It has been confirmed that the occurrence of a variety of chronic diseases including female infertility is closely related to bisphenol A (BPA) exposure. BPA is now being gradually replaced by its analogues. Although the adverse health effects of BPA have been extensively studied, little is known about the female reproductive toxicity of its analogues, particularly BPS, BPF and BPAF. The present study evaluated the effects of BPA and its analogues BPS, BPF and BPAF on mitochondrial mass and potential to induce apoptosis in KGN cells. We observed that BPA and its analogues, especially BPA and BPAF exposure can significantly reduce mitochondrial mass. This reduction in mitochondrial mass was confirmed by flow cytometry after labelling the NAO probe. The significant induction effect of BPA and its analogues on KGN cell apoptosis was detected using flow cytometry. Compared with BPA and BPAF, the interference effect of BPS and BPF on KGN cells was smaller, although there were significant differences between the high-concentration treatment groups and the control group. Our study revealed the possible mechanisms of BPA and its analogues on granulosa cell damage and female sterility. In addition, it also suggests that the safety of BPA analogues in female reproduction needs to be reconsidered.
Bisphenol A (BPA) is an environmental endocrine disruptor and has been strongly associated with the development of numerous diseases, including ovarian follicle development disorders. BPA is being replaced by structurally similar chemicals, such as bisphenol S (BPS), bisphenol F (BPF) and bisphenol AF (BPAF). However, the toxicity of these analogues in female reproduction is unclear. Here, we investigated the induction of cytotoxicity and mitochondrial dysfunction in the human granulosa cell line KGN by BPA and its selected analogues. We found that BPA and its analogues, especially BPAF, significantly reduced cell viability and caused cytotoxicity. Furthermore, we observed that BPA and BPAF significantly reduced mitochondrial function, including decreasing ATP generation, promoting ROS production and increasing intracellular Ca 2+ levels. An oxidative-antioxidant imbalance was also detected after exposure to these chemicals. In contrast, the total antioxidant capacity was significantly reduced. To our knowledge, this is the first report on the evaluation of the potential of BPA and its analogues to induce cytotoxicity and mitochondrial dysfunction in ovarian granulosa cells. Our study revealed the possible mechanism of BPA and its analogues inducing granulosa cell damage and suggested that mitochondrial dysfunction may play an important regulatory role in bisphenol-induced follicular development disorders.
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