亚砷酸盐
氧化应激
脂质过氧化
程序性细胞死亡
活性氧
生物
体内
线粒体
体外
GPX4
细胞生物学
化学
细胞凋亡
生物化学
超氧化物歧化酶
谷胱甘肽过氧化物酶
砷
遗传学
有机化学
作者
Meng Pan,Shanshan Zhang,Xuejun Jiang,Shuqun Cheng,Jun Zhang,Xianqing Cao,Xia Qin,Zhen Zou,Chengzhi Chen
标识
DOI:10.1016/j.ecoenv.2020.110360
摘要
Ferroptosis is a newly identified form of cell death characterized by accumulation of intracellular iron and requirement of lipid peroxidation. However, whether arsenite triggers testicular cell death via ferroptosis remains unclear. In this study, after administrating of adult male mice with 0.5, 5 and 50 mg/L arsenite for six months via drinking water, the results showed that arsenite caused the pathological changes in mouse testis and significantly reduced the number of sperm. Mitochondrial injuries were observed as the major ultrastructural damages induced by arsenite, and these damages were accompanied by the apparent mitochondrial oxidative damage in the testis, manifested by accumulation of iron, production of reactive oxygen species and lipid peroxidation products. We also demonstrated that arsenite significantly activated ferroptosis-related signal pathways in the mouse testis. To further verify the results obtained in the animal model, GC-2spd cells were employed as the in vitro culture system. Consistently, the results revealed arsenite remarkably triggered the ferroptotic cell death in vitro, and inhibition of ferroptosis by ferrostatin-1 could attenuate this adverse effect in cells. These findings together indicate that arsenite can trigger oxidative stress thus leading to testicular cell death by ferroptosis, suggesting that inhibition of ferroptosis would be a potential strategy for treatment of arsenite-related male reproductive toxicity.
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