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Journal ArticleDOI

Influence of adrenal cortex on testicular activity in the toad during the breeding season.

18 Feb 2000-Life Sciences (Pergamon)-Vol. 66, Iss: 13, pp 1253-1260

TL;DR: It is concluded that adrenocortical hormone plays an indirect role in testicular activity in toads during the breeding season.

AbstractThe aim of the present study was to determine the role of adrenals in gonadal activity in the male toad during the breeding season. Exogenous administration of corticosterone or metapyrone for 6 days inhibited adrenal Δ 5 -3β(delta 5−3 beta) hydroxysteroid (Δ 5 -3β-HSD) and testicular 17β (17 beta) hydroxysteroid dehydrogenase (17β-HSD) activities, decreased the serum levels of testosterone and inhibited spermatogenesis. When toads were treated with corticosterone a significant rise of serum corticosterone was noted while metapyrone treatment appeared to decrease serum corticosterone levels. It is concluded that adrenocortical hormone plays an indirect role in testicular activity in toads during the breeding season.

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Citations
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Journal Article
TL;DR: The results suggests that the changes that occurred after excessive magnesium in testis were not for the enhanced adrenocortical activities or for the generation of oxidative stress in reproductive organs, but for the direct action of excess magnesium on male gonads.
Abstract: The available information on the effect of excess dietary magnesium on male reproduction is inadequate, though consumption of hard water rich in magnesium salt is not uncommon in many geographical areas. The present study has thus been undertaken to evaluate the morphological as well as cytological and functional changes in testis of magnesium administered sexually mature male Wistar rats. Significant increase in the activities of androgenic enzymes viz. delta(5)3beta-hydroxysteroid dehydrogenase and 17beta-hydroxysteroid dehydrogenase with concomitant increase in serum testosterone level, followed by progressive development in cytoarchitechture of genital organs, without any significant alteration in quantitative spermatogenesis were observed. The results were more marked in the groups treated for longer duration. The results further suggests that the changes that occurred after excessive magnesium in testis were not for the enhanced adrenocortical activities or for the generation of oxidative stress in reproductive organs, but for the direct action of excess magnesium on male gonads. Magnesium supplementation thus has an apparent beneficial effect on male gonadal system.

55 citations

Journal ArticleDOI
TL;DR: Overall observations suggest that excessive dietary calcium enhances the generation of free-radicals resulting in structural and functional disruption of male reproduction.
Abstract: Calcium is essential for functioning of different systems including male reproduction. However, it has also been reported as chemo-castrative agent. The study has been undertaken to elucidate the effect of excessive dietary calcium on male reproductive system in animals with possible action. Adult male healthy rats fed CaCl2 at different doses (0.5, 1.0 and 1.5 g%) in diet for 13 and 26 days to investigate reproductive parameters as well as the markers of oxidative stress. Significant alteration was found (P < 0.05) in testicular and accessory sex organs weight, epididymal sperm count, testicular steroidogenic enzyme (Δ5 3β-HSD and 17β-HSD) activities, serum testosterone, LH, FSH, LPO, activities of antioxidant enzymes, testicular histoarchitecture along with adrenal Δ5 3β-HSD activity with corticosterone level in dose- and time-dependent manner. Overall observations suggest that excessive dietary calcium enhances the generation of free-radicals resulting in structural and functional disruption of male reproduction.

37 citations

Book ChapterDOI
01 Jan 2011
TL;DR: The chapter summarizes recent developments in understanding of the neural and endocrine pathways that mediate stressor effects on reproduction and the role of glucocorticoids in energy metabolism during reproduction in amphibians.
Abstract: Publisher Summary This chapter reviews the evidence that exposure to stressors alters the activity of the hypothalamus–pituitary–adrenal axis and influences reproduction in amphibians. The competing selective pressures of successfully reproducing and avoiding predation can have an impact on many aspects of an animal's behavior and physiology. At stake in this trade-off is survival, as animals engaged in reproduction may deplete energy stores necessary for avoiding predation and may be more vulnerable to predation or pathogens while engaged in reproductive behavior. The impact of this trade-off in shaping endocrine and neuronal pathways is seen clearly in amphibians. The chapter summarizes recent developments in understanding of the neural and endocrine pathways that mediate stressor effects on reproduction and the role of glucocorticoids in energy metabolism during reproduction in amphibians. Special attention is given to how multiple stressors related to changes in habitat quality may have an impact on reproduction and the health of amphibian populations.

