Conclusions
Taken together, our study demonstrated that mitochondrial dysfunction and ER stress-induced oxidative stress and DNA damage are the major cause of poor oocyte quality after PHE exposure.
Results
In this study, we set up PHE exposure model and found that PHE exposure compromised oocytes maturation competence by inhibiting spindle assembly and chromosomes alignment. Moreover, PHE exposure induced mitochondrial dysfunction and endoplasmic reticulum (ER) stress, leading to increased reactive oxygen species (ROS) and aberrant calcium levels in cytoplasm, eventually induced oxidative stress and DNA damage in oocytes. Furthermore, we found that oral administration of PHE caused the occurrence of oxidative stress and apoptosis in female ovary. In addition, the oocyte exhibited aberrant spindle morphology and failure of actin cap formation in metaphase II oocytes. Conclusions: Taken together, our study demonstrated that mitochondrial dysfunction and ER stress-induced oxidative stress and DNA damage are the major cause of poor oocyte quality after PHE exposure.