Exposure to phenanthrene affects oocyte meiosis by inducing mitochondrial dysfunction and endoplasmic reticulum stress. Issue 1 (20th September 2022)

• Record Type: Journal Article
• Authors: Wang, Yi; Li, Si‐Hong; Yang, Shu‐Jie; Li, Xiao‐Qing; Liu, Lu; Ma, Xiang; Niu, Dong; Duan, Xing
• Is Part Of: Cell proliferation. Volume 56:Issue 1(2023)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2022-09-20
• Subjects: Cell proliferation -- Periodicals; 571.84
• DOI: 10.1111/cpr.13335
• Languages: English
• ISSNs: 0960-7722

Abstract

Abstract: 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. Abstract : Mechanism of abnormal meiotic progression caused by PHE exposure. The current study indicated that PHE exposure caused ER stress and mitochondrial dysfunction by disrupting intracellular redox and Ca 2+ homeostasis, eventually inducing DNA damage and aberrant oocyte maturation.