31 citations

Journal Article
TL;DR: It is suggested that copper has got a dose-dependent effect on testicular steroidogenic enzyme activity and stimulation of testicular spermatogenesis and serum testosterone and LH level in maturing male rats.
Abstract: Background: Copper is essential as a trace element for metabolic processes. Exposure to copper in industries develops toxicity among the workers. Previous findings on adverse effects of copper on male reproductive function in adult albino rats led to investigate the effects of this metal on reproductive function of maturing male rats in the present experiment. Methodology: To study these effects, immature (30 to 35 days old) Wistar strain albino rats weighing about 50-60 g were treated intraperitoneally with copper chloride at doses of 1000, 2000 and 3000 µg/kg body weight/day for 26 days. Result: Significant fall in accessory sex organ weight and inhibition of testicular 17β-hydroxysteroid dehydrogenase activity along with degeneration of testicular growing spermatogenic cells and reduction in serum testosterone, FSH and LH level were observed at the doses of 2000 and 3000µg/kg/day. On the other hand, at the dose of 1000 µg/kg/day significant increase in testicular steroidogenic enzyme activity and stimulation of testicular spermatogenesis along with rise in serum testosterone and LH level were observed, though no significant change was observed in serum FSH level. This suggests that copper has got a dose-dependent effect on testicular steroidogenesis and spermatogenesis and serum testosterone and LH level in maturing male rats.

31 citations

Journal ArticleDOI
TL;DR: This is the first study to report the direct measurement of GnRH secretion in a poikilothermic tetrapod and revealed potent but sometimes paradoxical effects of steroid hormones, especially E(2), on the reproductive regulation of the male R. pipiens.
Abstract: Several lines of evidence suggest reproduction in the ranid frogs is potently regulated by the gonadal steroids, in particular 5α-dihydrotestosterone (DHT) and 17β-estradiol (E2), and a non-gonadal steroid, the stress hormone corticosterone (Cort). Little is known about how these steroid hormones act upon the GnRH system to regulate the downstream reproductive events. We address these gaps in our knowledge by investigating the effects of Cort, E2, and DHT administration on the in vitro release of GnRH and on the spermatogenesis of adult male leopard frog, Rana pipiens. R. pipiens were implanted for 20 days with silastic capsules containing cholesterol (Ch; control), Cort, E2, or DHT. Upon sacrifice, acute hypothalamic explants were cultured and measured for GnRH release, and testes processed for histological analysis. Although only E2 implant significantly reduced the gonadosomatic index, all three steroid hormones altered spermatogenesis. Cort modestly but significantly reduced the presence of spermatids. The effects of E2 and DHT were both stimulatory and inhibitory, depending on the stage of spermatogenesis. None of the steroid hormones altered baseline GnRH release. Interestingly, only E2 significantly stimulated veratridine-induced GnRH release, suggesting E2 treatment increased the releasable pool of GnRH and/or enhance the excitability of GnRH neurons. In sum, this is the first study to report the direct measurement of GnRH secretion in a poikilothermic tetrapod. Our results revealed potent but sometimes paradoxical effects of steroid hormones, especially E2, on the reproductive regulation of the male R. pipiens.

25 citations


References
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Book
15 Jan 1968
TL;DR: The Radiation Inactivation Method as a Tool to Study Structure-Function Relationships in Proteins Immunoassay with Electrochemical Detection and Theory and Newer Technology Assays for Superoxide Dismutase are studied.
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4,556 citations

