Mitochondrial Dysfunction and Ca2+ Overload in Injured Sertoli Cells Exposed to Bisphenol A. Issue 3 (18th May 2016)

• Record Type: Journal Article
• Authors: Wang, Chengmin; Qi, Suqin; Liu, Changjiang; Yang, Aixia; Fu, Wenjuan; Quan, Chao; Duan, Peng; Yu, Tingting; Yang, Kedi
• Is Part Of: Environmental toxicology. Volume 32:Issue 3(2017)
• Page Start: 823
• Page End: 831
• Publication Date: 2016-05-18
• Subjects: bisphenol‐A -- mitochondria -- Sertoli cell -- Ca2+ -- apoptosis; Water quality bioassay -- Periodicals; Water -- Pollution -- Toxicology -- Periodicals; Microbiological assay -- Periodicals; Toxicity testing -- Periodicals; Environmental toxicology -- Periodicals; Environmental Pollution -- Periodicals; Environmental Pollutants -- Periodicals; Environmental Monitoring -- Periodicals; Écotoxicologie -- Périodiques; Pollution -- Périodiques; 615.902
• DOI: 10.1002/tox.22282
• Languages: English
• ISSNs: 1520-4081

Abstract

ABSTRACT: 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 Ca 2+ concentration were examined. We have found BPA caused the cellular mitochondria dysfunction and followed by cell death in Sertoli cells. Moreover cytoplasm Ca 2+ 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.