Studies in Testicular Function. I. Quantitative Effects of FSH, LH, Testosterone and Dihydro-testosterone on Restoration and Maintenance of Spermatogenesis in the Hypophysectomized Rat

Js, Elkington; Aw, Blackshaw

doi:10.1071/bi9740047

Cited by 33 publications

(12 citation statements)

References 24 publications

(39 reference statements)

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“…Subsequent administration of T to GnRH-immunized rats has been shown to quantitatively restore complete spermatogenesis and fertility [6,22] over an 8-wk period, indicating that FSH is clearly not an absolute requirement for restoration of spermatogenesis despite widespread speculation to the contrary. This result, combined with the observed inability of T to restore spermatogenesis quantitatively in hypophysectomized rats [33][34][35][36], suggests that pituitary hormones other than, or in addition to, FSH may play a major role in the restoration of spermatogenesis.…”

Section: Discussionmentioning

confidence: 61%

Maintenance of Sexual Function with Testosterone in the Gonadotropin-Releasing Hormone-Immunized Hypogonadotropic Infertile Male Rat

Awoniyi¹,

Reece²,

Hurst³

et al. 1993

Biology of Reproduction

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We have previously shown that active immunization against GnRH in the mature male rat can predictably produce hypogonadotropic hypogonadism and azoospermia and, further, that normospermia and normal fertility can be restored by testosterone (T) administration alone. The objective of this study was to explore the hypothesis that GnRH-immunized azoospermic rats could be supplemented with T doses sufficient to restore sexual behavior, but insufficient to support adequate spermatogenesis or to allow restoration of fertility. Adult male rats of proven fertility were immunized against GnRH and supplemented with 2-, 4-, or 8-cm T implants or with empty implants. Eight weeks later, fertility was evaluated; concentrations of serum T, LH, FSH, growth hormone (GH), prolactin (PRL), and thyroid-stimulating hormone (TSH) were determined; sperm number was obtained from the testis; and weights of androgen-dependent organs were measured. GnRH immunization and T supplementation resulted in restoration of organ weights and of fertility in a dose-dependent manner. GnRH immunization with or without T supplementation resulted in the absence of circulating gonadotropins, but had no effect on serum GH, PRL, or TSH levels. Whereas all control animals were fertile, rats that received either empty or 2-cm T implants were completely infertile. Rats that received 4-cm or 8-cm T implants were fertile in 60% and 100% of cases, respectively. Sexual behavior of rats with empty and with 2-cm T implants was compared at 10-18 wk after immunization with GnRH. GnRH-immunized rats given empty implants displayed negligible sexual activity, but those with 2-cm T implants displayed sexual activity equivalent to that of untreated controls despite complete infertility.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionmentioning

confidence: 61%

Maintenance of Sexual Function with Testosterone in the Gonadotropin-Releasing Hormone-Immunized Hypogonadotropic Infertile Male Rat

Awoniyi¹,

Reece²,

Hurst³

et al. 1993

Biology of Reproduction

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mentioning

confidence: 80%

“…FSH will potentiate the action of LH during these steps (1,5,8,10), although FSH alone was observed to have no effect on the maturation of the spermatids in some (8,10,11), but not all (5), studies. It was suggested that the conversion of late spermatocytes to early spermatids is probably not hormonally sensitive (5,8), although this step was suppressed in testosterone-induced restoration experiments (9). Other studies showed that spermatogenesis can be qualitatively maintained in adult rats by testosterone alone (12), while a combination of testosterone and FSH appeared to be necessary for initiation of spermatogenesis at puberty in both rat (6,13) and man (14).…”

mentioning

confidence: 80%

“…3, the decreased SC/ SG ratio in the HPX groups compared to that in the intact groups suggests that a pituitary factor as well as testosterone are involved in this conversion. Previous studies have suggested that either testosterone (10) or FSH and testosterone (5,39) were effective in promoting this conversion. This study, thus, confirms the need for both hormones in maintaining the conversion of spermatogonia to spermatocytes.…”

