Fumonisin B1 exposure deteriorates oocyte quality by inducing organelle dysfunction and DNA damage in mice

被引:22
|
作者
Wang, Yue [1 ]
Xu, Yao [1 ]
Ju, Jia-Qian [1 ]
Liu, Jing-Cai [1 ]
Sun, Shao-Chen [1 ]
机构
[1] Nanjing Agr Univ, Coll Anim Sci & Technol, Nanjing 210095, Peoples R China
关键词
Fumonisin; Oocyte; Meiosis; Oxidative stress; Apoptosis; OXIDATIVE STRESS; IN-VITRO; B-1; APOPTOSIS; AUTOPHAGY; TOXICITY; DEOXYNIVALENOL; HEPATOTOXICITY; PROLIFERATION; OCHRATOXIN;
D O I
10.1016/j.ecoenv.2021.112598
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
Oocyte quality is critical for fertilization and early embryo development. Fumonisin B1 (FB1) is a Fusarium mycotoxin and it is commonly found in contaminated food and feedstuff, posing a potential health hazard to both animals and human. FB1 is reported to have hepatotoxicity, neurotoxicity, nephrotoxicity, immunotoxicity and embryotoxicity. However, the effects of FB1 on mouse oocyte quality are still unknown. Here, we explored the toxic effects and potential mechanisms of FB1 on oocyte maturation quality in mice. FB1 exposure inhibited the first polar body extrusion at concentrations of 30 mu M and 50 mu M, which further induced oocyte meiotic arrest. Besides, disrupted spindle structure was found in oocytes after FB1 exposure. Our results also showed that FB1 exposure impaired mitochondria dysfunction, which further induced oxidative stress and early apoptosis. In addition, we reported that FB1 exposure induced the accumulation of lysosome and occurrence of autophagy. Aberrant ER distribution and ER stress were also found in FB1-exposed oocytes. Moreover, DNA damage was also observed. These results together suggested that FB1 exposure affected oocyte quality by destroying spindle structure, leading to mitochondria, lysosome and ER dysfunction, which further induced oxidative stress, apoptosis, autophagy and DNA damage in mouse oocytes.
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页数:9
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