Hormonal control of mammalian spermatogenesis.

Steinberger, Emil

doi:10.1152/physrev.1971.51.1.1

Cited by 658 publications

(267 citation statements)

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“…In general, many researchers accept the hypothesis that inhibition of testicular testosterone production by E 2 administration is mediated by a decrease of serum LH level through the action of E 2 on the hypothalamic-pituitary axis [10,26]. In fact, in the report of Blanco-Rodriguez and Martinez-Garcia [2], who administered EB using the same protocol as used here, the serum LH level was reduced to 1/ 3 of that before EB treatment, but serum testosterone was undetectable at days 1 through 5 after a single EB treatment.…”

Section: Discussionmentioning

confidence: 99%

“…Both 17β-estradiol (E 2 ) and estradiol-3-benzoate (EB), a synthetic estrogen agonist, are known to have the same effect on testosterone production [2,10,15,26,27,29] in rats. Although some investigators have documented that estrogen exerts its effects via direct action on the testes [15,29], it is generally thought that estrogen's effects are due to indirect action of E 2 via the hypothalamus and pituitary [2,10,26]. Leydig cells synthesize testosterone from cholesterol [22].…”

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Administration of Estradiol-3-Benzoate Down-Regulates the Expression of Testicular Steroidogenic Enzyme Genes for Testosterone Production in the Adult Rat.

et al. 2002

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ABSTRACT. To study the role of estrogen in the testes, testosterone and testicular steroidogenic enzyme mRNA levels were investigated in male Sprague-Dawley rats 24 hr after intramuscular administration of a single dose of estradiol-3-benzoate (EB). EB administration resulted in a greater decrease in intra-testicular and serum testosterone in 10-week-old rats than in 3-or 5-week-old rats. A dose of 2 µg EB/kg had the lowest observed effect. The level of serum luteinizing hormone (LH) was unchanged at any dose. Semiquantitative RT-PCR analysis revealed that, of the four major testicular steroidogenic enzymes, mRNA levels of cytochrome P450 side-chain cleavage and 17β-hydroxysteroid dehydrogenase type-III were significantly reduced, and mRNA levels of cytochrome P450 17α-hydroxylase/ C 17-20 lyase (P450c17) were reduced severely and significantly, by EB administration. However, the level of 3β-hydroxysteroid dehydrogenase type-I mRNA was not changed. In addition, the P450c17 mRNA level in EB-treated rats was much lower than that in the testes of hypophysectomized rats, with the level in the latter being equal to that in control rats. LH is secreted into blood periodically, the effects of estrogen on the LH secretion pattern of the pituitary gland, for example, in frequency and amplitude of LH pulse, were difficult to detect with the methods of the present study. The results indicated, at least, that EB administration down-regulates P450c17 gene expression predominantly, resulting in the inhibition of testosterone production. From the differences in the steroidogenic enzyme expressions between hypophysectomized and EB-treated rats, it was suggested that EB acts on the testis directly or indirectly though not via alteration of LH secretion and induces reduction of P450c17 mRNA level. KEY WORDS: estrogen, rat, steroidogenic enzyme, testis, testosterone.J. Vet. Med. Sci. 64(2): 107-113, 2002 It has been documented that estrogen receptor (ER) α is expressed in Leydig cells, rete testes, and efferent ducts [6], and that ERβ is expressed in Sertoli cells and spermatogenic cells [32]. Eddy et al. found that testes in knockout mice lacking a functional ERα (ERKO) were atrophic with disruptions to the seminiferous epithelium and had gross dilations of the seminiferous tubule lumen in adulthood [5].Further studies on ERKO mice demonstrated that the disruption to spermatogenesis in this line was caused by a back pressure of fluid accumulating in the seminiferous tubules due to a lack of reabsorption of fluid in the efferent ductules, which were stimulated by estrogen in the normal male mouse [9]. These reports suggest that estrogen plays important roles in the male reproductive system.Testosterone plays a fundamental role in spermatogenesis and is synthesized by Leydig cells in the testicular interstitium. Estrogen inhibits testosterone production in the testes of many vertebrates, human [18], rat, frog [23], and fish [8]. Both 17β-estradiol (E 2 ) and estradiol-3-benzoate (EB), a synthetic estrogen agonist, are known to h...

