Effects of Acute Fluorene-9-Bisphenol Exposure on Mouse Oocyte in vitro Maturation and Its Possible Mechanisms.
Xiao-Fei JiaoQiu-Man LiangDi WuZhi-Ming DingJia-Yu ZhangFan ChenYong-Sheng WangShou-Xin ZhangYi-Liang MiaoLi-Jun HuoPublished in: Environmental and molecular mutagenesis (2018)
Fluorene-9-bisphenol (BHPF), a substitute of bisphenol A (BPA) used in the production of the so-called "BPA-free" plastics, has now been shown to be released from commercial plastic bottles into drinking water and has strong anti-estrogenic activity in mice, which suggests that BHPF is also an environmental toxin. However, whether BHPF exposure has effects on mouse oocyte development is unknown. In this study, the influence of acute exposure to BHPF (50-150 μM, 12 hr) on mouse oocyte maturation and its possible mechanisms were investigated. Of note, 50-μM BHPF had no effects on the maturation of mouse oocytes, whereas 100- and 150-μM BHPF significantly blocked germinal vesicle breakdown and led to the failure of first polar body extrusion. Particularly, 100-μM BHPF exposure severely decreased the cellular adenosine triphosphate in a time-dependent manner, which finally brought out the loss of spindles. In addition, the actin cytoskeleton was also impaired. The defective mitochondrial dynamics and decreased mitochondrial DNA implied the damage of mitochondria in BHPF-treated oocytes. Increased PINK1, Beclin1, and LC3B protein level and decreased TOMM20 and TOMM17A protein level illustrated that mitophagy was induced, which also confirmed that BHPF exposure impaired the cellular mitochondria. Moreover, BHPF induced reactive oxygen species accumulation and early apoptosis. Oocyte quality was also impaired by BHPF exposure through altering histone modifications evidenced by increased H3K9me3 and H3K27me3 levels. Collectively, our results indicated that BHPF exposure disrupted mouse oocyte maturation and reduced oocyte quality through affecting cytoskeleton architecture, mitochondrial function, oxidative stress, apoptosis, and histone modifications. Environ. Mol. Mutagen. 60:243-253, 2019. © 2018 Wiley Periodicals, Inc.
Keyphrases
- oxidative stress
- drinking water
- reactive oxygen species
- diabetic rats
- mitochondrial dna
- cell death
- endoplasmic reticulum stress
- drug induced
- liver failure
- escherichia coli
- copy number
- dna damage
- respiratory failure
- gene expression
- quality improvement
- high glucose
- induced apoptosis
- cell proliferation
- endothelial cells
- endoplasmic reticulum
- climate change
- binding protein
- insulin resistance
- mechanical ventilation
- signaling pathway
- ionic liquid
- estrogen receptor
- high fat diet induced
- solid phase extraction
- amino acid