Male Hormonal Contraception

Nieschlag, Eberhard

doi:10.1007/978-3-642-02062-9_11

Cited by 11 publications

(9 citation statements)

References 86 publications

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“…Sertoli cells cultured alone for 6 days were also processed for electron microscopy as described. 26 Cells were post-fixed in 1% OsO 4 [v/v] in 0.1 M sodium cacodylate buffer and stained with uranyl acetate. After dehydration in ascending grades of ethanol, cells were detached from dishes with propylene oxide and subsequently embedded in EPON (Electron Microscopy Sciences).…”

Section: Animalsmentioning

confidence: 99%

“…1,2 In contrast to hormonal approaches which disrupt spermatogenesis by interfering with the hypothalamic-pituitary-testicular axis, [3][4][5] adjudin exerts its effects behind the blood-testis barrier (BTB) in a specialized microenvironment known as the adluminal compartment. The most obvious phenotype following administration of adjudin to adult rats is the loss of developing germ cells from the seminiferous epithelium, most notably elongating/elongated spermatids, followed by round spermatids and spermatocytes but not spermatogonia residing outside of the BTB.…”

Section: Introductionmentioning

confidence: 99%

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Testin and actin are key molecular targets of adjudin, an anti-spermatogenic agent, in the testis

Mruk

Cheng

2011

Spermatogenesis

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Section: Animalsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Testin and actin are key molecular targets of adjudin, an anti-spermatogenic agent, in the testis

Mruk

Cheng

2011

Spermatogenesis

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“…Suppression of the high ITT by inhibition of LH secretion provides the mechanism of the most widely tested method of hormonal male contraception (8, 10, 11). This is achieved by treatment with exogenous T at doses that slightly increase the normal circulating T concentration, thereby enhancing the negative feedback inhibition of gonadotropin secretion.…”

mentioning

confidence: 99%

Overlapping dose responses of spermatogenic and extragonadal testosterone actions jeopardize the principle of hormonal male contraception

et al. 2014

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Testosterone (T), alone or in combination with progestin, provides a promising approach to hormonal male contraception. Its principle relies on enhanced negative feedback of exogenous T to suppress gonadotropins, thereby blocking the testicular T production needed for spermatogenesis, while simultaneously maintaining the extragonadal androgen actions, such as potency and libido, to avoid hypogonadism. A serious drawback of the treatment is that a significant proportion of men do not reach azoospermia or severe oligozoospermia, commensurate with contraceptive efficacy. We tested here, using hypogonadal luteinizing hormone/choriongonadotropin receptor (LHCGR) knockout (LHR−/−) mice, the basic principle of the T-based male contraceptive method, that a specific T dose could maintain extragonadal androgen actions without simultaneously activating spermatogenesis. LHR−/− mice were treated with increasing T doses, and the responses of their spermatogenesis and extragonadal androgen actions (including gonadotropin suppression and sexual behavior) were assessed. Conspicuously, all dose responses to T were practically superimposable, and no dose of T could be defined that would maintain sexual function and suppress gonadotropins without simultaneously activating spermatogenesis. This finding, never addressed in clinical contraceptive trials, is not unexpected in light of the same androgen receptor mediating androgen actions in all organs. When extrapolated to humans, our findings may jeopardize the current approach to hormonal male contraception and call for more effective means of inhibiting intratesticular T production or action, to achieve consistent spermatogenic suppression.—Oduwole, O. O., Vydra, N., Wood, N. E. M., Samanta, L., Owen, L., Keevil, B., Donaldson, M., Naresh, K., Huhtaniemi, I. T. Overlapping dose responses of spermatogenic and extragonadal testosterone actions jeopardize the principle of hormonal male contraception.

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“…One of the aims of this study was to determine whether the pre-or coadministration of NETE influences testosterone-induced effects on prostate growth, as testosterone is being increasingly used in aging men with a high tendency to develop BPH and experimentally in hormonal male contraception [13] . Utilizing our model of castrated macaques, we observed that the administration of NETE resulted in a direct inhibiting effect on testosterone-induced prostate growth, independent of the time of treatment, be it before or parallel to TU administration.…”

Section: Discussionmentioning

confidence: 99%

Testosterone-Induced Prostate Growth Is Blocked by Co- and Preadministration of Norethisterone Enanthate in Castrated Cynomolgus Monkeys

Wistuba¹,

Nieschlag²,

Semjonow

et al. 2012

Urol Int

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Introduction: Prostate size and function are regulated by testosterone. However, the progesterone receptor is expressed in the primate prostate. Progestins affect the prostate by endocrine suppression, but can also act directly. Examining the role of progestins, we studied the effects of norethisterone (NET) on testosterone undecanoate (TU)-induced prostate growth in castrated macaques. Materials and Methods: Two groups (n = 6 for each group) received TU every 9 weeks. Using a crossover setting, group I received norethisterone enanthate (NETE) 3 times at 3-week intervals, while group II received placebo. After 9 weeks, placebo was administered to group I, and group II received NETE. Results: In group II, the prostate grew under TU and placebo over the first period. In group I, coadministered with NETE, the increase was lower. After the crossover, prostates of animals previously treated with NETE did not increase to normal values under placebo. Prostates of animals treated with TU and placebo in the first period shrank following NETE administration after the crossover. The long half-life of NET can explain the lack of a TU effect on animals coadministered with NETE after the crossover. Conclusions: Pre- and coadministration of NET reduces testosterone-induced prostate growth with possible implications for the treatment of benign prostate hyperplasia and hormonal male contraception.

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Male Hormonal Contraception

Cited by 11 publications

References 86 publications

Testin and actin are key molecular targets of adjudin, an anti-spermatogenic agent, in the testis

Testin and actin are key molecular targets of adjudin, an anti-spermatogenic agent, in the testis

Overlapping dose responses of spermatogenic and extragonadal testosterone actions jeopardize the principle of hormonal male contraception

Testosterone-Induced Prostate Growth Is Blocked by Co- and Preadministration of Norethisterone Enanthate in Castrated Cynomolgus Monkeys

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