How much androgen is required for maintenance of spermatogenesis?

Rommerts, F. F. G.

doi:10.1677/joe.0.1160007

Cited by 67 publications

(29 citation statements)

References 14 publications

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“…Some of the concentrations of testosterone employed in this work which induced an electrophysiological response in Sertoli cells are similar to the values found normally within the testes of the rat (0.2 -0.3 M) [27,28]. Turner et al [15] reported values of 0.2 -0.25 mM in the testis of the rat and Jarrow et al [29] found values around 0.2 mM in rat and 2.0 mM in human aspirated testicular fluid.…”

Section: Discussionsupporting

confidence: 83%

Rapid Effect of Testosterone on Rat Sertoli Cell Membrane Potential. Relationship with K⁺ _ATPChannels

et al. 2002

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For this study, we investigated the changes in the electrophysiological parameters of Sertoli cells in seminiferous tubules from 17 - 19 day-old rats induced by testosterone. Using conventional intracellular microelectrode techniques, we analysed the membrane potential and its input resistance. The entire tubules were fixed in a superfusion chamber continuously perfused with Krebs-Ringer bicarbonate buffer (pH 7.4, 32 degrees C). Visual control of cell impalement was achieved using an inverted microscope. The parameters analysed were passed through an amplifier and recorded using a proprietary software system. The topical application of testosterone (0.1 to 10 microM) led to an immediate (within 30 seconds) and significant dose-dependent depolarization of the membrane potential of the cell at all concentrations used. Concomitantly, the input resistance of the cell membrane underwent a significant increment at 30 seconds. These changes returned to resting values after washout. Topical administration of 17beta-estradiol or progesterone (10 microM) did not change the membrane potential. The addition of the K +ATP channel agonist diazoxide to the perfusion buffer nullified the depolarization effect of testosterone at 30 seconds. This result suggests that the immediate action of testosterone is associated with the closing of K +ATP channels, thereby depolarizing the membrane.

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Section: Discussionsupporting

confidence: 83%

Rapid Effect of Testosterone on Rat Sertoli Cell Membrane Potential. Relationship with K⁺ _ATPChannels

et al. 2002

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“…Thus, in the present study, to more closely examine spermatogenesis, we observed more than 500 seminiferous tubules per animal and demonstrated that DES administration at 15 weeks of age had little or no effect on spermatogenesis. Some rat-based studies have demonstrated that Sertoli cells require high levels of testicular testosterone to support spermatogenesis [43][44][45]. Testosterone is known to preferentially induce conversion of round spermatids between stages VII and VIII [46][47][48][49], and this coincides with the maximal immunoexpression of AR protein in Sertoli cells [50].…”

Section: Discussionmentioning

confidence: 99%

Effects of Maternal Exposure to Low Doses of DES on Testicular Steroidogenesis and Spermatogenesis in Male Rat Offspring

