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Submitted on August 4, 2004
Accepted on October 13, 2004
Department of Biology, and Molecular and Cellular Biology Program, Morrill Science Center, University of Massachusetts, Amherst, MA 01003
* To whom correspondence should be addressed. E-mail: tzoeller{at}bio.umass.edu.
Considering the importance of thyroid hormone (TH) in brain development, it is of potential concern that a wide variety of environmental chemicals can interfere with thyroid function or, perhaps of greater concern, with TH action at its receptor (TR). Recently, bisphenol-A (BPA, 4,4' isopropylidenediphenol) was reported to bind to the rat TR and act as an antagonist in vitro. BPA is a high production volume chemical, with over 800 million kg of BPA produced annually in the United States alone. It is detectable in serum of pregnant women and in cord serum taken at birth, is 5-fold higher in amniotic fluid at 15-18 weeks gestation compared with maternal serum, and was found in concentrations of up to 100 ng/g in placenta. Thus, the human population is widely exposed to BPA and it appears to accumulate in the fetus. We now report that dietary exposure to BPA of Sprague Dawley rats during pregnancy and lactation causes an increase in serum total T4 in pups on postnatal day 15, but serum TSH was not different from controls. The expression of the TH-responsive gene RC3/Neurogranin, measured by in situ hybridization, was significantly up-regulated by BPA in the dentate gyrus. These findings suggest that BPA acts as a TH antagonist on the 
TR, which mediates the negative feedback effect of TH on the pituitary gland, but that BPA is less effective at antagonizing TH on the 
TR, leaving TR-mediated events to respond to elevated T4.
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