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.

已建议使用全氟辛烷酸（PFOA）（一种典型的全氟化学品）来干扰男性的生殖功能。在这项研究中，小鼠精原GC-1细胞在体外用PFOA（250、500或750μM）处理24小时，以研究PFOA的细胞毒性及其潜在机制。我们的结果表明，暴露于中剂量和高剂量的PFOA以浓度依赖的方式抑制了GC-1细胞的活力。此外，PFOA处理显着增强了活性氧和丙二醛的生成，同时降低了超氧化物歧化酶的活性。特别是，PFOA的暴露引起线粒体膜电位和ATP产量的下降。此外，用PFOA治疗后，凋亡指数和caspase-3活性显着升高。另外，PFOA的孵育导致LC3B-II / LC3B-I比率增加。同时，PFOA导致自噬体在细胞质中过度积累。在一起在体外，这可能与线粒体的氧化损伤，细胞凋亡和自噬的诱导有关。