Journal ArticleDOI
TL;DR: The direct inhibitory effect of glucocorticoids on testicular LH receptor content and steroidogenesis is demonstrated, suggesting the adrenal glucocORTicoids may regulate testis functions.
Abstract: The direct effects of glucocorticoids on testicular LH receptor content and steroidogenesis were studied in vivo and in vitro. Immature hypophysectomized rats were treated with varying doses of dexamethasone, corticosterone, or a synthetic progestin, 17,21-dimethyl-19-nor-pregna-4,9-diene-3,20-dione (R5020). Some animals were also treated concomitantly with FSH to prevent the hypophysectomy-induced decrease in testis functions. At the end of 5 days of treatment, testicular LH/hCG receptor content was measured by [125I]hCG binding assay while steroidogenic responsiveness was measured by in vitro incubation of testes. Dexamethasone decreased testicular LH receptor in control and FSH-treated hypophysectomized rats in doses as low as 10 microgram/day, whereas corticosterone (10 microgram/day) decreased testicular LH receptor in the FSH-treated rats but had no effect in rats not treated with FSH. In contrast, R5020 had no effect on testicular LH receptor content. In vivo treatment of hypophysectomized rats with FSH increased both basal and hCG-stimulated production of androstanediol in vitro. In contrast, concomitant treatment with dexamethasone, but not R5020, decreased both basal and hCG-stimulated testicular androstanediol production. The direct effect of glucocorticoids on testicular steroidogenic potentials was also studied in primary culture of testicular cells obtained from adult hypophysectomized rats. Treatment of cultured testicular cells wtih hCG increased testosterone production. The addition of various natural and synthetic glucocorticoids, but not R5020, to hCG-treated cells decreased testosterone production in a dose- and time-related manner (triamcinolone greater than or equal to dexamethasone greater than cortisol greater than or equal to corticosterone). A 40% decrease in testosterone production was apparent at 6 h after addition of 10(-7) M dexamethasone to hCG-treated cells. These results demonstrate the direct inhibitory effect of glucocorticoids on testicular LH receptor content and steroidogenesis, suggesting the adrenal glucocorticoids may regulate testis functions.

348 citations

Journal ArticleDOI
TL;DR: Methods for the extensive purification of a soluble 17@-hydroxysteroid dehydrogenasel of human placenta are described, which appears to be responsible for the entire 17/3estradiol-mediated transfer of hydrogen between pyridine nucleotides in soluble extracts of this tissue.
Abstract: This paper describes methods for the extensive purification of a soluble 17@-hydroxysteroid dehydrogenasel of human placenta. This single enzyme appears to be responsible for the entire 17/3estradiol-mediated transfer of hydrogen between pyridine nucleotides in soluble extracts of this tissue. Experiments which were reported in 1958 (2, 3) showed that soluble enzyme preparations derived from human placenta promoted a reversible transhydrogenation between pyridine nucleotides in the presence of low concentrations of 17&hydroxyst,eroids or 17-ketosteroids, notably 17/I-estradiol or estrone. These enzyme preparations also contained an active 17/3-hydroxysteroid dehydrogenase which interconverts 17@estradiol and estrone, and reacts with diphosphopyridine nucleotide (DPN) or triphosphopyridine nucleotide (TPN) (8, 9, 11). We suggested (2, 3) that the 17/3-estradiol-mediated transfer of hydro

248 citations

Journal ArticleDOI
TL;DR: The finding on the negative regulation of P450(17 alpha) protein synthesis by testosterone suggest that the steroidogenic P450 enzymes in Leydig cells are negatively regulated by steroid hormones acting via their cognate receptors.
Abstract: The regulation of cholesterol side-chain cleavage enzyme (P450scc) by glucocorticoids was investigated in mouse Leydig cell cultures. We recently demonstrated that P450scc is constitutively synthesized in Leydig cells and that the rate of P450scc synthesis is increased by chronic treatment of the cultures with 8-bromo-cAMP. We now report that glucocorticoids, specifically, decrease the constitutive and cAMP-induced synthesis of P450scc protein as well as the accumulation of P450scc mRNA. The treatment of cultures with as little as 10 nM dexamethasone resulted in a 50-60% decrease in the rate of synthesis of P450scc protein and mRNA content. The glucocorticoid-mediated decrease in P450scc synthesis was prevented when cultures were treated with the antiglucocorticoid RU-486. RU-486 alone had no effect on the rate of protein synthesis. The effect was specific for glucocorticoids; corticosterone (100 nM) or cortisol (100 nM) brought about a similar decrease as dexamethasone. Treatment of cultures with the progesterone agonist R5020 (100 nM), testosterone (2 microM), or estradiol (50 nM) had no effect on the rate of specific protein synthesis. The synthesis of iron sulfur protein reductase (ISP-reductase) and F1-ATPase were not affected by dexamethasone, indicating that the effect was specific for P450scc. The amount of P450scc mRNA was decreased 61% by dexamethasone and increased 144% by treatment with 8-bromo-cAMP. These data together with our previous finding on the negative regulation of P450(17 alpha) protein synthesis by testosterone suggest that the steroidogenic P450 enzymes in Leydig cells are negatively regulated by steroid hormones acting via their cognate receptors.

166 citations