Adrenal steroidogenesis following prenatal dexamethasone exposure in the spiny mouse

Quinn, Tracey A., Ratnayake, Udani, Castillo-Melendez, Margie, Moritz, Karen M., Dickinson, Hayley and Walker, David W. (2014) Adrenal steroidogenesis following prenatal dexamethasone exposure in the spiny mouse. Journal of Endocrinology, 221 2: 347-362. doi:10.1530/JOE-13-0514

Author Quinn, Tracey A.
Ratnayake, Udani
Castillo-Melendez, Margie
Moritz, Karen M.
Dickinson, Hayley
Walker, David W.
Title Adrenal steroidogenesis following prenatal dexamethasone exposure in the spiny mouse
Journal name Journal of Endocrinology   Check publisher's open access policy
ISSN 0022-0795
Publication date 2014-05-01
Year available 2014
Sub-type Article (original research)
DOI 10.1530/JOE-13-0514
Open Access Status Not Open Access
Volume 221
Issue 2
Start page 347
End page 362
Total pages 16
Place of publication Bristol, United Kingdom
Publisher BioScientifica
Language eng
Formatted abstract
Antenatal stress disturbs the development of the fetal hypothalamic–pituitary–adrenal axis and adrenal steroidogenesis. We investigated the effect of brief maternal exposure to high glucocorticoids (dexamethasone (DEX)) at mid- and late-pregnancy on adrenal structure and production of steroids in spiny mouse. Pregnant spiny mice were treated for 60 h with 125 μg/kg DEX or saline s.c. by osmotic minipump at day 20 (0.5) or 30 (0.75) of gestation. Immunohistochemical expression of steroidogenic acute regulatory-protein (StAR), 3β-hydroxysteroid dehydrogenase (3βHSD), 17-hydroxylase,17-20lyase (P450C17), and cytochromeb5 (CYTB5) was determined in adrenals on postnatal (P) day 170±20. DHEA, testosterone, and cortisol were measured by RIA. Maternal DEX at 20 days significantly reduced the expression of STAR, P450C17 (CYP17A1), and CYTB5 in the adrenal zona reticularis (ZR) of adult offspring, with greater change in male vs female offspring (P<0.05). Plasma DHEA was decreased in male offspring from DEX-treated (6.84±1.24 ng/ml) vs saline-treated (13±0.06 ng/ml; P=0.01) dams, and the DHEA:cortisol ratio was lower in males (P<0.05). Testosterone levels increased in male offspring from DEX (266.03±50.75 pg/ml) vs saline (83.47±32.3 pg/ml, P<0.05)-treated dams. DEX treatment at 0.75 gestation had no significant effect on any parameters measured. This study shows that brief exposure to excess glucocorticoid has long-term impacts on the ZR and adrenal steroidogenesis, affecting the secretion of DHEA and testosterone in male offspring, an effect produced at 0.5 but not at 0.75 gestation. DHEA is important for brain development, and its suppression in adult life might contribute to the neurobehavioral pathologies that can arise after illness and stress during pregnancy.
Keyword Dhea
Prenatal stress
Adrenal cortex
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2015 Collection
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