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Submitted on September 1, 2005
Accepted on October 18, 2005
Graduate School of Pharmaceutical Sciences (J.M., J.T., K.O., T.I., Y.I. H.Y.), Kyushu University, Fukuoka 812-8582; Department of Cell Fate Modulation (T.K.), Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto 860-0811; Division of Active Transport (T.K.), National Institute for Physiological Sciences, Aichi 444-8585, Japan
* To whom correspondence should be addressed. E-mail: yamada{at}xenoba.phar.kyushu-u.ac.jp.
Reproductive and developmental disorders are the most sensitive toxic effects caused by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). TCDD is thought to produce many, if not all, of these toxic effects by impairing steroidogenesis and/or steroid action during the prenatal or early postnatal stages. However, the mechanism of the anti-sex steroid effect of TCDD is not well understood. This study revealed that steroidogenic acute-regulatory protein (StAR), a key transporter of cholesterol for steroidogenesis, in the testes of fetal rats are down-regulated by maternal exposure to TCDD. It was also shown that many mRNAs of steroidogenetic enzymes, including cytochromes P450 11A1, 17 and 11B1, and 3
-hydroxysteroid dehydrogenase, are reduced in fetuses of TCDD-treated dams in a testis-specific manner. The same was also observed for the expression of estrogen 
receptors and androgen receptors. While StAR expression was not affected by TCDD in cultured fetal testis, the fetal serum content of LH (LH), a pituitary regulator of StAR, was significantly reduced by TCDD. In agreement with this, pituitary expression of LH subunit mRNA in fetuses was reduced by maternal exposure to TCDD, while the -subunit remained unchanged. The reduction in LH is suggested to occur by a mechanism different from the reduction in the gonadotropin-releasing hormone level. Direct supply of exogenous gonadotropin to TCDD-exposed fetuses completely abolished the reduction of StAR expression. Taken together, these results demonstrate that TCDD impairs steroidogenesis in the fetus by targeting pituitary gonadotropins.
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