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Section: Discussionmentioning

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Administration of Estradiol-3-Benzoate Down-Regulates the Expression of Testicular Steroidogenic Enzyme Genes for Testosterone Production in the Adult Rat.

et al. 2002

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“…' The hormonal regulation of spermatogenesis involves an interplay of sex steroids and pituitary gonadotrophic hormones acting on specific cells of the testis. Several reviews have brought together earlier work on spermatogenesis (Steinberger, 1971 ;Courot et at., 1970 ;Bishop and Walton, 1960 ;Clermont and Harvey, 1967). Recent progress has led to the identification of target cells for pituitary hormones and steroid hormones within the testis and to the elucidation of molecular mechanisms for hormone action.…”

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Hormonal regulation of Sertoli cell function in the rat

Hansson¹,

Purvis²,

Ritzén³

et al. 1978

Ann. Biol. anim. Bioch. Biophys.

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“…Steinberger and Nelson (1955), using very large doses of oestradiol (222/kg/day) or stilboestrol (1 mg/day), which would completely suppress pituitary gonadotropins (Steinbergcr and Duckett 1967), observed quantitative spermatogenic arrest similar to that observed after hypophysectomy. Steinberger and Duckett (1967) have proposed that the qualitative progress of spermatogenesis is relatively independent of hormonal control up to the late pachytene stage of the primary spermatocytes, but that the reduction division requires testosterone rather than gonadotropic hormones as suggested by Cutuly and Cutuly (1940). Previous work (Elkington and Blackshaw 1970) has shown that testosterone and pregnant mare serum gonadotropin prevent the decline in enzymatic activity and qualitative histology of the oestrogen-treated rat testis.…”

Section: Discussionmentioning

confidence: 99%

Effect of Oestradiol-3,17ß Dipropionate on Spermatogenesis and Lysosomal Enzymes in the Rat Tests

Elkington¹,

Blackshaw²

1971

Aust. Jnl. Of Bio. Sci.

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Daily intramuscular injections (20 f-Lgjday) of oestradiol-3, 17,8 dipropionate in adult male rats depressed body growth and reduced the weight of the testes and seminal vesicles between 4 and 8 days of treatment.The proportion of soluble acid phosphatase (E.C. 3.1.3.2), acid proteinase (E.C. 3.4.4.23), and ,8-glucuronidase (E.C. 3.2.1.31), increased during oestradiol treatment. There was also an increase in the total amount of acid proteinase and ,8.glucuronidase but no significant change in total acid phosphatase activity with oestrogen treatment. These changes in hydrolase activity coincided with a decrease in the yield of late primary spermatocytes from early primary spermatocytes, and long spermatidsfromroundspermatids. Histochemical evidence supported the biochemical and histochemical findings, with increasing tubular staining of acid phosphatase and lipid in the testis during treatment.It is concluded that lysosomal enzymes are important in testicular degeneration and probably in normal spermatogenesis.

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Hormonal control of mammalian spermatogenesis.

Cited by 658 publications

References 0 publications

Administration of Estradiol-3-Benzoate Down-Regulates the Expression of Testicular Steroidogenic Enzyme Genes for Testosterone Production in the Adult Rat.

Administration of Estradiol-3-Benzoate Down-Regulates the Expression of Testicular Steroidogenic Enzyme Genes for Testosterone Production in the Adult Rat.

Hormonal regulation of Sertoli cell function in the rat

Effect of Oestradiol-3,17ß Dipropionate on Spermatogenesis and Lysosomal Enzymes in the Rat Tests

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