The Joint Annual Scientific Meetings of the Endocrine Society of Australia and the Society for Reproductive Biology 2018

Maternal corticosterone exposure in pregnant mice alters the expression of placental oxidative stress, antioxidant enzymes and mitochondrial content in a sex specific manner. (#341)

Lucy Bartho 1 , Olivia Holland 1 , Karen Moritz 2 , Anthony Perkins 1 , James Cuffe 1 2
  1. Griffith University, Southport, QLD, Australia
  2. School of Biomedical Science, University of Queensland, Brisbane, QLD, Australia

Many of our most debilitating chronic diseases are caused in part by events that occur before birth. Maternal health is essential for maintaining a healthy pregnancy and optimal birth outcomes. The placenta is an essential organ for pregnancy as it forms the interface between the mother and baby. It is required for nutrient delivery, oxygen transfer and waste removal from the foetus. Maternal stress during pregnancy can impair placental development and foetal growth, which can contribute to the development of chronic disease within offspring in adulthood. Maternal stress increases concentrations of stress hormones, known as glucocorticoids (GCs). GCs hinder placental development, although the mechanisms remain unknown. This study aimed to investigate the role of oxidative stress and antioxidants in glucocorticoid induced placental dysfunction.     

Pregnant C57bl6 mice were exposed to corticosterone for 60 hours from embryonic day 12.5 (E12.5). Placentas were collected at E14.5, RNA extracted and reverse transcribed and gene expression of Thioredoxin Reductase 1 and 2 (TXNRD1 and TXNRD2), Glutathione Peroxidase 1 and 3 (GPX1 and GPX3) and Superoxide Dismutase 1 and 2 (SOD1 and SOD2) was analysed by QPCR. Protein was extracted and used for protein carbonyl assays.

Maternal corticosterone exposure significantly increased TXNRD1 gene expression in female placentae. Interestingly, males from the corticosterone treated placentas had significantly decreased TXNRD2 gene expression. Maternal corticosterone did not affect GPX1, GPX3, SOD1 and SOD2 within the placenta in both sexes. Corticosterone exposure significantly increased protein carbonyl levels in female placentae. Mitochondrial content was significantly reduced in female placentas affected by maternal corticosterone.

The sex specific changes in the expression of mitochondrial content, antioxidant enzymes and protein carbonyl levels demonstrated in the current study may infer different levels of protection from glucocorticoids in males and females. These outcomes may underlie the increased disease outcomes in male offspring compared to females.