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: Chengmin Wang, Suqin Qi, Changjiang Liu, Aixia Yang, Wenjuan Fu, Chao Quan, Peng Duan, Tingting Yu, Kedi Yang
• Journal: Environmental toxicology (Environ Toxicol) Vol. 32 Issue 3 Pg. 823-831 (Mar 2017) ISSN: 1522-7278 [Electronic] United States
• PMID: 27189055 (Publication Type: Journal Article)
• Copyright: © 2016 Wiley Periodicals, Inc.

Chemical References

• Benzhydryl Compounds
• Endocrine Disruptors
• Phenols
• Reactive Oxygen Species
• ATP Synthetase Complexes
• bisphenol A
• Calcium
• Acetylcysteine

Topics

• ATP Synthetase Complexes (metabolism)
• Acetylcysteine (pharmacology)
• Animals
• Apoptosis (drug effects)
• Benzhydryl Compounds (toxicity)
• Calcium (metabolism)
• Cells, Cultured
• Cytoplasm (metabolism)
• Endocrine Disruptors (toxicity)
• Male
• Mitochondria (drug effects, enzymology, metabolism)
• Phenols (toxicity)
• Rats
• Rats, Sprague-Dawley
• Reactive Oxygen Species (metabolism)
• Sertoli Cells (cytology, drug effects, metabolism)