1. The role of Fas-FasL-FADD signaling pathway in arsenic-mediated neuronal apoptosis in vivo and in vitro
- Author
-
Hongna, Sun, Yanmei, Yang, Muyu, Gu, Yang, Li, Zhe, Jiao, Chunqing, Lu, Bingyu, Li, Yuting, Jiang, Lixin, Jiang, Fang, Chu, Wenjing, Yang, Dianjun, Sun, and Yanhui, Gao
- Subjects
Male ,Neurons ,Caspase 8 ,Fas Ligand Protein ,Dose-Response Relationship, Drug ,Caspase 3 ,Fas-Associated Death Domain Protein ,General Medicine ,Toxicology ,Arsenic ,Rats ,Up-Regulation ,Rats, Sprague-Dawley ,Random Allocation ,Gene Expression Regulation ,Cell Line, Tumor ,Animals ,Humans ,Environmental Pollutants ,RNA, Messenger ,fas Receptor ,Signal Transduction - Abstract
The molecular mechanisms underlying arsenic-induced neurotoxicity have not been completely elucidated. Our study aimed to determine the role of the Fas-FasL-FADD signaling pathway in arsenic-mediated neuronal apoptosis. Pathological and molecular biological tests were performed on the cerebral cortex of arsenic-exposed rats and SH-SY5Y neuroblastoma cells. Arsenic induced apoptosis in the cortical neurons, which corresponded to abnormal ultrastructural changes. Mechanistically, arsenic activated the Fas-FasL-FADD signaling pathway and the downstream caspases both in vivo and in vitro. ZB4 treatment reversed the apoptotic effects of arsenic on the SHSY5Y cells. Taken together, arsenic induces neurotoxicity by activating the Fas-FasL-FADD signaling pathway.
- Published
- 2022