Effect of Immobilization Stress on Plasma Luteinizing Hormone, Testosterone, and Corticosterone Concentrations and on 3 -Hydroxysteroid Dehydrogenase Activity in the Testes of Adult Rats

Srivastava, Rajesh K.; Taylor, Matthew F.; Mann, David R.

doi:10.3181/00379727-204-43658

Cited by 58 publications

(36 citation statements)

References 6 publications

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“…The ability of stress to inhibit reproductive function is well documented (27,28,37,38,39,40,50,55,56,64,72). A sharp decline of serum testosterone is one of the first signs of IMO.…”

Section: Discussionmentioning

confidence: 99%

“…17), whereas other investigators reported a stimulatory effect of this peptide on steroidogenesis in the mouse testis (29,33). It is well documented that plasma levels of CRH and glucocorticoids increase during stress (30,31,32,55,56,72) and that adrenal glucocorticoids may mediate some of the effects of acute stress on the gonadal axis (24,26,27,28,32,55). Because one determinant in setting the level of glucocorticoid activity in Leydig cells is whether the steroid is metabolized, we followed the expression 11␤HSD transcripts.…”

Section: Discussionmentioning

confidence: 99%

“…A sharp decline of serum testosterone is one of the first signs of immobilization stress (IMO). Acute stress-induced reduction of testosterone production appears to be related to the inhibition of the activities of testicular steroidogenic enzymes (50,55,56,72). On the contrary, in prolonged or repeated stress, testosterone production starts to recover, suggesting that the increased steroidogenic capacity of Leydig cells is somehow associated with restored activity of steroidogenic machinery (39,40).…”

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confidence: 95%

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Repeated immobilization stress disturbed steroidogenic machinery and stimulated the expression of cAMP signaling elements and adrenergic receptors in Leydig cells

Stojkov

Janjic

Bjelic

et al. 2012

American Journal of Physiology-Endocrinology and Metabolism

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Stojkov NJ, Janjic MM, Bjelic MM, Mihajlovic AI, Kostic TS, Andric SA. Repeated immobilization stress disturbed steroidogenic machinery and stimulated the expression of cAMP signaling elements and adrenergic receptors in Leydig cells. Am J Physiol Endocrinol Metab 302: E1239 -E1251, 2012. First published February 28, 2012 doi:10.1152/ajpendo.00554.2011.-This study was designed to evaluate the effect of acute (2 h daily) and repeated (2 h daily for 2 or 10 consecutive days) immobilization stress (IMO) on: 1) the steroidogenic machinery homeostasis; 2) cAMP signaling; and the expression of receptors for main markers of 3) adrenergic and 4) glucocorticoid signaling in Leydig cells of adult rats. The results showed that acute IMO inhibited steroidogenic machinery in Leydig cells by downregulation of Scarb1 (scavenger receptor class B), Cyp11a1 (cholesterol side-chain cleavage enzyme), Cyp17a1 (17␣-hydroxylase/17,20 lyase), and Hsd17b3 (17␤-hydroxysteroid dehydrogenase) expression. In addition to acute IMO effects, repeated IMO increased transcription of Star (steroidogenic acute regulatory protein) and Arr19 (androgen receptor corepressor 19 kDa) in Leydig cells. In the same cells, the transcription of adenylyl cyclases (Adcy7, Adcy9, Adcy10) and cAMPspecific phosphodiesterases (Pde4a, Pde4b, Pde4d, Pde7a, Pde8a) was stimulated, whereas the expression of the genes encoding protein kinase A subunits were unaffected. Ten times repeated IMO increased the levels of all adrenergic receptors and ␤-adrenergic receptor kinase (Adrbk1) in Leydig cells. The transcription analysis was supported by cAMP/testosterone production. In this signaling scenario, partial recovery of testosterone production in medium/content was detected. The physiological significance of the present results was proven by ex vivo application of epinephrine, which increased cAMP/testosterone production by Leydig cells from control rats in greater fashion than from stressed. IMO did not affect the expression of transcripts for Crhr1/Crhr2 (corticotropin releasing hormone receptors), Acthr (adrenocorticotropin releasing hormone receptor), Gr (glucocorticoid receptor), and Hsd11b1 [hydroxysteroid (11-␤) dehydrogenase 1], while all types of IMO stimulated the expression of Hsd11b2, the unidirectional oxidase with high affinity to inactivate glucocorticoids. Thus, presented data provide new molecular/transcriptional base for "fight/adaptation" of Leydig cells and new insights into the role of cAMP, epinephrine, and glucocorticoid signaling in recovery of stress-impaired Leydig cell steroidogenesis.

