全氟辛酸
细胞毒性
化学
生物化学
体外
环境化学
作者
Tingting Lin,Yurong Zhang,Xinbao Ding,Tao Huang,Wenjuan Zhang,Weiying Zou,Haibin Kuang,Bei Yang,Lei Wu,Dalei Zhang
出处
期刊:Chemosphere
[Elsevier BV]
日期:2020-07-07
卷期号:260: 127545-127545
被引量:17
标识
DOI:10.1016/j.chemosphere.2020.127545
摘要
Perfluorooctane acid (PFOA), a typical perfluorinated chemical, has been suggested to interfere with male reproductive function. In this study, mouse spermatogonial GC-1 cells were in vitro treated with PFOA (250, 500 or 750 μM) for 24 h to investigate the cytotoxicity of PFOA and its underlying mechanisms. Our results indicated that exposure to intermediate and high doses of PFOA suppressed the viability of GC-1 cells in a concentration-dependent manner. Furthermore, PFOA treatment markedly enhanced the generation of reactive oxygen species and malondialdehyde, with diminished activity of superoxide dismutase. Particularly, PFOA exposure evoked a decline in mitochondrial membrane potential and ATP production. Furthermore, the apoptotic index and caspase-3 activity were significantly elevated after treatment with PFOA. In addition, PFOA incubation caused an increase in LC3B-II/LC3B–I ratio. Meanwhile, PFOA resulted in an excessive accumulation of autophagosomes in the cytoplasm. Taken together, exposure to PFOA can elicit cytotoxicity to spermatogonial GC-1 cells in vitro, which may be link to the mitochondrial oxidative damage and induction of apoptosis and autophagy.
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