title: Mitochondrial Dysfunction and Ca2+Overload in Injured Sertoli Cells Exposed to Bisphenol A.
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 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.
authors.affiliation: MOE Key Laboratory of Environment and Health, Department of Occupational and Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, People's Republic of China.|Department of Environmental Health, School of Public Health, Anhui Medical University, Hefei, 230032, People's Republic of China.
authors.forename: Chengmin
authors.initials: C
authors.lastname: Wang
authors.affiliation: MOE Key Laboratory of Environment and Health, Department of Occupational and Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, People's Republic of China.|Wuhan Hospital for the Prevention and Treatment of Occupational Disease, Wuhan, 430015, People's Republic of China.
authors.forename: Suqin
authors.initials: S
authors.lastname: Qi
authors.affiliation: MOE Key Laboratory of Environment and Health, Department of Occupational and Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, People's Republic of China.
authors.forename: Changjiang
authors.initials: C
authors.lastname: Liu
authors.affiliation: Center of Experimental Medicine, Wuhan No.1 Hospital, Wuhan, 430022, People's Republic of China.
authors.forename: Aixia
authors.initials: A
authors.lastname: Yang
authors.affiliation: MOE Key Laboratory of Environment and Health, Department of Occupational and Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, People's Republic of China.
authors.forename: Wenjuan
authors.initials: W
authors.lastname: Fu
authors.affiliation: MOE Key Laboratory of Environment and Health, Department of Occupational and Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, People's Republic of China.
authors.forename: Chao
authors.initials: C
authors.lastname: Quan
authors.affiliation: MOE Key Laboratory of Environment and Health, Department of Occupational and Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, People's Republic of China.
authors.forename: Peng
authors.initials: P
authors.lastname: Duan
authors.affiliation: MOE Key Laboratory of Environment and Health, Department of Occupational and Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, People's Republic of China.
authors.forename: Tingting
authors.initials: T
authors.lastname: Yu
authors.affiliation: MOE Key Laboratory of Environment and Health, Department of Occupational and Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, People's Republic of China.
authors.forename: Kedi
authors.initials: K
authors.lastname: Yang
mesh_terms: D025181:ATP Synthetase Complexes / Q000378:metabolism; D000111:Acetylcysteine / Q000494:pharmacology; D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D001559:Benzhydryl Compounds / Q000633:toxicity*; D002118:Calcium / Q000378:metabolism; D002478:Cells, Cultured; D003593:Cytoplasm / Q000378:metabolism; D052244:Endocrine Disruptors / Q000633:toxicity*; D008297:Male; D008928:Mitochondria / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism; D010636:Phenols / Q000633:toxicity*; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism; D012708:Sertoli Cells / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D000098826:Bisphenol A Compounds
chemical_list: D025181:ATP Synthetase Complexes; D000111:Acetylcysteine; D001559:Benzhydryl Compounds; D002118:Calcium; D052244:Endocrine Disruptors; D010636:Phenols; D017382:Reactive Oxygen Species; C006780:bisphenol A; D000098826:Bisphenol A Compounds
keywords: Ca2+; Sertoli cell; apoptosis; bisphenol-A; mitochondria