Section: Spermatocytesmentioning

confidence: 97%

“…In general, the hormonally sensitive steps in the spermatogenic process have been identified as spermatogonial proliferation (4)(5)(6)(7), the conversion from early to late spermatocytes (5,8), and the conversion from early to late spermatids (5,8,9). FSH will potentiate the action of LH during these steps (1,5,8,10), although FSH alone was observed to have no effect on the maturation of the spermatids in some (8,10,11), but not all (5), studies.…”

mentioning

confidence: 93%

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Quantitative Cytological Studies of Spermatogenesis in Intact and Hypophysectomized Rats: Identification of Androgen-Dependent Stages*

et al. 1990

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A stereological study of the numbers of germ cells in various stages of spermatogenesis was undertaken in testosterone-treated intact and hypophysectomized (HPX) rats. Adult Sprague-Dawley rats were given testosterone by Silastic implants, which either inhibited (3-cm length) or partially maintained (10 cm) spermatogenesis over a 13-week period. The numbers of nuclei of the various germ cell categories (spermatogonia, spermatocytes, and round spermatids) in the testes were estimated by profile counting and measurement of nuclear diameter. The numbers of elongated spermatids were determined separately in testicular homogenates. Testis weight, seminiferous tubule volume, and tubule diameter were significantly decreased in intact rats with 3- and 10-cm testosterone implants and in HPX rats, although they were partially maintained in groups with 10-cm implants compared to those in groups with 3-cm implants (P less than 0.05). The effect of 3-cm testosterone implants in the intact group was to suppress the number of spermatogonia to 57%, reduce the conversion of spermatogonia to spermatocytes to 85%, and reduce the conversion of round to elongated spermatids to 19% of the control value. This latter effect was largely overcome with 10-cm testosterone implants. In HPX rats, only 10-cm implants were effective in maintaining the conversion of round spermatids to elongated spermatids. However, testosterone alone was less effective in maintaining the conversion of spermatocytes to round spermatids, suggesting that a pituitary factor, probably FSH, was involved. It is concluded that testosterone has a major effect on the conversion of round to elongated spermatids. The conversion of spermatogonia to spermatocytes and the conversion of spermatocytes to round spermatids depend on the synergistic action of both FSH and testosterone. However, the effect of FSH is greatest on the conversion of spermatocytes to spermatids, i.e. meiosis.

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Can Spermatogenesis Be Maintained Quantitatively in Intact Adult Rats with Exogenously Administered Dihydrotestosterone?

CHEN,

CHANDRASHEKAR,

ZIRKIN

1994

Journal of Andrology

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It is well established that testosterone (T) is required to maintain spermatogenesis in the mammalian testis, presumably acting through a receptor mechanism, as elsewhere. It is puzzling, however, that the T concentration that is required to maintain spermatogenesis quantitatively in intact adult rats (15–20 ng/ml) is well in excess of the concentration required to saturate testicular androgen receptors. If, indeed, T regulation of spermatogenesis is mediated through the androgen receptor, 5α‐dihydrotestosterone (DHT) would be expected to more effectively maintain spermatogenesis than T because of its greater affinity for, and slower rate of dissociation from, the androgen receptor. To test this hypothesis experimentally, the quantitative relationship between the intratesticular concentration of exogenously administered DHT and the maintenance of germ cell production was examined in intact rats in which endogenous T production was suppressed. To this end, rats received increasing doses of DHT via polydimethylsiloxane implants of 6–36 cm in length for 8 weeks. In each DHT‐treated rat, serum luteinizing hormone (LH) concentration was reduced to below the limit of detectability by radioimmunoassay (RIA), and intratesticular T concentration was reduced by >90%. Serum and intratesticular DHT concentrations increased with increasing implant size. The serum and intratesticular concentrations of 5α‐androstane‐3α, 17β‐diol (3α‐Diol) were consistently higher than DHT concentrations because of conversion of DHT to 3α‐Diol. Spermatogenesis was maintained qualitatively in some rats that received implants of 6 cm, in most rats that received implants of 12 cm, and in all rats that received implants of 18 cm. Spermatogenesis was maintained quantitatively in most rats that received implants of 24 cm and 36 cm. The minimal average intratesticular concentration of DHT associated with the quantitative maintenance of spermatogenesis was approximately 50% of the T concentration shown previously to be minimally required. These results indicate that DHT, with its greater affinity for, and slower rate of dissociation from, the androgen receptor, more effectively maintains spermatogenesis than T at comparable intratesticular concentrations.

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Studies in Testicular Function. I. Quantitative Effects of FSH, LH, Testosterone and Dihydro-testosterone on Restoration and Maintenance of Spermatogenesis in the Hypophysectomized Rat

Cited by 33 publications

References 24 publications

Maintenance of Sexual Function with Testosterone in the Gonadotropin-Releasing Hormone-Immunized Hypogonadotropic Infertile Male Rat

Maintenance of Sexual Function with Testosterone in the Gonadotropin-Releasing Hormone-Immunized Hypogonadotropic Infertile Male Rat

Quantitative Cytological Studies of Spermatogenesis in Intact and Hypophysectomized Rats: Identification of Androgen-Dependent Stages*

Can Spermatogenesis Be Maintained Quantitatively in Intact Adult Rats with Exogenously Administered Dihydrotestosterone?

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