AI Article Synopsis
- BPA (Bisphenol A) negatively impacts bone development by reducing cell viability and osteogenic activity while promoting oxidative stress and apoptosis in both in vitro (hFOB1.19 cells) and in vivo (larval zebrafish) models.
- The study found that BPA exposure led to increased levels of apoptotic proteins (Caspases 3 and 9) and disrupted transcription of key genes involved in bone development and apoptosis, like bmp2, runx2, and bcl2.
- Results highlighted that BPA's harmful effects on bone health are linked to oxidative stress and changes in cell death processes, emphasizing the need for further research on its mechanisms.
Article Abstract
Bisphenol A (BPA), an ingredient in consumer products, has been suggested that it can interfere with bone development and maintenance, whereas the molecule mechanism remains unclear. The objective of this study is to investigate the effect of BPA on early bone differentiation and metabolism, and its potential molecule mechanism by employing hFOB1.19 cell as an in vitro model, as well as larval zebrafish as an in vivo model. The in vitro experiments indicated that BPA decreased cell viability, inhibited osteogenic activity (such as ALP, RUNX2), increased ROS production, upregulated transcriptional or protein levels of apoptosis-related molecules (such as Caspase 3, Caspase 9), while suppressed transcriptional or protein levels of pyroptosis-specific markers (TNF-α, TNF-β, IL-1β, ASC, Caspase 1, and GSDMD). Moreover, the evidences from in vivo model demonstrated that exposure to BPA distinctly disrupted pharyngeal cartilage, craniofacial bone development, and retarded bone mineralization. The transcriptional level of bone development-related genes (bmp2, dlx2a, runx2, and sp7), apoptosis-related genes (bcl2), and pyroptosis-related genes (cas1, nlrp3) were significantly altered after treating with BPA in zebrafish larvae. In summary, our study, combining in vitro and in vivo models, confirmed that BPA has detrimental effects on osteoblast activity and bone development. These effects may be due to the promotion of apoptosis, the initiation of oxidative stress, and the inhibition of pyroptosis.
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| http://dx.doi.org/10.1016/j.envpol.2024.123731 | DOI Listing |
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