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Submitted on October 31, 2003
Accepted on March 15, 2004
-mediated inhibition of male germ cell line development in mice by endogenous estrogens during perinatal life*
1-Unité de Gamétogenèse et génotoxicité., INSERM U566 - CEA - Université Paris 7- Denis Diderot, 92265 Fontenay-aux-Roses, France; 2- IGBMC - INSERM U184, CNRS/INSERM/ULP, Collège de France, BP 163, 37404 Illkirch-Cedex, France.
* To whom correspondence should be addressed. E-mail: christine.levacher{at}cea.fr.
Epidemiological, clinical and experimental studies have suggested that excessive exposure to estrogens during fetal/neonatal life can lead to reproductive disorders and sperm abnormalities in adulthood. However, it is unknown whether endogenous concentrations of estrogens affect establishment of the male fetal germ cell lineage. We addressed this question by studying the testicular development of mice in which the ER
or the ER
gene was inactivated. The homozygous inactivation of ER (ER-) increased the number of gonocytes by 50% in two- and six-day-old neonates. The numbers of Sertoli and Leydig cells and the level of testicular testosterone production were unaffected, suggesting that estrogens act directly on the gonocytes. The increase in the number of gonocytes did not occur during fetal life, but instead occurred just after birth, when gonocytes resumed mitosis and apoptosis. It seems to result from a decrease in apoptosis rate evaluated by TUNEL method and cleaved caspase-3 immunohistochemical detection. Lastly, mice heterozygous for the ER gene inactivation behaved similarly to their ER- littermates in terms of the number of gonocytes, apoptosis and mitosis, suggesting that these cells are highly sensitive to the binding of estrogens to ER. ER inactivation had no effect on the number of neonatal gonocytes and Sertoli cells. In conclusion, this study provides the first demonstration that endogenous estrogens can physiologically inhibit germ cell growth in the male. This finding may have important implications concerning the potential action of environmental estrogens.
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