Bisphenol S exposure induces cytotoxicity in mouse Leydig cells

• Published in: Food and chemical toxicology 2022-02, Vol.160, p.112805-112805, Article 112805
• Main Authors: Zhang, Wenjuan, Huang, Tao, Sun, Zhangbei, Kuang, Haibin, Yuan, Yangyang, Zou, Weiying, Liu, Fangming, Zhang, Fan, Yang, Bei, Wu, Lei, Zhang, Dalei
• Format: Article
• Language: English
• Subjects: Animals; Apoptosis; Apoptosis - drug effects; Autophagy; Autophagy - drug effects; Benzhydryl Compounds - toxicity; Bisphenol S; Cell Line; Leydig Cells - cytology; Leydig Cells - drug effects; Leydig Cells - metabolism; Male; Membrane Potential, Mitochondrial - drug effects; Mice; Mitochondria - drug effects; Mitochondria - metabolism; Mitochondrial dysfunction; Oxidative stress; Oxidative Stress - drug effects; Phenols - toxicity; Reactive Oxygen Species - metabolism
• ISSN: 0278-6915; 1873-6351
• DOI: 10.1016/j.fct.2021.112805

Bisphenol S (BPS), an increasingly used alternative to bisphenol A, has been linked to testosterone deficiency and male reproductive dysfunction in laboratory animals. This study aimed to examine the cytotoxicity of BPS exposure to Leydig cells and to investigate its possible mechanisms. After treatment with BPS (100, 200 and 400 μM) for 48 h in vitro, TM3 mouse Leydig cells exhibited a dose-dependent decrease in the viability. Furthermore, BPS challenge triggered oxidative stress manifested by compromised activities of superoxide dismutase and catalase with exaggerated formation of reactive oxygen species. Especially, BPS exposure resulted in augmented mitochondrial permeability transition pore opening, dissipated mitochondrial membrane potential and reduced ATP generation, along with an altered energy metabolism. Moreover, BPS stimulation enhanced BAX expression and caspase-3 activity and inhibited BCL-2 expression. In addition, BPS-treated TM3 cells showed an accumulation of autophagic vacuoles, together with increased Beclin1 and P62 expression and elevated LC3B-II/LC3B-I ratio. These results demonstrated that in vitro exposure to BPS exerted cytotoxicity to TM3 Leydig cells through inducing oxidative stress, mitochondrial impairment, autophagic disturbance and apoptosis. •BPS exposure impaired the viability of mouse TM3 Leydig cells in vitro.•BPS induced mitochondrial dysfunction and energy metabolism disorder in TM3 cells.•BPS treatment caused autophagic disturbance and apoptosis in TM3 cells.