Maternal exposure to 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD) causes a number of toxic effects on development such as growth retardation and sexual immaturity in the offspring. However, the toxic mechanism remains unknown. Our previous studies have revealed that single oral administration of TCDD (1 jg/kg) to pregnant rats at gestational day (GD) 15 attenuates the fetal expression of testicular steroidogenic proteins such as steroidogenic acute-regulatory protein (StAR) and cytochrome P450 (CYP) 17 by targeting the fetal production of pituitary gonadotropins. In addition, we provided evidence that TCDD-produced damage on the fetal pituitary-gonad axis leads to imprint defects in sexual behaviors at adulthood. In this study, we investigated whether TCDD also affects fetal steroidogenesis in the adrenal gland. When pregnant Wistar rats were orally treated with TCDD, the fetal expression of CYP21, CYP11B1 and CYP11B2 mRNAs was either induced or tended to be induced in the male adrenal gland during GD17 and GD19, while the expression of mRNAs coding for StAR, CYP11A1 and 313-hydroxysteroid dehydrogenase was insensitive to TCDD treatment. The above alterations did not seem to be caused through a change in the upstream regulator, because TCDD exhibited little ability to attenuate the expression of adrenocorticotropin, a pituitary hormone stimulating adrenal steroidogenesis, in the male and female fetuses. In contrast to the males, TCDD effect on the adrenal gland was not observed in the female fetuses. These results suggest that maternal exposure to TCDD disrupts fetal steroidogenesis in adrenal as well as gonadal glands in a male specific manner, and the mechanism underlying the effect on adrenal gland is independent of the alteration of pituitary regulator.
|Number of pages||9|
|Publication status||Published - Jan 1 2013|
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