BPA induces placental trophoblast proliferation inhibition and fetal growth restriction by inhibiting the expression of SRB1

Cao, Yuming; Chen, Sihan; Lu, Jing; Zhang, Ming; Shi, Lei; Qin, Juling; Lv, Jing; Li, Danyang; Ma, Ling; Zhang, Yuanzhen

doi:10.1007/s11356-023-26850-4

Cited by 9 publications

(4 citation statements)

References 55 publications

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“…Over a long period of time, a series of studies have been conducted on BPA, from small beetle dapits to mammalian mice to human embryos, and we can find that BPA is far more harmful to living things than we thought [ 32 ]. Excessive levels of BPA in daphnia can cause disturbances in the digestive, nervous, and antioxidant systems [ 39 ]; Mice exposed to certain doses of BPA have been shown to suffer severe damage in both female and male mice. BPA was more severe during perinatal exposure, causing dysregulation of the hypothalamic-pituitary-ovarian axis in both young and adult mice, leading to axial precocious puberty [ 40 – 42 ].…”

Section: Discussionmentioning

confidence: 99%

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

Wang,

He,

et al. 2024

J Ovarian Res

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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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Section: Discussionmentioning

confidence: 99%

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

Wang,

He,

et al. 2024

J Ovarian Res

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“…In the last decade, several studies have examined the effects of BPA on mouse placenta [57][58][59][60][61]. Many investigations showed that BPA interferes with the placental epigenome of mammals.…”

Section: Effects On the Placentamentioning

confidence: 99%

An Overview of the Health Effects of Bisphenol A from a One Health Perspective

Molina-López

Bujalance-Reyes

Ayala-Soldado

et al. 2023

Animals

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Bisphenol A (BPA) is a chemical compound, considered as an “emerging pollutant”, that appears ubiquitously, contaminating the environment and food. It is an endocrine disruptor, found in a multitude of consumer products, as it is a constituent of polycarbonate used in the manufacture of plastics and epoxy resins. Many studies have evaluated the effects of BPA, using a wide range of doses and animal models. In this work, we carried out a review of relevant research related to the effects of BPA on health, through studies performed at different doses, in different animal models, and in human monitoring studies. Numerous effects of BPA on health have been described; in different animal species, it has been reported that it interferes with fertility in both females and males and causes alterations in their offspring, as well as being associated with an increase in hormone-dependent pathologies. Similarly, exposure to BPA has been related to other diseases of great relevance in public health such as obesity, hypertension, diabetes, or neurodevelopmental disorders. Its ubiquity and nonmonotonic behavior, triggering effects at exposure levels considered “safe”, make it especially relevant when both animal and human populations are constantly and inadvertently exposed to this compound. Its effects at low exposure levels make it essential to establish safe exposure levels, and research into the effects of BPA must continue and be focused from a “One Health” perspective to take into account all the factors that could intervene in the development of a disease in any exposed organism.

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“…The placenta, characterized by unique hypomethylated patterns, plays a crucial role in fetal growth and development, with altered placental DNAm levels considered a mediator between prenatal environmental exposures and adverse health outcomes . However, only a few human studies have elucidated mechanisms regarding placental DNAm and gene expression underlying the association between prenatal BPs exposure and fetal growth restriction. , Direct evidence linking these alterations to developmental outcomes, especially reproductive outcomes, remains limited.…”

Section: Introductionmentioning

confidence: 99%

“…22 However, only a few human studies have elucidated mechanisms regarding placental DNAm and gene expression underlying the association between prenatal BPs exposure and fetal growth restriction. 23,24 Direct evidence linking these alterations to developmental outcomes, especially reproductive outcomes, remains limited.…”

Section: Introductionmentioning

confidence: 99%

The Role of Placental DNA Methylation at Reproduction-Related Genes in Associations between Prenatal Bisphenol Analogues Exposure and the Digit Ratio in Children at Age 4: A Birth Cohort Study

Chen,

Zhu,

Chen

et al. 2024

Environ. Sci. Technol.

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BPA induces placental trophoblast proliferation inhibition and fetal growth restriction by inhibiting the expression of SRB1

Cited by 9 publications

References 55 publications

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

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

An Overview of the Health Effects of Bisphenol A from a One Health Perspective

The Role of Placental DNA Methylation at Reproduction-Related Genes in Associations between Prenatal Bisphenol Analogues Exposure and the Digit Ratio in Children at Age 4: A Birth Cohort Study

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