Bisphenol A induced spermatogenic cell damage by regulating Chchd10 mediated mitochondrial dynamics in mice
摘要：Mitochondrial fusion and fission（mitochondrial dynamics） are homeostatic processes that safeguard normal cellular function and seems to be critical for spermatogenesis. So far, the effects and mechanisms of Bisphenol A（BPA） on mitochondrial dynamics in spermatogenic cells are less-well understood. Here, we utilized BPA exposure in vivo and in vitro model to assess the effects of BPA on spermatogenic cell and explored the molecular mechanism involved in. The results showed that the sperm motility decreased and the head abnormality of sperm increased significantly compared to the control after BPA（30 mg/kg/d） exposure for 35 days. Meanwhile, some pathological changes including the vacuoles, exfoliated as well as abnormal mitochondria were found in seminiferous tubules or germ cells in mice. In addition, we found that the number of long tubular mitochondria decreased significantly in BPA treated GC-2 cells. Affymetrix GeneChip results showed that multiple mitochondrial related genes were differentially expressed after BPA treatment, and the expression of Chchd10, a mitochondrial inner membrane structural protein was significantly up-regulated after BPA treatment, which was verified both in vivo and in vitro model. Furthermore, interfering with the expression of Chchd10 can improve the fragmented mitochondria caused by BPA induced mitochondrial fusion and fission imbalance in GC2 cells. Together, these results suggested that mitochondria are the important target organelles in BPA induced spermatogenic cell damage and Chchd10 mediated mitochondrial fission/fusion imbalance in BPA induced spermatogenic cell damage in mice.