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This Article Accepted manuscript (PDF) Supplementary data All Versions of this Article: JOE-09-0050v1 202/2/287    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by de Waal, P. Articles by Bogerd, J. Search for Related Content PubMed PubMed Citation Articles by de Waal, P. Articles by Bogerd, J.

P de Waal, Department of Biology, Faculty of Science, Utrecht University, Utrecht, Netherlands
M Leal, Department of Morphology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Brazil
Á García-López, Department of Biology, Faculty of Science, Utrecht University, Utrecht, Netherlands
S Liarte, Department of Cell Biology, Faculty of Biology, University of Murcia, Murcia, Spain
H de Jonge, Department of Biology, Faculty of Science, Utrecht University, Utrecht, Netherlands
N Hinfray, Unité d'évaluation des risques écotoxicologiques, Direction des Risques Chroniques, Institut National de l'Environnement Industriel et des Risques, Verneuil-en-Halatte, France
F Brion, Unité d'évaluation des risques écotoxicologiques, Direction des Risques Chroniques, Institut National de l'Environnement Industriel et des Risques, Verneuil-en-Halatte, France
R Schulz, Department of Biology, Faculty of Science, Utrecht University, Utrecht, Netherlands
J Bogerd, Department of Biology, Faculty of Science, Utrecht University, Utrecht, Netherlands

Correspondence: Jan Bogerd, Email: j.bogerd{at}uu.nl

Androgens can induce complete spermatogenesis in immature or prepubertal teleost fish. However, many aspects of the role of androgens in adult teleost spermatogenesis have remained elusive. Since oestrogens inhibit androgen synthesis, we used an oestrogen-induced androgen depletion model to identify androgen-dependent stages during adult zebrafish spermatogenesis. Exposure to 10 nM 17β-oestradiol in vivo at least halved the mass of differentiating germ cells (from type B spermatogonia to spermatids), while type A spermatogonia accumulated. Studies on the cellular dynamics revealed that a reduction of spermatogonial proliferation together with an inhibition of their differentiation to type B spermatogonia were the basis for the oestrogen-mediated disturbance of spermatogenesis. The capacity of the zebrafish testis to produce 11-ketotestosterone as well as the expression of steroidogenesis-related genes was markedly decreased after in vivo oestrogen exposure. Moreover, the androgen release response to recombinant zebrafish luteinizing hormone was lost after oestrogen exposure. We conclude that oestrogen exposure caused a state of androgen insufficiency in adult male zebrafish. Since the down-regulation of the steroidogenic system as well as disturbance of spermatogenesis in testicular explants exposed to 17β-oestradiol ex vivo was much less severe than after in vivo exposure, the main inhibitory effect appears to be exerted via feedback inhibition of gonadotropin release. This experimental set-up helped to identify spermatogonial proliferation and their differentiation as androgen targets in adult zebrafish spermatogenesis.