Analysis of apoptosis induced by perfluorooctane sulfonates (PFOS) in mouse Leydig cells in vitro

• Published in: Toxicology mechanisms and methods Vol. 25; no. 1; pp. 21 - 25
• Main Authors: Zhang, De-Yong, Xu, Xiao-Lu, Shen, Xiu-Ying, Ruan, Qin, Hu, Wen-Lang
• Format: Journal Article
• Language: English
• Published: England Informa Healthcare USA, Inc 01.01.2015; Informa Healthcare
• Subjects: Alkanesulfonic Acids - toxicity; Animals; Apoptosis; Apoptosis - drug effects; bcl-2-Associated X Protein - metabolism; Cells, Cultured; Dose-Response Relationship, Drug; Environmental Pollutants - toxicity; Fluorocarbons - toxicity; Leydig Cells - drug effects; Leydig Cells - metabolism; Leydig Cells - pathology; Male; Membrane Potential, Mitochondrial - drug effects; Mice; Mitochondria - drug effects; Mitochondria - metabolism; Mitochondria - pathology; mitochondria pathway; mouse Leydig cells; oxidative stress; Oxidative Stress - drug effects; perfluorooctane sulfonates; Proto-Oncogene Proteins c-bcl-2 - metabolism; Reactive Oxygen Species - metabolism; Signal Transduction - drug effects; Time Factors; perfluorooctane sulfonates; mitochondria pathway; mouse Leydig cells; oxidative stress; Apoptosis
• ISSN: 1537-6516; 1537-6524
• DOI: 10.3109/15376516.2014.971140

Abstract To explore the possible mechanism of perfluorooctane sulfonates (PFOS's) reproductive toxicity, mouse Leydig cells cultured in vitro were exposed to a serial concentration of PFOS for four more days of culture. Apoptosis during the process was checked. After 24 h, apoptosis occurred to all of the groups  50 μg/mL PFOS. After 72 h, 37.5 μg/mL dose also showed apoptosis, and the most apoptosis signals, averagely 18 per well, were observed in 62.5 μg/mL dose group. An increase in ROS (p < 0.05) and a decrease of mitochondrial membrane potential (p < 0.01) was confirmed in those groups with  12.5 μg/mL dose. ROS levels peaked in 50 μg/mL and 62.5 μg/mL groups, nearly two-folds higher than control. PFOS was also observed to down-regulate the protein expression of Bcl-2 and to up-regulate that of Bax. The apoptosis induced by PFOS in mouse Leydig cells was shown to be related to mitochondrially mediated pathways and to involve oxidative stress.