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INHIBITION OF TESTICULAR STEROIDOGENESIS BY THE XENOESTROGEN BISPHENOL A IS ASSOCIATED WITH REDUCED PITUITARY LH SECRETION AND DECREASED STEROIDOGENIC ENZYME GENE EXPRESSION IN RAT LEYDIG CELLS
Citation:
Akingbemi, B. T., C. M. Sottas, A. I. Koulova, G R. Klinefelter, AND M. P. Hardy. INHIBITION OF TESTICULAR STEROIDOGENESIS BY THE XENOESTROGEN BISPHENOL A IS ASSOCIATED WITH REDUCED PITUITARY LH SECRETION AND DECREASED STEROIDOGENIC ENZYME GENE EXPRESSION IN RAT LEYDIG CELLS. ENDOCRINOLOGY 145(2):592-603, (2004).
Description:
Exposure of humans to bisphenol A (BPA), a monomer in polycarbonate plastics and constituent of resins used in food packaging and denistry, is significant. In this report, exposure of rats to 2.4 ug/kg/day (a dose that approximates BPA levels in the environment) from postnatal days 21 to 35 suppressed serum luteinizing hormone (LH) and testosterone (T) levels compared to controls. This was associated with decreased LHB and increased estrogen receptor-B (ERB) pituitary mRNA levels. Treatment of adult Leydig cells with 0.01 nM BPA decreased T biosynthesis by 25% as a result of decreased expression of steroidogenic enzyme 17a-hydroxylase/17-20 lyase. BPA decreased serum 17B-estradiol (E2) levels in adult rats exposed to 2.4 ug/kg/day and higher from days 21-35 of age; this was due to compromised Leydig cell aromatase activity. Exposure of pregnant and nursing dams, i.e. from gestation day 12 to postnatal day 21, decreased T levels in testicular interstitial fluid at adulthood, implying that the perinatal period is a sensitive window of exposure. Since BPA has been measured in several human populations, further studies are warranted to assess BPA effects on male fertility.