BPZ inhibits early mouse embryonic development by disrupting maternal-to-zygotic transition and mitochondrial function
The use of Bisphenol A (BPA) has been widely restricted due to its adverse health effects. Bisphenol Z (BPZ) is used as an alternative to BPA, and humans are widely exposed to BPZ through various routes. Recent studies have shown that BPZ exposure adversely affects mouse oocyte meiotic maturation. T...
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Elsevier
2025-01-01
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| Series: | Ecotoxicology and Environmental Safety |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S0147651325000296 |
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| author | Zhiming Ding Huilei Chen Huiru Cheng Caiyun Wu Hongzhen Ruan Bingjing Zhu Ping Zhou Zuying Xu Huifen Xiang |
| author_facet | Zhiming Ding Huilei Chen Huiru Cheng Caiyun Wu Hongzhen Ruan Bingjing Zhu Ping Zhou Zuying Xu Huifen Xiang |
| author_sort | Zhiming Ding |
| collection | DOAJ |
| description | The use of Bisphenol A (BPA) has been widely restricted due to its adverse health effects. Bisphenol Z (BPZ) is used as an alternative to BPA, and humans are widely exposed to BPZ through various routes. Recent studies have shown that BPZ exposure adversely affects mouse oocyte meiotic maturation. This study investigates the impact of BPZ exposure on early mouse embryonic development alongside an exploration of the underlying mechanisms. The findings reveal that exposure to BPZ leads to a reduction in early embryo quality and hinders developmental progression. RNA sequencing analysis has identified 593 differentially expressed genes as a result of BPZ exposure, highlighting considerable changes in early embryonic gene expression. Mechanistically, BPZ exposure inhibits the activation of the zygotic genome and impedes maternal mRNA degradation, thereby interfering with maternal-to-zygotic transition (MZT). Further analysis indicates compromised mitochondrial function, as evidenced by abnormal distribution, diminished membrane potential, and lower ATP levels. Consequently, BPZ-exposed embryos exhibit elevated levels of reactive oxygen species, superoxide anions, and oxidative DNA damage. Moreover, BPZ exposure is associated with an increase in γ-H2A.X expression. Additionally, BPZ exposure alters the expression levels of histone modifications, including H3K27me2, H3K27me3, H3K9me3, and H3K27ac, in early embryos. Collectively, BPZ exposure significantly impairs early embryo quality by disrupting mitochondrial function, inducing oxidative stress and DNA damage, altering histone modifications, and inhibiting MZT, ultimately resulting in hindered blastocyst formation. These findings underscore the profound adverse effects of BPZ on early embryonic development, indicating the need for caution when considering it as a safe alternative to BPA. |
| format | Article |
| id | doaj-art-5db51d61082149e2b093b78c4a3edb79 |
| institution | Kabale University |
| issn | 0147-6513 |
| language | English |
| publishDate | 2025-01-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Ecotoxicology and Environmental Safety |
| spelling | doaj-art-5db51d61082149e2b093b78c4a3edb792025-01-23T05:26:08ZengElsevierEcotoxicology and Environmental Safety0147-65132025-01-01289117693BPZ inhibits early mouse embryonic development by disrupting maternal-to-zygotic transition and mitochondrial functionZhiming Ding0Huilei Chen1Huiru Cheng2Caiyun Wu3Hongzhen Ruan4Bingjing Zhu5Ping Zhou6Zuying Xu7Huifen Xiang8NHC Key Laboratory of Study on Abnormal Gametes and Reproductive Tract, Anhui Medical University, No.81 Meishan Road, Hefei 230032, China; Reproductive Medicine Center, Department of Obstetrics and Gynecology, The First Affiliated Hospital of Anhui Medical University, No.218 Jixi Road, Hefei 230022, ChinaNHC Key Laboratory of Study on Abnormal Gametes and Reproductive Tract, Anhui Medical University, No.81 Meishan Road, Hefei 230032, China; Reproductive Medicine Center, Department of Obstetrics and Gynecology, The First Affiliated Hospital of Anhui Medical University, No.218 Jixi Road, Hefei 230022, China; Reproductive Medicine Center, Department of Obstetrics and Gynecology, The First Affiliated Hospital of Bengbu Medical University, No.287 Changhuai Road, Bengbu 233000, ChinaNHC Key Laboratory of Study on Abnormal Gametes and Reproductive Tract, Anhui Medical University, No.81 Meishan Road, Hefei 230032, China; Reproductive Medicine Center, Department of Obstetrics and Gynecology, The First Affiliated Hospital of Anhui Medical University, No.218 Jixi Road, Hefei 230022, ChinaNHC Key Laboratory of Study on Abnormal Gametes and Reproductive Tract, Anhui Medical University, No.81 Meishan Road, Hefei 230032, China; Reproductive Medicine Center, Department of Obstetrics and Gynecology, The First Affiliated Hospital of Anhui Medical University, No.218 Jixi Road, Hefei 230022, ChinaNHC Key Laboratory of Study on Abnormal Gametes and Reproductive Tract, Anhui Medical University, No.81 Meishan Road, Hefei 230032, China; Reproductive Medicine Center, Department of