Abstract
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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