1. Tetrabromobisphenol A-Induced Apoptosis in Neural Stem Cells Through Oxidative Stress and Mitochondrial Dysfunction
- Author
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Yujeong Lee, Hyeyoung Jeon, Seonguk Yang, Ah Hyun Kim, Won-Jong Lee, Jung-Hyun Cho, Seulah Lee, Jaewon Lee, Jeanho Yun, and Young-Suk Jung
- Subjects
0301 basic medicine ,Polybrominated Biphenyls ,Apoptosis ,Hippocampal formation ,Toxicology ,medicine.disease_cause ,03 medical and health sciences ,chemistry.chemical_compound ,Mice ,0302 clinical medicine ,Neural Stem Cells ,medicine ,Cytotoxic T cell ,Animals ,Cells, Cultured ,Flame Retardants ,Chemistry ,General Neuroscience ,Neurogenesis ,Neurotoxicity ,medicine.disease ,Neural stem cell ,Cell biology ,Mitochondria ,Oxidative Stress ,030104 developmental biology ,Tetrabromobisphenol A ,030217 neurology & neurosurgery ,Oxidative stress ,Signal Transduction - Abstract
Tetrabromobisphenol A (TBBPA) is widely used in materials like plastics and textiles as a fire retardant. In a previous study, we reported TBBPA might disrupt hippocampal neurogenesis and neurocognitive function in mice. However, the mechanism responsible for these effects has not been established. The present study was undertaken to investigate the potential involvement of oxidative stress and mitochondrial dysfunction in TBBPA-mediated neurotoxicity in neural stem cells. We confirmed TBBPA was more cytotoxic to neural stem cells than to neurons, astrocytes, or fibroblasts, and found that TBBPA-induced neural stem cell apoptosis was accompanied by increased reactive oxygen species generation and mitochondrial dysfunction. At a molecular level, TBBPA-induced apoptosis was determined to be mediated by c-Jun N-terminal kinase-p53 pathway activation. Taken together, these findings suggest that the adverse effects of TBBPA on hippocampal neurogenesis are due to the inhibition of neural stem cell expansion.
- Published
- 2019