Endocrine Abstracts (2018) 59 P038 | DOI: 10.1530/endoabs.59.P038

QRT-PCR analysis of the effect of in utero exposure to sewage sludge on steroidogenic gene expression in ovine foetal adrenal gland

Erin A Cooper1, Sreedath Reddy2, Abbie Z Allenson1, Duncan P Cooper1, Paul A Fowler3, Michael T Rae2 & Steven D Morley1,4


1University of Edinburgh Medical School, Edinburgh, UK; 2School of Life, Sport and Social Sciences, Edinburgh Napier University, Edinburgh, UK; 3Centre for reproductive Endocrinology & Medicine, University of Aberdeen, Aberdeen, UK; 4Division of Health Sciences, University of Edinburgh, Edinburgh, UK.


Endocrine disruptors are chemicals which in low concentrations can disturb gene expression in a range of endocrine glands and organs including the fetal and adult adrenal glands, potentially resulting in altered steroidogenic flux. With exposure to endocrine disruptors affecting both animals and humans, it is important to assess both the mechanisms and consequences of disruption in steroidogenic pathways, particularly as foetal development may be especially sensitive to endocrine disruption. Indeed, disruption of foetal development could affect key foetal functions such as organ maturation and the onset of parturition. Sewage sludge, a biosolid by-product of soil water purification, is commonly used as a fertiliser on livestock pasture and has been shown to have endocrine disrupting effects in multiple organs, including the foetal adrenal gland. However, it is not yet known exactly where in the steroidogenic pathway disruption might occur. The purpose of the present study was to compare the effects on fetal steroidogenic gene expression in experimental groups of sheep maintained before and after fetal conception on pasture exposed to sewage sludge or to an organic fertiliser. Expression of candidate ‘rate determining’ steroidogenic genes selected following review of the literature was determined in sewage sludge-exposed E110 ovine fetal adrenal glands by QRT-PCR and compared to organic fertiliser controls. This suggests that flux through the glucocorticoid synthetic pathway may be enhanced during late fetal development, while interconversion of active cortisol and in active cortisone may be suppressed.

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