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Perfluorooctanoic acid inhibits the maturation rate of mouse oocytes cultured in vitro by triggering mitochondrial and DNA damage
Author(s) -
Guo Conghui,
Zhao Zhihong,
Zhao Kun,
Huang Jianhao,
Ding Linshu,
Huang Xiaogang,
Meng Li,
Li Li,
Wei Hengxi,
Zhang Shouquan
Publication year - 2021
Publication title -
birth defects research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.845
H-Index - 17
ISSN - 2472-1727
DOI - 10.1002/bdr2.1899
Subject(s) - apoptosis , dna damage , perfluorooctanoic acid , mitochondrion , reactive oxygen species , oxidative stress , mitochondrial dna , biology , oocyte , microbiology and biotechnology , in vitro , andrology , chemistry , gene , biochemistry , dna , embryo , medicine
Background Perfluorooctanoic acid (PFOA) is widely used in the manufacture of household and industrial products. It has certain toxicity and leaves many residues in the environment. Numerous studies have shown that PFOA exhibits endocrine disrupting properties and immunotoxicity and induces developmental defects. However, there is very little information regarding its toxicity on oocytes. Methods We cultured denuded oocytes in maturation medium supplemented with 0, 300, or 500 PFOA during IVM and evaluated the maturation of oocytes from the aspects of ROS(DCFH‐DA), mitochondria(MitoOrange and JC‐1), DNA damage(P‐H2AX), and cytoskeleton(β‐tubulin). Results Compared with the control group, the PFOA treatment group exhibited significantly reduced proportion of oocytes matutation. Furthermore, the DCFH‐DA test showed that PFOA significantly increased reactive oxygen species (ROS) levels. PFOA disrupted mitochondrial distribution and decreased mitochondrial function as assessed using MitoOrange and JC‐1. In addition, PFOA‐treated oocytes exhibited a significantly higher percentage of P‐H2AX, defective β‐tubulin, abnormal chromosome alignment, lower expression of the anti‐apoptotic gene Bcl‐2, and higher expression of the apoptotic genes caspase3 and Bax. Conclusion In summary, PFOA could negatively and directly affect oocyte maturation in vitro and cause oxidative stress, mitochondrial function disruption, DNA damage, cytoskeleton damage, and apoptosis.