Transport and Toxicity of Methylmercury-Cysteine in Cultured BeWo Cells
Autor: | Srividya Ganapathy, Elisa R. Farrell, Simran Vaghela, Lucy Joshee, Earl G. Ford, Olga Uchakina, Robert J. McKallip, Jennifer L. Barkin, Christy C. Bridges |
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Jazyk: | angličtina |
Rok vydání: | 2022 |
Předmět: |
autophagy
Time Factors mercury placenta Cell Survival QH301-705.5 syncytiotrophoblast Tritium Models Biological Catalysis Article Cell Line Substrate Specificity Inorganic Chemistry Methionine Malondialdehyde Humans oxidative stress Cysteine Physical and Theoretical Chemistry Biology (General) Molecular Biology Cell Shape QD1-999 Spectroscopy Organic Chemistry Biological Transport General Medicine Methylmercury Compounds Glutathione Computer Science Applications Mitochondria Chemistry embryonic structures Lipid Peroxidation toxicology Biomarkers |
Zdroj: | International Journal of Molecular Sciences, Vol 23, Iss 394, p 394 (2022) International Journal of Molecular Sciences International Journal of Molecular Sciences; Volume 23; Issue 1; Pages: 394 |
ISSN: | 1661-6596 1422-0067 |
Popis: | Mercury is a heavy metal toxicant that is prevalent throughout the environment. Organic forms of mercury, such as methylmercury (MeHg), can cross the placenta and can lead to lasting detrimental effects in the fetus. The toxicological effects of MeHg on the placenta itself have not been clearly defined. Therefore, the purpose of the current study was to assess the transport of MeHg into placental syncytiotrophoblasts and to characterize the mechanisms by which MeHg exerts its toxic effects. Cultured placental syncytiotrophoblasts (BeWo) were used for these studies. The transport of radioactive MeHg was measured to identify potential mechanisms involved in the uptake of this compound. The toxicological effects of MeHg on BeWo cells were determined by assessing visible pathological change, autophagy, mitochondrial viability, and oxidative stress. The findings of this study suggest that MeHg compounds are transported into BeWo cells primarily by sodium-independent amino acid carriers and organic anion transporters. The MeHg altered mitochondrial function and viability, decreased mitophagy and autophagy, and increased oxidative stress. Exposure to higher concentrations of MeHg inhibited the ability of cells to protect against MeHg-induced injury. The findings show that MeHg is directly toxic to syncytiotrophoblasts and may lead to disruptions in the fetal/maternal transfer of nutrients and wastes. |
Databáze: | OpenAIRE |
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