Bisphenol A triggers apoptosis in mouse pre-antral follicle granulosa cells via oxidative stress

Abstract Background Bisphenol A (BPA), an endocrine disrupting chemical with weak estrogenic and anti-androgenic activity, is widely present in various environmental media and organisms. It has certain reproductive toxicity and can cause a variety of female reproductive system diseases. Although BPA...

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Main Authors: Chen Wang, Chaofan He, Shumin Xu, Yuanyuan Gao, Kaixian Wang, Meng Liang, Ke Hu
Format: Article
Language:English
Published: BMC 2024-01-01
Series:Journal of Ovarian Research
Subjects:
Online Access:https://doi.org/10.1186/s13048-023-01322-y
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author Chen Wang
Chaofan He
Shumin Xu
Yuanyuan Gao
Kaixian Wang
Meng Liang
Ke Hu
author_facet Chen Wang
Chaofan He
Shumin Xu
Yuanyuan Gao
Kaixian Wang
Meng Liang
Ke Hu
author_sort Chen Wang
collection DOAJ
description Abstract Background Bisphenol A (BPA), an endocrine disrupting chemical with weak estrogenic and anti-androgenic activity, is widely present in various environmental media and organisms. It has certain reproductive toxicity and can cause a variety of female reproductive system diseases. Although BPA-stimulated apoptosis of granulosa cells has been widely elaborated, the effect of BPA on mouse pre-antral follicle granulosa cells (mpGCs) has not been well elucidated. Results In this study, the results of live-dead cell staining showed that high concentrations of BPA severely impaired mpGCs growth viability and affected the cell cycle transition of mpGCs. We confirmed that BPA promotes the production of reactive oxygen species (ROS) and facilitates oxidative stress in mpGCs. In addition, immunofluorescence, transmission electron microscopy, and flow cytometry experiments demonstrated that BPA treatment for mpGCs resulted in apoptotic features, such as rounding, cytoplasmic crinkling, and mitochondrial damage. This was accompanied by a large production of ROS and apoptosis-inducing factor (AIF) translocation from the mitochondria to the nucleus. RNA-seq data showed that several apoptosis-related pathways were enriched in the high concentration BPA-treated group compared with the normal group, such as the p53 pathway, MAPK pathway, etc. Conclusions These results suggest that cells undergo oxidative stress effects and apoptosis after BPA treatment for mpGCs, which affects normal follicle development. The potential mechanism of BPA-induced female reproductive toxicity was elucidated, while providing a research basis for the prevention and treatment of female reproductive diseases.
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spelling doaj.art-b29070166a734e818969e157471bdd262024-01-21T12:30:36ZengBMCJournal of Ovarian Research1757-22152024-01-0117111110.1186/s13048-023-01322-yBisphenol A triggers apoptosis in mouse pre-antral follicle granulosa cells via oxidative stressChen Wang0Chaofan He1Shumin Xu2Yuanyuan Gao3Kaixian Wang4Meng Liang5Ke Hu6School of Life Science, Bengbu Medical UniversitySchool of Life Science, Bengbu Medical UniversitySchool of Life Science, Bengbu Medical UniversitySchool of Life Science, Bengbu Medical UniversitySchool of Life Science, Bengbu Medical UniversitySchool of Life Science, Bengbu Medical UniversitySchool of Life Science, Bengbu Medical UniversityAbstract Background Bisphenol A (BPA), an endocrine disrupting chemical with weak estrogenic and anti-androgenic activity, is widely present in various environmental media and organisms. It has certain reproductive toxicity and can cause a variety of female reproductive system diseases. Although BPA-stimulated apoptosis of granulosa cells has been widely elaborated, the effect of BPA on mouse pre-antral follicle granulosa cells (mpGCs) has not been well elucidated. Results In this study, the results of live-dead cell staining showed that high concentrations of BPA severely impaired mpGCs growth viability and affected the cell cycle transition of mpGCs. We confirmed that BPA promotes the production of reactive oxygen species (ROS) and facilitates oxidative stress in mpGCs. In addition, immunofluorescence, transmission electron microscopy, and flow cytometry experiments demonstrated that BPA treatment for mpGCs resulted in apoptotic features, such as rounding, cytoplasmic crinkling, and mitochondrial damage. This was accompanied by a large production of ROS and apoptosis-inducing factor (AIF) translocation from the mitochondria to the nucleus. RNA-seq data showed that several apoptosis-related pathways were enriched in the high concentration BPA-treated group compared with the normal group, such as the p53 pathway, MAPK pathway, etc. Conclusions These results suggest that cells undergo oxidative stress effects and apoptosis after BPA treatment for mpGCs, which affects normal follicle development. The potential mechanism of BPA-induced female reproductive toxicity was elucidated, while providing a research basis for the prevention and treatment of female reproductive diseases.https://doi.org/10.1186/s13048-023-01322-yBisphenol AmpGCsReactive oxygen speciesOxidative stressApoptosis
spellingShingle Chen Wang
Chaofan He
Shumin Xu
Yuanyuan Gao
Kaixian Wang
Meng Liang
Ke Hu
Bisphenol A triggers apoptosis in mouse pre-antral follicle granulosa cells via oxidative stress
Journal of Ovarian Research
Bisphenol A
mpGCs
Reactive oxygen species
Oxidative stress
Apoptosis
title Bisphenol A triggers apoptosis in mouse pre-antral follicle granulosa cells via oxidative stress
title_full Bisphenol A triggers apoptosis in mouse pre-antral follicle granulosa cells via oxidative stress
title_fullStr Bisphenol A triggers apoptosis in mouse pre-antral follicle granulosa cells via oxidative stress
title_full_unstemmed Bisphenol A triggers apoptosis in mouse pre-antral follicle granulosa cells via oxidative stress
title_short Bisphenol A triggers apoptosis in mouse pre-antral follicle granulosa cells via oxidative stress
title_sort bisphenol a triggers apoptosis in mouse pre antral follicle granulosa cells via oxidative stress
topic Bisphenol A
mpGCs
Reactive oxygen species
Oxidative stress
Apoptosis
url https://doi.org/10.1186/s13048-023-01322-y
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