Endocrine-disrupting compounds (EDCs) are found in the environment due to their use in industrial and manufacturing
activities. Exposure of the population to bisphenol A (BPA) and di (2-ethylhexyl) phthalate (DEHP) is
significant because they are present in many consumer products. EDCs target the reproductive tract because they
express high levels of steroid hormone receptors, which act as transcriptional factors to regulate reproductive
development. In the present study, timed-pregnant Long-Evans female rats (n=8–10) were administered BPA
and DEHP by oral gavage at 2.5 or 25 μg/kg body weight and 5 or 50 μg/kg body weight, respectively. Exposures
to chemicals were limited to the period between gestational days 12 and 21 followed by assessment of testicular
development in male offspring in the postnatal period. Leydig cells and Sertoli cells are the two major somatic
cells present in the testis. The 17β-hydroxysteroid dehydrogenase (17β-HSD) steroidogenic enzyme is a marker
for Leydig cell maturation, whereas transferrin is a marker for Sertoli cell differentiation. At day 10 post-partum,
testes were obtained from cohorts of control and chemical-exposed male rats and processed to measure 17β-HSD
and transferrin expression levels in western blots. Compared to control, 17βHSD enzyme protein was increased
in BPA-treated rats but levels were decreased in animals exposed to DEHP (P < 0.05). Transferrin protein was
decreased in male rats exposed to both BPA and DEHP compared to control animals (P < 0.05). To assess
qualitative cellular changes within the spermatogenic epithelium, testes were obtained from separate cohorts of
male rats at 35 days of age and processed for histopathological analysis. Results showed that prenatal exposures
of male rats to BPA and DEHP caused disruption of the spermatogenic epithelium evident as disorganization and
atrophy of seminiferous tubules as well as desquamation of germ cells into the tubular lumen. Together, results
from the present study support the view that developmental exposures to environmentally relevant levels of BPA
and DEHP are associated with disruptions of testicular cell development, which have implications for endocrine
and exocrine functions of testis.