Inhibition of testicular steroidogenesis by the xenoestrogen bisphenol A is associated with reduced pituitary luteinizing hormone secretion and decreased steroidogenic enzyme gene expression in rat Leydig cells (PDF)
Akingbemi,Benson T.; Sottas,Chantal M.; Koulova,Anna I.; Klinefelter,Gary R.; Hardy,Matthew P.
Endocrinology 145(2): 592-603
Publication date: 2004
Exposure of humans to bisphenol A (BPA), a monomer in polycarbonateplastics and a constituent of resins used in food packagingand dentistry, is significant. In this report exposure of ratsto 2.4 µg/kg·d (a dose that approximates BPA levelsin the environment) from postnatal d 21-35 suppressedserum LH (0.21 ± 0.05 ng/ml; vs. control, 0.52 ±0.04; P < 0.01) and testosterone (T) levels (1.62 ±0.16 ng/ml; vs. control, 2.52 ± 0.21; P < 0.05), inassociation with decreased LHß and increased estrogenreceptor ß pituitary mRNA levels as measured by RT-PCR.Treatment of adult Leydig cells with 0.01 nM BPA decreased Tbiosynthesis by 25% as a result of decreased expression of thesteroidogenic enzyme 17-hydroxylase/17-20 lyase. BPA decreasedserum 17ß-estradiol levels from 0.31 ± 0.02ng/ml (control) to 0.22 ± 0.02, 0.19 ± 0.02, and0.23 ± 0.03 ng/ml in rats exposed to 2.4 µg, 10µg, or 100 mg/kg·d BPA, respectively, from 21-35d of age (P < 0.05) due to its ability to inhibit Leydigcell aromatase activity. Exposures of pregnant and nursing dams,i.e. from gestation d 12 to postnatal d 21, decreased T levelsin the testicular interstitial fluid from 420 ± 34 (control)to 261 ± 22 (P < 0.05) ng/ml in adulthood, implyingthat the perinatal period is a sensitive window of exposureto BPA. As BPA has been measured in several human populations,further studies are warranted to assess the effects of BPA onmale fertility.
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