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Reprod Toxicol. 2019 Jul 29. pii: S0890-6238(19)30108-X. doi: 10.1016/j.reprotox.2019.07.017. [Epub ahead of print]

Prenatal exposures to bisphenol A and di (2-ethylhexyl) phthalate disrupted seminiferous tubular development in growing male rats.

Author information

1
Department of Anatomy, Physiology and Pharmacology, Faculty of Veterinary Medicine, Auburn University, USA; Department of Anatomy and Histology, Faculty of Veterinary Medicine, Assiut University, Egypt.
2
Department of Pathology and Clinical pathology, Faculty of Veterinary Medicine, Sohag University, Egypt.
3
Department of Anatomy, Physiology and Pharmacology, Faculty of Veterinary Medicine, Auburn University, USA. Electronic address: akingbt@auburn.edu.

Abstract

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.

KEYWORDS:

Chemicals; Leydig cells; Male rat; Prenatal exposure; Sertoli cells; Spermatogenesis

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