hypogonadotropic hypogonadic men: tamoxifen and testicular response to hCG.
17OHP rose with hCG alone, but not with hCG + Tx in both groups. E, SHBG and 17OHP/T ratio did not change after treatments. hCG tests: E increased 24 h following hCG administration in every test. The ratio 17OHP/T rose at 24 h in the first and second test but in the third test it did not change. These results support the role of E in the acute hCG-induced Leydig cell desensitization.
Jenetic
Modulation of Leydig Cell Androgen Biosynthesis and Cytochrome P-450 Levels during Estrogen Treatment and Human Chorionic Gonadotropin induced Desensitization
The similarity of estrogen dependent lesions to those produced by hCG treatment further indicates the involvement of endogenous estrogen in the development of the microsomal enzymatic lesions in gonadotropin-induced desensitization of testicular androgen production.
Tamoxifen suppresses gonadotropin-induced 17 alpha-hydroxyprogesterone accumulation in normal men.
Simultaneous administration of hCG and the estrogen antagonist tamoxifen (20 mg twice daily) almost completely abolished the hCG-induced steroidogenic block localized between 17 OHP and T (17 OHP to T ratio at 24 h, 1.1 +/- 0.1 times baseline; P < 0.01 vs. hCG alone). These data indirectly suggest that, in man, the hCG-induced steroidogenic lesion might be mediated through its estrogen-stimulating effect.
Effect of an antiestrogen on the testicular response to acute and chronic administration of hCG in normal and hypogonadotropic hypogonadic men: tamoxifen and testicular response to hCG.
17OHP rose with hCG alone, but not with hCG + Tx in both groups. E, SHBG and 17OHP/T ratio did not change after treatments. hCG tests: E increased 24 h following hCG administration in every test. The ratio 17OHP/T rose at 24 h in the first and second test but in the third test it did not change. These results support the role of E in the acute hCG-induced Leydig cell desensitization.
Jenetic
