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Exposure to diisononyl phthalate deteriorates the quality of porcine oocytes by inducing the apoptosis

文献类型： 外文期刊

作者： Wang, Rui 1 ; Chen, Jingyue 1 ; Cui, Zhaokang 1 ; Li, Yu 1 ; Gao, Qian 4 ; Miao, Yilong 1 ; Wang, Huili 3 ; Xiong, Bo 1 ;

作者机构： 1.Nanjing Agr Univ, Coll Anim Sci & Technol, Nanjing 210095, Peoples R China

2.Chinese Acad Agr Sci, State Key Lab Mol Biol Special Econ Anim & Plant S, Changchun 130112, Peoples R China

3.Jiangsu Acad Agr Sci, Institue Anim Sci, Nanjing 210014, Peoples R China

4.Nanjing Agr Univ, Coll Vet Med, Nanjing 210095, Peoples R China

关键词： Diisononyl phthalate; Oocyte quality; Fertilization ability; Apoptosis; Autophagy

期刊名称：ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY （ 影响因子：6.8； 五年影响因子：6.9 ）

ISSN： 0147-6513

年卷期： 2023 年 254 卷

页码：

收录情况： SCI

摘要： Diisononyl phthalate (DINP), a mixture of chemical compounds composed of diverse isononyl esters of phthalic acid, is commonly applied as a plasticizer to substitute for di (2-ethylhexyl) phthalate (DEHP). It has been demonstrated that DINP exposure impairs the functions of kidney and liver in animals. However, the effects and potential mechanisms of DINP exposure on the female reproduction, especially the oocyte quality are still poorly understood. Here, we discovered that DINP exposure weakened the porcine oocyte meiotic competency (78.9% vs 53.6%, P < 0.001) and fertilization ability (78.5% vs 34.1%, P < 0.0001) during in vitro maturation. Specifically, DINP exposure induced the persistent spindle assembly checkpoint (SAC) activation caused by the disorganized spindle/chromosome apparatus (spindle: 20.0% vs 83.3%, P < 0.001; chromosome: 20.0% vs 80.0%, P < 0.01) to arrest meiotic progression of oocytes at metaphase I stage. In addition, DINP exposure disturbed the dynamics of sperm binding (146.7 vs 58.6, P < 0.0001) and fusion proteins (19.5 vs 11.6, P < 0.0001) in oocytes to compromise their fertilization ability. In particular, transcriptome data uncovered that the action mechanism of DINP on the oocyte maturation was associated with oxidative phosphorylation, apoptosis and autophagy pathways. Lastly, we validated that DINP exposure resulted in the mitochondrial dysfunction (27.2 vs 19.8, P < 0.0001) and elevated levels of reactive oxygen species (ROS; 8.9 vs 19.9, P < 0.0001) to trigger the occurrence of apoptosis (7.2 vs 13.1, P < 0.0001) and protective autophagy (68.6 vs 139.3, P < 0.01). Altogether, our findings not only testify that DINP has a potentially adverse impact on the mammalian oocyte quality, but also provide a scientific reference regarding how environment pollutants act on the female germ cell development.

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