PMID- 24594617
OWN - NLM
STAT- MEDLINE
DCOM- 20140630
LR  - 20140513
IS  - 1479-6805 (Electronic)
IS  - 0022-0795 (Linking)
VI  - 221
IP  - 2
DP  - 2014 May
TI  - Adrenal steroidogenesis following prenatal dexamethasone exposure in the spiny 
      mouse.
PG  - 347-62
LID - 10.1530/JOE-13-0514 [doi]
AB  - 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 mug/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), 
      3beta-hydroxysteroid dehydrogenase (3betaHSD), 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.
FAU - Quinn, Tracey A
AU  - Quinn TA
AD  - Monash Institute of Medical Research, The Ritchie Centre, Monash University, 
      27-31 Wright Street, Clayton, Victoria 3168, Australia The Florey Institute of 
      Neuroscience and Mental Health, University of Melbourne, Melbourne, Victoria 
      3010, Australia School of Biomedical Sciences, The University of Queensland, St 
      Lucia, Queensland 4072, Australia Department of Obstetrics and Gynaecology, 
      Monash Medical Centre, Monash University, Clayton, Victoria 3168, Australia.
FAU - Ratnayake, Udani
AU  - Ratnayake U
FAU - Castillo-Melendez, Margie
AU  - Castillo-Melendez M
FAU - Moritz, Karen M
AU  - Moritz KM
FAU - Dickinson, Hayley
AU  - Dickinson H
FAU - Walker, David W
AU  - Walker DW
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140512
PL  - England
TA  - J Endocrinol
JT  - The Journal of endocrinology
JID - 0375363
RN  - 0 (Adrenal Cortex Hormones)
RN  - 7S5I7G3JQL (Dexamethasone)
SB  - IM
MH  - Adrenal Cortex Hormones/*biosynthesis
MH  - Adrenal Glands/embryology/growth & development/*metabolism
MH  - Animals
MH  - Animals, Newborn
MH  - Dexamethasone/*adverse effects
MH  - Embryo, Mammalian
MH  - Female
MH  - Gene Expression Regulation, Developmental/drug effects
MH  - Gene Expression Regulation, Enzymologic/drug effects
MH  - Gestational Age
MH  - Male
MH  - *Maternal Exposure
MH  - Mice
MH  - Pregnancy
MH  - Prenatal Exposure Delayed Effects/*metabolism/physiopathology
OTO - NOTNLM
OT  - DHEA
OT  - P450C17
OT  - adrenal cortex
OT  - glucocorticoids
OT  - prenatal stress
EDAT- 2014/03/07 06:00
MHDA- 2014/07/01 06:00
CRDT- 2014/03/06 06:00
PHST- 2014/03/06 06:00 [entrez]
PHST- 2014/03/07 06:00 [pubmed]
PHST- 2014/07/01 06:00 [medline]
AID - JOE-13-0514 [pii]
AID - 10.1530/JOE-13-0514 [doi]
PST - epublish
SO  - J Endocrinol. 2014 May 12;221(2):347-62. doi: 10.1530/JOE-13-0514. Print 2014 
      May.