Prenatal bisphenol a exposure leads to reproductive hazards on male offspring via the Akt/mTOR and mitochondrial apoptosis pathways.

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 32: 1007-1023, 2017.