TRIM24-DTNBP1-ATP7A mediated astrocyte cuproptosis in cognition and memory dysfunction caused by Y2O3 NPs.
Sci Total Environ
; 954: 176353, 2024 Sep 19.
Article
in En
| MEDLINE
| ID: mdl-39304169
ABSTRACT
Yttrium oxide nanoparticles (Y2O3 NPs), extensively utilized rare earth nanoparticles, exhibited a diverse range of applications across various fields, which leading to increased human exposure. Moreover, potential neurotoxic risks have been associated with their use, yet the underlying mechanism remains unclear. The present study aimed to investigate the effects of Y2O3 NPs on cognitive function in rats with a particular focus on elucidating the pivotal role played by astrocytes in this process. The results demonstrated that Y2O3 NPs induced cognitive and memory impairment in rats, copper (Cu) accumulation and cuproptosis of astrocytes as contributing factors. Furthermore, we elucidated that Y2O3 NPs induced astrocytes cuproptosis by inhibiting TRIM24/DTNBP1/ATP7A signaling pathway-mediated cellular Cu efflux. We provide, for the first time, the important involvement of astrocytes in Y2O3 NPs-induced neurotoxicity, elucidating that cuproptosis as the primary mode of cell death. These results offer valuable insights for the future safe application of rare earth nanoparticles in field of neurology.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Language:
En
Journal:
Sci Total Environ
Year:
2024
Document type:
Article
Affiliation country:
China
Country of publication:
Netherlands