In utero and lactational exposure of the male rat to 2,3,7,8-tetrachlorodibenzo-p-dioxin impairs prostate development. 1. Effects on gene expression

Toxicology and Applied Pharmacology
B L Roman, Richard E Peterson

Abstract

In utero and lactational 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure decreases rat prostate weight without decreasing circulating androgen concentrations. Because one mechanism by which TCDD is thought to cause toxicity is by aryl hydrocarbon receptor (AhR)-mediated alterations in gene transcription, the goals of this study were to determine whether the developing prostate expresses the AhR and its dimerization partner, the AhR nuclear translocator (ARNT); to determine whether in utero and lactational TCDD exposure is capable of directly activating gene transcription in the developing prostate; and to identify prostatic mRNAs that exhibit altered abundance in response to in utero and lactational TCDD exposure. Pregnant Holtzman rats were administered TCDD (1.0 microgram/kg po) or vehicle on Gestation Day (GD) 15, and male offspring were euthanized between Postnatal Days (PNDs) 1 and 63. Using reverse transcriptase-polymerase chain reaction (RT-PCR), mRNAs encoding the AhR and ARNT were detected in both ventral and dorsolateral prostates from control animals throughout postnatal development. ARNT protein was expressed in the majority of stromal nuclei early in development, whereas ARNT expression in the prostate epitheli...Continue Reading

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Jun 3, 2000·Annual Review of Pharmacology and Toxicology·J F Waring, R G Ulrich
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