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17ß-Estradiol Treatment Decreases Steroidogenic Enzyme Messenger Ribonucleic Acid Levels in the Rainbow Trout Testis¹

Institut National de la Recherche Agronomique, Laboratoire Institut National de la Recherche Agronomique-Station Commune de Recherches en Ichtyophysiologie, Biodiversité et Environement, Campus de Beaulieu (M.G., H.M., Y.G.), 35042 Rennes Cedex, France; and National Diagnostics Center, BioResearch Ireland, National University of Ireland (O.M.M., T.J.S.), Galway, Ireland

Address all correspondence and requests for reprints to: Dr. Yann Guiguen, Laboratoire Institut National de la Recherche Agronomique-Station Commune de Recherches en Ichtyophysiologie, Biodiversité et Environement, Campus de Beaulieu, 35042 Rennes Cedex, France. E-mail: guiguen{at}beaulieu.rennes.inra.fr

In fish, estrogens are well known for their involvement in ovarian differentiation and have been shown to be very potent feminizing agents when administrated in vivo during early development. However, the mechanism of action of exogenous estrogens is poorly understood. We report here on the feminizing effects of estrogen treatment on the testicular levels of some steroidogenic enzyme messenger RNAs [mRNAs; cholesterol side-chain cleavage (P450scc), 17-hydroxylase/lyase (P450c17), 3ß-hydroxysteroid dehydrogenase (3ßHSD), 11ß-hydroxylase (P45011ß), and aromatase (P450aro)] in the rainbow trout, Oncorhynchus mykiss. Treatment was carried out by dietary administration of 17ß-estradiol (E₂; dosage of 20 mg/kg diet) to a genetically all male population. Steroidogenesis in the differentiating testis was demonstrated to be strongly altered by E₂, as this treatment resulted in considerable decrease in P450c17, 3ßHSD, and P45011ß mRNAs after only 10 days of treatment. In contrast, P450scc and P450aro mRNA levels were unaffected by E₂, with P450scc mRNA levels remaining unaltered and P450aro not stimulated by this feminizing estrogen treatment. To better characterize this E₂ effect, the same treatment was applied on postdifferentiating males, and roughly the same expression pattern was detected with a considerable decrease in testicular P450c17, 3ßHSD, and P45011ß mRNAs and a significant, but reduced, decrease in P450scc mRNA. In the interrenal, these steroidogenic enzyme mRNAs were not significantly affected by this E₂ treatment, except for a slight, but significant, decrease in P450scc mRNA. These results clearly demonstrate that estrogens have profound effects on testicular steroidogenesis and that they are acting specifically on the testis by decreasing mRNA steady state levels of many steroidogenic enzyme genes. The decrease in P45011ß mRNA, and thus inhibition of the synthesis of testicular 11-oxygenated androgens, may be an important step required for the active feminization of these genetic males.

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