Open AccessExposure to phenanthrene affects oocyte meiosis by inducing mitochondrial dysfunction and endoplasmic reticulum stress
Author(s) -
Wang Yi,
Li SiHong,
Yang ShuJie,
Li XiaoQing,
Liu Lu,
Ma Xiang,
Niu Dong,
Duan Xing
Publication year - 2023
Publication title -
cell proliferation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.647
H-Index - 74
eISSN - 1365-2184
pISSN - 0960-7722
DOI - 10.1111/cpr.13335
Subject(s) - oocyte , oxidative stress , endoplasmic reticulum , mitochondrion , reactive oxygen species , dna damage , microbiology and biotechnology , biology , chemistry , andrology , endocrinology , biochemistry , medicine , embryo , dna
Objectives Phenanthrene (PHE) is one of the most abundant polycyclic aromatic hydrocarbons (PAHs), which is a widespread environmental contaminant. Various studies showed that PHE has adverse impacts on animals and human health. It has been shown that PHE exposure induced follicular atresia and endocrine dyscrasia in female mice. However, the potential mechanism regarding how PHE affects female reproductive system especially the oocyte quality has not been elucidated. Methods and 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.