Mitochondrial Dysfunction and Ca²⁺ Overload in Injured Sertoli Cells Exposed to Bisphenol A

Bisphenol-A (BPA) is well known as one of endocrine-disrupting chemicals and testicular toxicant. In this present study, we determined whether BPA caused cell injury through mitochondria impairment and ROS overproduction. The cellular ROS production, mitochondrial ATP synthetase activity and Ca²⁺ concentration were examined. We have found BPA caused the cellular mitochondria dysfunction and followed by cell death in Sertoli cells. Moreover cytoplasm Ca²⁺ overload was also involved. Furthermore, pretreatment with N-acetyl-L-cysteine (NAC) could alleviate the damage by causing a remarkable decrease in ROS production and mitochondrial dysfunction. Collectively, our results showed that BPA exposure induced Sertoli cell apoptosis because of excessive ROS generation and mitochondrial dysfunction. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 823-831, 2017.