Role of glucocorticoids in the stress-induced suppression of testicular steroidogenesis in adult male rats

Orr, T. Edward; Mann, David R.

doi:10.1016/0018-506x(92)90005-g

Cited by 157 publications

(96 citation statements)

References 35 publications

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“…Elevations in circulating corticosteroid after stresses result in a significant drop in testosterone secretion [6,7]. A similar pattern is observed in rats subjected to restrained stress [8][9][10][11]. In humans, the severe psychological stress brought on by the death of a relative or spouse consistently lowers the sperm count [12].…”

Section: Stress and Leydig Cell Functionmentioning

confidence: 65%

“…Sharp increases in glucocorticoid levels accompany exposure to stressors such as restrained [8][9][10][11] and psychosocial interaction with a dominant male [17,18] are associated with the decline of testosterone levels in these animals. Apparently, the classic GRs are involved in these glucocorticoid actions.…”

Section: Stress and Leydig Cell Functionmentioning

confidence: 99%

“…Glucocorticoids act directly on Leydig cells to inhibit testosterone biosynthesis [16,48,49]. Elevations in circulating glucocorticoids during stress including restraint stresses [8][9][10][11] and psychosocial stresses of subordinate rats [17,18] can, therefore, cause suppression in androgen secretion at the level of the testis. Following this view, 11βHSD in Leydig cells normally acts as a protective gatekeeper, maintaining testosterone biosynthesis in the presence of basal glucocorticoid concentrations: testosterone secretion is suppressed only if the oxidative capacity of 11βHSD is exceeded or the dehydrogenase component of the enzyme is inhibited.…”

Section: A Rapid Action Of Glucocorticoids Via 11βhsd1mentioning

confidence: 99%

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Rapid mechanisms of glucocorticoid signaling in the Leydig cell☆

Lian

Lin

et al. 2008

Steroids

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Stress-mediated elevations in circulating glucocorticoid levels lead to corresponding rapid declines in testosterone production by Leydig cells in the testis. In previous studies we have established that glucocorticoids act on Leydig cells directly, through the classic glucocorticoid receptor (GR), and that access to the GR is controlled prior to the GR by a metabolizing pathway mediated by the type 1 isoform of 11β-hydroxysteroid dehydrogenase (11βHSD1). This enzyme is bidirectional (with both oxidase and reductase activities) and in the rat testis is exclusively localized in Leydig cells where it is abundantly expressed and may catalyze the oxidative inactivation of glucocorticoids. The predominant reductase direction of 11βHSD1 activity in liver cells is determined by an enzyme, hexose-6-phosphate dehydrogenase (H6PDH), on the luminal side of the smooth endoplasmic reticulum (SER). Generation of the pyridine nucleotide cofactor NADPH by H6PDH stimulates the reductase direction of 11βHSD1 resulting in increased levels of active glucocorticoids in liver cells. Unlike liver cells, steroidogenic enzymes including 17β-hydroxysteroid dehydrogenase 3 (17βHSD3) forms the coupling with 11βHSD1. Thus the physiological concentrations of androstenedione serve as a substrate for 17βHSD3 utilizing NADPH to generate NADP+, which drives 11βHSD1 in Leydig cells primarily as an oxidase; thus eliminating the adverse effects of glucocorticoids on testosterone production. At the same time 11βHSD1 generates NADPH which promotes testosterone biosynthesis by stimulating 17βHSD3 in a cooperative cycle. This enzymatic coupling constitutes a rapid mechanism for modulating glucocorticoid control of testosterone biosynthesis. Under stress conditions, glucocorticoids also have rapid actions to suppress cAMP formation thus to lower testosterone production.

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Section: Stress and Leydig Cell Functionmentioning

confidence: 65%

Section: Stress and Leydig Cell Functionmentioning

confidence: 99%

Section: A Rapid Action Of Glucocorticoids Via 11βhsd1mentioning

confidence: 99%

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Rapid mechanisms of glucocorticoid signaling in the Leydig cell☆

Lian

Lin

et al. 2008

Steroids

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“…The inhibitory effect of chronic immobilization on plasma T has been a common finding in adult rats (5-7,10,11) attributed to reduced LH concentration (7,20). The precise mechanism of the inhibitory effect of prolonged stress on plasma T, however, is not fully understood since the changes in androgenic response are not always associated with altered LH levels (8,11,21). It was suggested that restraint stress may induce Leydig cell hyposensitivity to gonadotropin leading to a blockade of T biosynthesis at normal LH levels (21).…”

Section: Discussionmentioning

confidence: 99%

“…Although short-or long-term immobilization is stressful to laboratory animals, the magnitude of the response depends on the intensity and duration of the stimulus (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11). Experiments are in progress in our laboratory using a model of aversive stimulation -6 h of daily immobilization -to investigate the effects of stress on the onset of puberty in male rats.…”

Section: Introductionmentioning

confidence: 99%

Decreased spermatogenic and androgenic testicular functions in adult rats submitted to immobilization-induced stress from prepuberty

Almeida

Petenusci

Anselmo-Franci

et al. 1998

Braz J Med Biol Res

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We investigated whether chronic stress applied from prepuberty to full sexual maturity interferes with spermatogenic and androgenic testicular functions. Male Wistar rats (40 days old) were immobilized 6 h a day for 60 days. Following immobilization, plasma concentrations of corticosterone and prolactin increased 135% and 48%, respectively, while plasma luteinizing hormone and testosterone presented a significant decrease of 29% and 37%, respectively. Plasma concentration of follicle-stimulating hormone was not altered in stressed rats. Chronic stress reduced the amount of mature spermatids in the testis by 16% and the spermatozoon concentration in the cauda epididymidis by 32%. A 17% reduction in weight and a 42% decrease in DNA content were observed in the seminal vesicle of immobilized rats but not in its fructose content. The growth and secretory activity of the ventral prostate were not altered by chronic stress.

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Fighting dynamics of male copperheads,Agkistrodon contortrix (Serpentes, Viperidae): Stress-induced inhibition of sexual behavior in losers

Schuett¹

1996

Zoo Biol.

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Role of glucocorticoids in the stress-induced suppression of testicular steroidogenesis in adult male rats

Cited by 157 publications

References 35 publications

Rapid mechanisms of glucocorticoid signaling in the Leydig cell☆

Rapid mechanisms of glucocorticoid signaling in the Leydig cell☆

Decreased spermatogenic and androgenic testicular functions in adult rats submitted to immobilization-induced stress from prepuberty

Fighting dynamics of male copperheads,Agkistrodon contortrix (Serpentes, Viperidae): Stress-induced inhibition of sexual behavior in losers

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