The effect of dexamethasone (DXM) on circulating testosterone (T) and luteinizing hormone (LH) in young postpubertal bulls;.

Theriogenology (Impact Factor: 1.85). 03/1976; 5(2):53-60. DOI: 10.1016/0093-691X(76)90168-0
Source: PubMed

ABSTRACT Testosterone (T) and luteinizing hormone (LH) in the peripheral plasma of 6 young postpubertal (52 weeks of age) bulls were measured by radioimmunoassay. For 3 bulls blood samples were collected at half-hour intervals for 6 hours one day before dexamethasone (DXM) injection (20 mg) and two days after. For the 3 others blood collection occurred two days before injection and two days after. On the days before treatment, T and LH concentrations fluctuated similarly to what was previously observed. After treatment LH decreased rapidly and remained between 0.25 and 1.0 ng/ml until the end of the experiment. We observed a small peak of T (between 1.9 and 6.1 ng/ml depending on the animal) immediately after DXM injection; this peak was followed by a decrease to low values (0.25 to 0.5 ng/ml) as soon as 4 hours after injection. It is concluded that DXM suppresses the testosterone secretion. Since we observed a large decrease of LH, we postulate that DXM lowers LH release and therefore indirectly lowers the T synthesis and/or release.

1 Bookmark
  • [Show abstract] [Hide abstract]
    ABSTRACT: The onset of sexual maturity and changes in weight and serum testosterone and cortisol concentrations were studied in male Weddell seals during October–December, 1986, at a breeding colony in McMurdo Sound, Antarctica. Ages were estimated from length or known from tagging history. Underwater copulatory and territorial activities were monitored by colored grease transfer and radiotelemetry, respectively. Hormone concentrations were measured by radioimmunoassay. Of 37 male seals visiting the colony, 22 were resident for ~5 weeks. About one-third of the male residents defended territories into estrus and were called territorial (T). Another one-third appeared unsuccessful at defending a territory and were called transitional (TN). The remaining one-third were nonterritorial (N). Males were closely matched in size (coefficient of variation ≤ 15% for length, girth, and weight). Most N males were 5–7 years old. T males (≥ 7 years old), being older (P < 0.05) than N males, attained 19 of 20 observed copulations. T males were heavier initially (P < 0.10) than TN or N males, and they lost more weight during the breeding season (P = 0.08, 3.2 vs. 2.1 kg/day) than N males. In all males, serum testosterone and cortisol concentrations declined, approaching nadir as estrus and the breeding season ended. Mean (±SE) daily concentrations ranged from 6.8 ± 2.4 ng/mL to nondetectable concentrations for testosterone and from 104.8 ± 13.2 to 54.7 ± 4.5 μg/dL for cortisol. Concentrations of both hormones were higher in T males than in N males. Hormone profiles of TN males initially resembled those of T males, but at estrus resembled those of N males. Coincident with a change in competitive behavior was a transient rise in cortisol accompanied by a drop in testosterone.
    Canadian Journal of Zoology 02/2011; 70(4):680-692. · 1.35 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: In rodents, livestock and primate species, a single dose of the synthetic glucocorticoid dexamethasone acutely lowers testosterone biosynthesis. To determine the mechanism of decreased testosterone biosynthesis, stallions were treated with 0.1mg/kg dexamethasone 12h prior to castration. Dexamethasone decreased serum concentrations of testosterone by 60% compared to saline-treated control stallions. Transcriptome analyses (microarrays, northern blots and quantitative PCR) of testes discovered that dexamethasone treatment decreased concentrations of glucocorticoid receptor alpha (NR3C1), alpha actinin 4 (ACTN4), luteinizing hormone receptor (LHCGR), squalene epoxidase (SQLE), 24-dehydrocholesterol reductase (DHCR24), glutathione S-transferase A3 (GSTA3) and aromatase (CYP19A1) mRNAs. Dexamethasone increased concentrations of NFkB inhibitor A (NFKBIA) mRNA in testes. SQLE, DHCR24 and GSTA3 mRNAs were predominantly expressed by Leydig cells. In man and livestock, the GSTA3 protein provides a major 3-ketosteroid isomerase activity: conversion of Δ(5)-androstenedione to Δ(4)-androstenedione, the immediate precursor of testosterone. Consistent with the decrease in GSTA3 mRNA, dexamethasone decreased the 3-ketosteroid isomerase activity in testicular extracts. In conclusion, dexamethasone acutely decreased the expression of genes involved in hormone signaling (NR3C1, ACTN4 and LHCGR), cholesterol synthesis (SQLE and DHCR24) and steroidogenesis (GSTA3 and CYP19A1) along with testosterone production. This is the first report of dexamethasone down-regulating expression of the GSTA3 gene and a very late step in testosterone biosynthesis. Elucidation of the molecular mechanisms involved may lead to new approaches to modulate androgen regulation of the physiology of humans and livestock in health and disease.
    The Journal of Steroid Biochemistry and Molecular Biology 07/2014; · 4.05 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: In order to determine the mechanism by which stress may affect the secretion and function of luteinizing hormone (LH) in primates, the response of the adrenal and gonadal axes was followed in male rhesus monkeys during brief restraint in primate chairs and during various hormone treatments. To further assess the responsiveness of the gonadal axis, gonadotropin releasing hormone (GnRH) was administered during the experiments. Corticosteroid levels were elevated throughout the first restraint trial as compared to those in subsequent trials. LH was elevated in the first sample of the first trial as compared to that in the following trials. The responses of LH to GnRH were equivalent in all trials, while the testosterone response to GnRH was attenuated in the first trial. A single injection of adrenocorti-cotropin (ACTH, 40 IU), while increasing circulating corticosteroids similarly to that observed during the first restraint trial, failed to cause an acute initial release of LH. However, ACTH did lower the testosterone response to GnRH. Following 5 days of ACTH treatment (40 IU twice daily), basal LH was suppressed, and the testosterone response to GnRH was decreased. Following 5 days of cortisol injections (100 mg twice daily), basal LH and testosterone were suppressed, but again only the testosterone response to GnRH was attenuated. Acute restraint stress, acting by some mechanism other than the activation of adrenal axis, stimulates a transient release of LH. While the stress-stimulated release of corticosteroids failed to affect the LH response following GnRH administration, it did act directly on the testes to prevent the normal release of testosterone. Finally, chronic elevation of corticosteroids, produced by ACTH or cortisol administration, suppressed basal serum LH and attenuated the response of testosterone to GnRH.
    American Journal of Primatology 01/1987; 12(3):263-273. · 2.14 Impact Factor