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“…The ability of stress to inhibit reproductive function is well documented (27,28,37,38,39,40,50,55,56,64,72). A sharp decline of serum testosterone is one of the first signs of IMO.…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 95%

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Repeated immobilization stress disturbed steroidogenic machinery and stimulated the expression of cAMP signaling elements and adrenergic receptors in Leydig cells

Stojkov

Janjic

Bjelic

et al. 2012

American Journal of Physiology-Endocrinology and Metabolism

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“…Immediately after the end of 2-to 3-h stress sessions, serum androgens, but not gonadotropins, are reduced (Orr & Mann 1992, Srivastava et al 1993, Akinbami et al 1994, Maric et al 1996, Kostic et al 1997, 1998a. The stress-induced decrease in serum androgens is accompanied by significant changes in the activities of two steroidogenic enzymes, 3 -hydroxysteroid dehydrogenase (3 HSD) and 17 -hydroxylase/C17-20 lyase (P450c17) (Srivastava et al 1993, Akinbami et al 1994, Maric et al 1996, Kostic et al 1997, 1998a. In vitro androgenesis by decapsulated testes from stressed rats exposed to human chorionic gonadotropin (hCG) for 3 h is also reduced, and this reduction coincides with an elevation in the testicular nitrite levels, a stable oxidation product of the nitric oxide pathway (Kostic et al 1998b).…”

Section: Introductionmentioning

confidence: 98%

Involvement of inducible nitric oxide synthase in stress-impaired testicular steroidogenesis

Kostic¹,

Andrić²,

Marić³

et al. 1999

Journal of Endocrinology

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The immobilization stress induces an acute inhibition of testicular steroidogenesis that is mediated by the nitric oxide (NO) signaling pathway. Here we compared the effects of 2-h immobilization stress on in vivo and in vitro rat steroidogenesis at two time points, 0 h and 6 h after the end of the stress session. As expected, serum androgens and human chorionic gonadotropin (hCG)-stimulated progesterone and testosterone production by testicular tissue were inhibited at 0 h, and also at the 6-h time point. Both the acute and sustained inhibitions of in vitro steroidogenesis were accompanied by a significant increase in nitrite, a stable oxidation product of NO. To clarify which subtype of NO synthase (NOS) (constitutive (cNOS) or inducible (iNOS)) participates in down-regulation of testicular steroidogenesis, aminoguanidine hydrochloride (AG), a selective iNOS inhibitor, was employed. Intratesticular injection of AG prevented the sustained, but not the acute, stress-induced decrease in serum testosterone.When added in vitro, it also prevented the sustained decrease in steroid production and increase in nitrite production by testicular tissue, both in a dose-dependent manner and with EC 50 of about 50 µM. Furthermore, AG added in vivo and in vitro effectively blocked the sustained decrease in 3 -hydroxysteroid dehydrogenase (3 HSD) and 17 -hydroxylase/C17-20 lyase (P450c17) activities. In all concentrations employed, AG did not affect serum androgens and in vitro steroid and nitrite production in unstressed animals. These results indicate that the NO signaling pathway participates in acute and sustained stress-induced down-regulation of testicular steroidogenesis, presumably through its direct action on 3 HSD and P450c17. The acute NO production is controlled by cNOS and the sustained production of this messenger is controlled by iNOS.

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“…In addition, TNF-a acutely elevates glucocorticoid levels [8,10]. Increased glucocorticoids causes primary hypogonadism and diminish androgen production [9,13]. Increased glucocorticoids and reduced androgen levels induce testicular germ cell apoptosis [13].…”

Section: Resultsmentioning

confidence: 99%

ACUTE EFFECTS OF TUMOR NECROSIS FACTOR-a ON TESTICULAR GERM CELL APOPTOSIS AND VASCULAR NEUTROPHIL ADHESION IN RATS

Yazawa

2000

Archives of Andrology

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Effect of Immobilization Stress on Plasma Luteinizing Hormone, Testosterone, and Corticosterone Concentrations and on 3 -Hydroxysteroid Dehydrogenase Activity in the Testes of Adult Rats

Cited by 58 publications

References 6 publications

Repeated immobilization stress disturbed steroidogenic machinery and stimulated the expression of cAMP signaling elements and adrenergic receptors in Leydig cells

Repeated immobilization stress disturbed steroidogenic machinery and stimulated the expression of cAMP signaling elements and adrenergic receptors in Leydig cells

Involvement of inducible nitric oxide synthase in stress-impaired testicular steroidogenesis

ACUTE EFFECTS OF TUMOR NECROSIS FACTOR-a ON TESTICULAR GERM CELL APOPTOSIS AND VASCULAR NEUTROPHIL ADHESION IN RATS

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