Prenatal bisphenol a exposure leads to reproductive hazards on male offspring via the Akt/mTOR and mitochondrial apoptosis pathways.
Environ Toxicol. 2016 Jun 14. Epub 2016 Jun 14. PMID: 27296223
BACKGROUND: Bisphenol A (BPA) exposure is ubiquitous, and in laboratory animals and humans, exposure has been associated with male spermatogenesis dysfunction. However, it is largely unknown if this association has a fetal origin.
OBJECTIVE: The aim of this research is to explore the mechanism whereby prenatal BPA exposure exerts its reproductive toxicities on spermatogenesis in male offspring.
METHODS: We fed pregnant SD rats BPA at doses ranging from 1 to 100 mg/kg body weight during gestation days 14-21. The male offspring were euthanized at postnatal day 21, and the levels of sex hormones and reactive oxygen species (ROS), expressions of proteins and genes in the Akt/mTOR, and mitochondrial apoptosis pathways were detected. Several closely linked autophagy indexes were also measured incidentally. Additionally, semen quality of adult offspring was tested at the end of the study.
RESULTS: The results revealed that prenatal BPA exposure can cause endocrine disruption and oxidative stress in male offspring, leading to inhibition of spermatogenesis by suppressing the Akt/mTOR pathway and activating the mitochondrial apoptosis pathway.
CONCLUSIONS: These preliminary results indicate noteworthy and far-reaching effects of BPA on the reproductive system of male offspring.© 2016 Wiley Periodicals, Inc. Environ Toxicol, 2016.