Kobayashi

Shirai

Sakaue

et al. 2009

Journal of Reproduction and Development

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Abstract.Our previous studies have demonstrated that prenatally administered diethylstilbestrol (DES) impairs testicular endocrine function in male offspring. The present study examined whether maternal DES treatment influences testicular steroidogenesis and spermatogenesis. DES was injected subcutaneously at 0.5 or 1.5 μg/kg/day (DES 0.5 and 1.5 groups, respectively) into pregnant SD rats on days 7-21 of gestation. Male offspring in the DES 0.5 and 1.5 groups were autopsied at 1, 3, 6 and 15 weeks after birth. At 1 week, DES treatment did not lead to a change in the volume of P450scc-positive cells (Leydig cells), suggesting that DES has no inhibitory effect on the development of Leydig cells. DES administration disrupted luteinizing hormone receptor (LHr) expression and exerted inhibitory effects on signal transduction from LHr to steroidogenic acute regulatory protein (StAR) in testicular steroidogenesis (P<0.05), although there were no changes in the mRNA expression levels of steroidogenic enzymes, such as P450scc, 3β-hydroxysteroid dehydrogenase (3β-HSD) and P45017α, which may have caused a decrease in the plasma testosterone level. DES treatment did not disrupt the cycle of spermatogenesis but did upregulate the expression levels of androgen receptor (AR) mRNA in both DES groups at 15 weeks (P<0.05). These results indicate that maternal DES treatment disrupts steroidogenesis but induces a high level of AR mRNA expression to counteract the low levels of testosterone during spermatogenesis. uring embryonic development, rat primordial germ cells appear in the yolk sac on embryonic day 10, and the gonadal primordium begins to develop as the genital ridge around embryonic day 11. Primordial germ cells begin to reach the genital ridge on embryonic day 12 [1]; thereafter, Sertoli and Leydig cells in the male differentiate from genital ridge cells, leading to a series of differentiation events. The duration of pregnancy is generally divided into periods of embryonic development (first trimester), organogenesis (second trimester) and organ maturation (third trimester).Diethylstilbestrol (DES), a synthetic non-steroidal estrogen, exhibits strong estrogenic activity by binding to estrogen receptors (ERs). It has been shown that the treatment of pregnant rats with DES dose-dependently (range: 10 to 300 μg/kg) suppresses testosterone levels in the blood and testes of male fetuses [2-4]. We administered doses of DES much lower (1.5 μg/kg) than those previously applied to pregnant rats at 7-21 days of gestation (in the second and third trimesters) and demonstrated that DES suppresses plasma testosterone levels in adolescent male offspring (6 weeks after birth) [5].Androgen plays an important role in the development and function of the testis and male reproductive tract via the androgen receptor (AR). Similarly, since ERs have been found in these tissues [6][7][8][9][10], estrogen may be involved in development of the male reproductive system. Nevertheless, it is apparent that male ER-or aromatase-knockout mice initially ...

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“…At least two observations support the hypothesis FSH and testosterone signaling in Sertoli cells 21 that testosterone may act through alternative mechanisms to complement classical AR actions in Sertoli cells. First, Sertoli cells require testicular testosterone levels greater than 70 nM to support full spermatogenesis even though testosterone binding to AR and gene expression responses to testosterone are saturated at 1 nM (Rommerts 1988, Zirkin et al 1989, Veldscholte et al 1992, Sharpe 1994. Second, [Ca 2þ ] i levels are elevated in primary Sertoli cells within seconds of androgen stimulation and thus cannot be dependent on AR-DNA interactions and initiation of gene expression (Steinsapir et al 1991, Gorczynska & Handelsman 1995, Lyng et al 2000.…”

Section: The Testosterone Paradoxmentioning

confidence: 99%

FSH and testosterone signaling in Sertoli cells

Walker¹,

Cheng²

2005

Reproduction

371

221

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Testosterone and follicle-stimulating hormone (FSH) are required to obtain full reproductive potential. In the testis, somatic Sertoli cells transduce signals from testosterone and FSH into the production of factors that are required by germ cells as they mature into spermatozoa. Recent advances in identifying new signaling pathways that are regulated by FSH and testosterone have allowed for refinement in the understanding of the independent, overlapping and synergistic actions of these hormones. In this review, we discuss the signaling pathways that are regulated by FSH and testosterone as well as the resulting metabolic and gene expression changes that occur as related to Sertoli cell proliferation, differentiation and the support of spermatogenesis.Reproduction (2005) 130 15-28

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How much androgen is required for maintenance of spermatogenesis?

Cited by 67 publications

References 14 publications

Rapid Effect of Testosterone on Rat Sertoli Cell Membrane Potential. Relationship with K⁺ _ATPChannels

Rapid Effect of Testosterone on Rat Sertoli Cell Membrane Potential. Relationship with K⁺ _ATPChannels

Effects of Maternal Exposure to Low Doses of DES on Testicular Steroidogenesis and Spermatogenesis in Male Rat Offspring

FSH and testosterone signaling in Sertoli cells

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How much androgen is required for maintenance of spermatogenesis?

Cited by 67 publications

References 14 publications

Rapid Effect of Testosterone on Rat Sertoli Cell Membrane Potential. Relationship with K+ ATPChannels

Rapid Effect of Testosterone on Rat Sertoli Cell Membrane Potential. Relationship with K+ ATPChannels

Effects of Maternal Exposure to Low Doses of DES on Testicular Steroidogenesis and Spermatogenesis in Male Rat Offspring

FSH and testosterone signaling in Sertoli cells

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Rapid Effect of Testosterone on Rat Sertoli Cell Membrane Potential. Relationship with K⁺ _ATPChannels

Rapid Effect of Testosterone on Rat Sertoli Cell Membrane Potential. Relationship with K⁺ _ATPChannels