Acrylamide impairs the developmental potential of germinal vesicle oocytes by inducing mitochondrial dysfunction and autophagy/apoptosis in mice

被引:12
|
作者
Gao, Ji-Guang [1 ,2 ]
Yang, Jian-Ke [2 ]
Zhu, Lei [3 ]
Xu, Cheng [4 ]
Nie, Liu-Wang [1 ]
机构
[1] Anhui Normal Univ, Prov Key Lab Conservat & Exploitat Res Biol Resou, Life Sci Coll, Wuhu, Peoples R China
[2] Wannan Med Coll, Sch Preclin Med, Wuhu, Peoples R China
[3] Wannan Med Coll, Sch Pharm, Wuhu, Peoples R China
[4] Wannan Med Coll, Sch Clin Med, Wuhu, Peoples R China
基金
中国国家自然科学基金;
关键词
Acrylamide; germinal vesicle oocyte; mitochondrial function; actin filament assembly; autophagy; apoptosis; ZONAE-PELLUCIDAE; CHROMATIN ORGANIZATION; MEIOTIC COMPETENCE; OXIDATIVE STRESS; ANTRAL OOCYTES; MOUSE EGG; APOPTOSIS; MATURATION; AUTOPHAGY; TOXICITY;
D O I
10.1177/09603271211045956
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
Background: Acrylamide (ACR), an important endogenous contaminant in carbohydrate-rich foods, has been involved in various negative effects on multiple organ networks, including the reproductive system. Previous studies have reported that ACR affects oocyte quality and fertility. Purpose: This study aimed to explore the toxic effects and regulatory mechanisms of ACR on mouse germinal vesicle (GV) oocytes. Research Design: In this study, adult female mice were exposed to ACR at 10 mg/kg/day/body weight through their drinking water continuously for 4 weeks. Study Sample and Data Analysis: The mitochondrial function, autophagy/apoptosis, and development potential of GV oocytes were investigated. Results: The results showed that ACR reduced the oocyte diameter, sperm-binding ability, parthenogenetic activation and in vitro fertilization (IVF) rate, and development potential of pre-implantation embryos. We also found that ACR exposure disrupted chromatin configuration, mitochondrial distribution, and membrane potential (Delta phi m) of oocytes. Actin filament expression was significantly reduced in both the membrane and cytoplasm of mouse oocytes. Moreover, ACR exposure increased LC3-positive signals, early apoptosis rate, aberrant ATG3, ATG5, LC3, Beclin1, and mTOR mRNA expression. Conclusions: These results suggest that ACR exposure can affect the developmental potential of GV oocytes by inducing mitochondrial dysfunction, actin filament assembly, and autophagy/apoptosis.
引用
收藏
页码:S370 / S380
页数:11
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