Obstetrics and Gynecology, The First Affiliated Hospital of Anhui Medical University, No.218 Jixi Road, Hefei 230022, ChinaNHC Key Laboratory of Study on Abnormal Gametes and Reproductive Tract, Anhui Medical University, No.81 Meishan Road, Hefei 230032, China; Reproductive Medicine Center, Department of Obstetrics and Gynecology, The First Affiliated Hospital of Anhui Medical University, No.218 Jixi Road, Hefei 230022, ChinaNHC Key Laboratory of Study on Abnormal Gametes and Reproductive Tract, Anhui Medical University, No.81 Meishan Road, Hefei 230032, China; Reproductive Medicine Center, Department of Obstetrics and Gynecology, The First Affiliated Hospital of Anhui Medical University, No.218 Jixi Road, Hefei 230022, China; Corresponding authors at: NHC Key Laboratory of Study on Abnormal Gametes and Reproductive Tract, Anhui Medical University, No.81 Meishan Road, Hefei 230032, China.NHC Key Laboratory of Study on Abnormal Gametes and Reproductive Tract, Anhui Medical University, No.81 Meishan Road, Hefei 230032, China; Reproductive Medicine Center, Department of Obstetrics and Gynecology, The First Affiliated Hospital of Anhui Medical University, No.218 Jixi Road, Hefei 230022, China; Corresponding authors at: NHC Key Laboratory of Study on Abnormal Gametes and Reproductive Tract, Anhui Medical University, No.81 Meishan Road, Hefei 230032, China.NHC Key Laboratory of Study on Abnormal Gametes and Reproductive Tract, Anhui Medical University, No.81 Meishan Road, Hefei 230032, China; Reproductive Medicine Center, Department of Obstetrics and Gynecology, The First Affiliated Hospital of Anhui Medical University, No.218 Jixi Road, Hefei 230022, China; Corresponding authors at: NHC Key Laboratory of Study on Abnormal Gametes and Reproductive Tract, Anhui Medical University, No.81 Meishan Road, Hefei 230032, China.The use of Bisphenol A (BPA) has been widely restricted due to its adverse health effects. Bisphenol Z (BPZ) is used as an alternative to BPA, and humans are widely exposed to BPZ through various routes. Recent studies have shown that BPZ exposure adversely affects mouse oocyte meiotic maturation. This study investigates the impact of BPZ exposure on early mouse embryonic development alongside an exploration of the underlying mechanisms. The findings reveal that exposure to BPZ leads to a reduction in early embryo quality and hinders developmental progression. RNA sequencing analysis has identified 593 differentially expressed genes as a result of BPZ exposure, highlighting considerable changes in early embryonic gene expression. Mechanistically, BPZ exposure inhibits the activation of the zygotic genome and impedes maternal mRNA degradation, thereby interfering with maternal-to-zygotic transition (MZT). Further analysis indicates compromised mitochondrial function, as evidenced by abnormal distribution, diminished membrane potential, and lower ATP levels. Consequently, BPZ-exposed embryos exhibit elevated levels of reactive oxygen species, superoxide anions, and oxidative DNA damage. Moreover, BPZ exposure is associated with an increase in γ-H2A.X expression. Additionally, BPZ exposure alters the expression levels of histone modifications, including H3K27me2, H3K27me3, H3K9me3, and H3K27ac, in early embryos. Collectively, BPZ exposure significantly impairs early embryo quality by disrupting mitochondrial function, inducing oxidative stress and DNA damage, altering histone modifications, and inhibiting MZT, ultimately resulting in hindered blastocyst formation. These findings underscore the profound adverse effects of BPZ on early embryonic development, indicating the need for caution when considering it as a safe alternative to BPA.http://www.sciencedirect.com/science/article/pii/S0147651325000296BPZDNA damageEmbryoMZTMitochondria |
| spellingShingle | Zhiming Ding Huilei Chen Huiru Cheng Caiyun Wu Hongzhen Ruan Bingjing Zhu Ping Zhou Zuying Xu Huifen Xiang BPZ inhibits early mouse embryonic development by disrupting maternal-to-zygotic transition and mitochondrial function Ecotoxicology and Environmental Safety BPZ DNA damage Embryo MZT Mitochondria |
| title | BPZ inhibits early mouse embryonic development by disrupting maternal-to-zygotic transition and mitochondrial function |
| title_full | BPZ inhibits early mouse embryonic development by disrupting maternal-to-zygotic transition and mitochondrial function |
| title_fullStr | BPZ inhibits early mouse embryonic development by disrupting maternal-to-zygotic transition and mitochondrial function |
| title_full_unstemmed | BPZ inhibits early mouse embryonic development by disrupting maternal-to-zygotic transition and mitochondrial function |
| title_short | BPZ inhibits early mouse embryonic development by disrupting maternal-to-zygotic transition and mitochondrial function |
| title_sort | bpz inhibits early mouse embryonic development by disrupting maternal to zygotic transition and mitochondrial function |
| topic | BPZ DNA damage Embryo MZT Mitochondria |
| url | http://www.sciencedirect.com/science/article/pii/S0147651325000296 |
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