Methylparaben induces cell-cycle arrest and caspase-3-mediated apoptosis in human placental BeWo cells
- Authors
- Kim, Ji-Young; Kim, Mi Jin; An, Mi-Jin; Shin, Geun-Seup; Lee, Hyun-Min; Kim, Chul-Hong; Kim, Jung-Woong
- Issue Date
- Nov-2020
- Publisher
- KOREAN SOCIETY TOXICOGENOMICS & TOXICOPROTEOMICS-KSTT
- Keywords
- Apoptosis; Methylparaben; Caspase-3; Human placenta; BeWo cells
- Citation
- MOLECULAR & CELLULAR TOXICOLOGY, v.16, no.4, pp 409 - 418
- Pages
- 10
- Journal Title
- MOLECULAR & CELLULAR TOXICOLOGY
- Volume
- 16
- Number
- 4
- Start Page
- 409
- End Page
- 418
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/43338
- DOI
- 10.1007/s13273-020-00097-3
- ISSN
- 1738-642X
2092-8467
- Abstract
- Background Parabens are frequently used as antimicrobial preservatives in various commercials, pharmaceutical products, and foods. Recent studies have suggested that the exposure of pregnant women to methylparaben has adverse effects on the fetus. However, the biological mechanisms underlying the effects of methylparaben on human placental cells are yet to be elucidated. Objective In this study, we determined that methylparaben induces cell death by affecting the growth, cell-cycle arrest, and apoptosis of human placental BeWo cells. We employed flow cytometry at the single-cell level for analyzing the expression of proteins related to cell cycle and apoptosis instead of using conventional methods. Results The results demonstrated that treatment with methylparaben significantly decreased cell viability. We observed that methylparaben increased the protein level of cyclin B1, which arrested the cell cycle at sub-G1 status, and decreased the proportion of BeWo cells in the G2/M phase. We also observed that methylparaben induced caspase-3-mediated apoptosis in a time- and dose-dependent manner. Conclusion These results suggested that methylparaben had cytotoxic adverse effects on human BeWo placenta cells through the induction of apoptosis and cell-cycle arrest.
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Collections - College of Natural Sciences > Department of Life Science > 1. Journal Articles
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