Cadmium cytotoxicity and possible mechanisms in human trophoblast HTR-8/SVneo cells.
Ying LiaoHong ZhengLangbo WuLei HeYu WangYangsong OuHongjun YangShiqin PengFengwang ChenXiaoyan WangJiayuan ZhaoPublished in: Environmental toxicology (2021)
The accumulation of cadmium (Cd) in the human body through food chain can lead to adverse pregnancy outcomes. In this study, Cd cytotoxicity and its mechanisms in HTR-8/SVneo cells were investigated. Cd disrupted the cellular submicrostructure and inhibited the cell viability in a time- and dose-dependent manner. The levels of reactive oxygen species, malondialdehyde content, and the activities of glutathione peroxidase (GSH-Px) and total superoxode dismutase (T-SOD) were concentration-dependently increased by Cd. In addition, Cd dose-dependently inducedcell apoptosis and decreased cell migration and invasion capacities. Finally, Cd significantly upregulated all the genes related to oxidative stress (SOD1, ROS1, and HSPA6), inflammatory response, cell cycle, apoptosis, and migration and invasion. This study will provide insights into the prevention and treatment of pregnancy-related diseases caused by Cd intoxication.
Keyphrases
- oxidative stress
- cell cycle arrest
- induced apoptosis
- cell cycle
- pregnancy outcomes
- cell death
- endothelial cells
- reactive oxygen species
- nk cells
- endoplasmic reticulum stress
- dna damage
- pregnant women
- nitric oxide
- emergency department
- mesenchymal stem cells
- mass spectrometry
- single molecule
- dna methylation
- hydrogen peroxide
- replacement therapy