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Submitted on September 5, 2003
Accepted on October 28, 2003
1 Center for Biomedical Research,Population Council, New York, New York 10021, Reproductive Toxicology Division,National Health and Environmental Effects Research Laboratory, United States Environmental Protection Agency, Research Triangle Park, North Carolina 27711
* To whom correspondence should be addressed. E-mail: m-hardy{at}popcbr.rockefeller.edu.
Exposures of humans to bisphenol A (BPA), a monomer in polycarbonate plastics and constituent of resins used in food packaging and dentistry, is significant. In this report, exposure of rats to 2.4 µg/kg/day (a dose that approximates BPA levels in the environment) from postnatal days 21 to 35 suppressed serum (ng/ml) LH (LH) (0.21 ± 0.05 vs. control, 0.52 ± 0.04; P < 0.01) and testosterone (T) levels (1.62 ± 0.16 vs. control, 2.52 ± 0.21; P < 0.05), in association with decreased LH
and increased estrogen receptor- (ER) pituitary mRNA levels as measured by RT-PCR. Treatment of adult Leydig cells with 0.01 nM BPA decreased T biosynthesis by 25% as a result of decreased expression of the steroidogenic enzyme 17
-hydroxylase/17-20 lyase. BPA decreased serum 17-estradiol (E2) levels from 0.31 ± 0.02 ng/ml (control) to 0.22 ± 0.02, 0.19 ± 0.02 and 0.23 ± 0.03 in rats exposed to 2.4 µg, 10 µg, or 100 mg/kg/day BPA, respectively, from 21 to 35 days of age (P < 0.05), due to its ability to inhibit Leydig cell aromatase activity. Exposures of pregnant and nursing dams, i.e. from gestation day 12 to postnatal day 21, decreased T levels in the testicular interstitial fluid (ng/ml) from 420 ± 34 (control) to 261 ± 22 (P < 0.05) in adulthood, implying that the perinatal period is a sensitive window of exposure to BPA. Since BPA has been measured in several human populations, further studies are warranted to assess BPA effects on male fertility.
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