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ToxSci Advance Access originally published online on June 14, 2007
Toxicological Sciences 2007 99(1):234-243; doi:10.1093/toxsci/kfm160
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© The Author 2007. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Developmental Changes in Testicular Sensitivity to Estrogens throughout Fetal and Neonatal Life

Géraldine Delbès, Clotilde Duquenne, Jessica Szenker, Julie Taccoen, René Habert and Christine Levacher1

Laboratory of Differentiation and Radiobiology of the Gonads, Université Paris 7—Denis Diderot and CEA, DSV/iRCM/SCSR/LDRG and INSERM, Unité 566, F-92265, Fontenay aux Roses, France

1 To whom correspondence should be addressed at LDRG/SCSR/IRCM /DSV, Centre CEA, BP6, F-92265, Fontenay aux Roses, France. Fax: +33-1-46-54-99-06. E-mail: christine.levacher{at}cea.fr.

Received April 6, 2007; accepted June 11, 2007


  Abstract

There is now compelling evidence that inappropriate exposure to estrogen during fetal or neonatal life could affect adult reproductive functions because the testis is sensitive to estrogens during specific periods of its development. Therefore, we investigated the effects of exogenous estrogens on gametogenesis and steroidogenesis during fetal and neonatal testicular development in the rat. We used in vitro systems, organ cultures, and dispersed testicular cell cultures, which allow the development of fetal and neonatal germ cells (gonocytes) and Leydig cells. Exogenous estrogens inhibited testosterone production in dispersed testicular cell cultures throughout fetal life, but this inhibition was observed only in the early fetal stages in organ culture. By using an aromatase inhibitor (letrozole, Novartis Pharma AG), we showed that the inhibitory effect of exogenous estrogens on testosterone production is masked in the whole testis at later stages (20.5 days postconception) due essentially to local production of estrogens. In both systems, additions of high concentrations (10–6M) of 17ß-estradiol or diethylstilbestrol decreased the number of gonocytes during the first fetal proliferative period but not during the neonatal period. Letrozole was without effect, suggesting that the aging-related loss of responsiveness of gonocytes is not due to any aromatase activity in the gonocytes.

Key Words: testis development; fetus; neonate; gonocyte; Leydig; testosterone; estrogen.


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