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This Article Full Text Full Text (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 Google Scholar Articles by de Waal, P. P Articles by Bogerd, J. PubMed PubMed Citation Articles by de Waal, P. P Articles by Bogerd, J.

¹ Division of Endocrinology and Metabolism, Department of Biology, Faculty of Science, Utrecht University, Hugo R Kruyt Building, Padualaan 8, 3584 CH Utrecht, The Netherlands
² Laboratory of Cellular Biology, Department of Morphology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte MG 31270-901, Brazil
³ Department of Cell Biology, Faculty of Biology, University of Murcia, 30100 Murcia, Spain
⁴ Unité d'évaluation des risques écotoxicologiques, Direction des Risques Chroniques, Institut National de l'Environnement Industriel et des Risques (INERIS), BP 2, F-60550 Verneuil-en-Halatte, France
⁵ Research Group Reproduction and Growth, Institute of Marine Research, PO Box 1870, Nordnes, 5817 Bergen, Norway

(Correspondence should be addressed to J Bogerd or R W Schulz at Division of Endocrinology and Metabolism, Department of Biology, Faculty of Science, Utrecht University; J Bogerd; Email: j.bogerd{at}uu.nl, R W Schulz; Email: r.w.schulz{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 (E₂) 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 Lh was lost after oestrogen exposure. We conclude that oestrogen exposure caused a state of androgen insufficiency in adult male zebrafish. Since the downregulation of the steroidogenic system as well as the disturbance of spermatogenesis in testicular explants exposed to E₂ 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.