Prenatal exposure to dexamethasone alters Leydig cell steroidogenic capacity in immature and adult rats

This study examines the effects of prenatal exposure to dexamethasone (DEX) on postnatal testosterone production in male rats. Pregnant female rats were treated on gestation days 14–19 with DEX (100 μg/kg body weight per day; n = 9) or vehicle (n = 9). Results show that 35‐day‐old male offspring fro...

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Bibliographic Details
Published in:Journal of andrology 2001-11, Vol.22 (6), p.973-980
Main Authors: Page, K. C, Sottas, C. M, Hardy, M. P
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
corticosterone
Corticosterone - blood
Dexamethasone - pharmacology
Drug toxicity and drugs side effects treatment
Female
luteinizing hormone
Luteinizing Hormone - blood
Male
Medical sciences
neuroendocrine
Pharmacology. Drug treatments
Pregnancy
Prenatal Exposure Delayed Effects
Rats
Reference Values
Sexual Maturation - drug effects
Spermatozoa
Testis
testosterone
Testosterone - blood
Toxicity: urogenital system
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Summary:This study examines the effects of prenatal exposure to dexamethasone (DEX) on postnatal testosterone production in male rats. Pregnant female rats were treated on gestation days 14–19 with DEX (100 μg/kg body weight per day; n = 9) or vehicle (n = 9). Results show that 35‐day‐old male offspring from DEX‐treated pregnant females (n = 42) had decreased levels of serum testosterone (45.6% lower, P< .05) compared with control offspring (n = 43), although serum luteinizing hormone (LH) levels were not significantly altered. These findings suggest that a direct programming of developing gonadal cells occurs in response to high levels of maternal glucocorticoid. Indeed, testosterone production was significantly reduced in Leydig cells isolated from immature offspring of DEX‐treated pregnant females compared with controls (48.3%, P < .001), and LH stimulation of these cells did not compensate for the lowered steroidogenic capacity. The hypothalamic‐pituitary‐adrenal axis was also affected, because significant reductions in both serum adrenocorticotropic hormone (ACTH; 26.2%, P < .001) and corticosterone (CORT; 32.3%, P < .001) were measured in DEX‐exposed immature male offspring. In contrast, adult male offspring from DEX‐treated dams had significantly higher levels of serum ACTH (39.2%, P
ISSN:0196-3635
1939-4640
DOI:10.1002/j.1939-4640.2001.tb03438.x