Effects on differentiation of reproductive organs and sexual behaviour in Japanese quail by excessive embryonic ERα activation
Anna Mattsson A B and Björn Brunström A B CA Department of Environmental Toxicology, Uppsala University, Norbyvägen 18A, SE-75236 Uppsala, Sweden.
B Centre for Reproductive Biology in Uppsala (CRU).
C Corresponding author. Email: bjorn.brunstrom@ebc.uu.se
Reproduction, Fertility and Development 22(2) 416-425 https://doi.org/10.1071/RD08293
Submitted: 13 December 2008 Accepted: 11 August 2009 Published: 4 January 2010
Abstract
Exposure of Japanese quail (Coturnix japonica) embryos to oestrogenic substances disrupts sexual differentiation of the reproductive tract of both sexes and impairs the copulatory behaviour of the adult male. To examine whether these effects can be induced by selective activation of oestrogen receptor α (ERα), Japanese quail eggs were injected with various doses of the selective ERα agonist 16α-lactone-oestradiol (16α-LE2). The natural oestrogen 17β-oestradiol (E2) was used as a positive control. Both 16α-LE2 and E2 induced formation of an ovary-like cortex in the left testis (ovotestis) and reduced the size of the right testis in male embryos. The asymmetry in testis size remained in sexually mature males. Both substances induced retention and malformation of the Müllerian ducts in embryos of both sexes and malformed oviducts in juveniles. Male copulatory behaviour was suppressed by embryonic exposure to E2 and the highest dose of 16α-LE2. However, the lower dose of 16α-LE2, which markedly affected development of the reproductive organs, was without effects on behaviour. It can therefore not be excluded that the behavioural demasculinisation at the 100-fold higher dose involved cross-activation of oestrogen receptor β (ERβ). In conclusion, our results suggest that oestrogen-induced disruption of reproductive organ development in Japanese quail can be mediated via ERα, whereas the role of ERα in demasculinisation of copulatory behaviour remains to be clarified.
Additional keywords: endocrine disruption, oestrogen receptors, ovotestis, sex differentiation.
Acknowledgements
Bayer Schering Pharma AG (Germany) is acknowledged for kindly providing 16α-LE2. We thank Margareta Mattsson for preparing the histological sections and Johanna Karlsson for performing the image analysis. We also thank Stefan Gunnarsson for advice on the image analysis and Jeanette Axelsson for helpful suggestions on the manuscript. Economic support was given by the Swedish Research Council Formas, and the Swedish Environmental Protection Agency, via the research program ReproSafe.
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