Department of Physiology, School of Basic Medical Sciences, Jiangxi Provincial Key Laboratory of Reproductive Physiology and Pathology, Nanchang University, Nanchang, 330006, PR China.
Medical College of Nanchang University, Nanchang, 330006, PR China.
Chemosphere. 2020 Dec;260:127545. doi: 10.1016/j.chemosphere.2020.127545. Epub 2020 Jul 7.
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.
全氟辛酸（PFOA）是一种典型的全氟化学物质，据报道其可能干扰男性生殖功能。在这项研究中，我们将 PFOA（250、500 或 750μM）体外处理 GC-1 细胞 24 小时，以研究 PFOA 的细胞毒性及其潜在机制。结果表明，PFOA 以浓度依赖性方式抑制 GC-1 细胞活力，且中、高剂量 PFOA 处理后，细胞内活性氧和丙二醛的生成显著增加，而超氧化物歧化酶的活性降低。此外，PFOA 暴露后线粒体膜电位和 ATP 生成减少。经 PFOA 处理后，细胞凋亡指数和 caspase-3 活性显著升高。此外，LC3B-II/LC3B-I 比值增加。同时，PFOA 导致过多的自噬体在细胞质中积累。综上所述，PFOA 暴露可引起体外 GC-1 细胞的细胞毒性，这可能与线粒体氧化损伤以及诱导细胞凋亡和自噬有关。
