Apoptosis, rather than neurogenesis, induces significant hippocampal-dependent learning and memory impairment in chronic low Cd2+ exposure.
Environ Toxicol
; 37(4): 814-824, 2022 Apr.
Article
en En
| MEDLINE
| ID: mdl-34989457
ABSTRACT
Cadmium (Cd), a ubiquitous toxic heavy metal, with the intractable trait of low degradation, can induce multiple organ damage. Whereas, far less is known about its neurotoxicity and the specific mechanism in the chronic low Cd exposure. To investigate the chronic neurotoxicity of Cd2+ , we traced its effects for up to 30 months in mice which were exposed to Cd2+ by drinking the mimicking Cd-polluted water. We found the toxicity of chronic Cd exposure was a process associated with the transition from autophagy to apoptosis, and the switch of autophagy-apoptosis was Cd dose-dependent with the threshold of [Cd2+ ] 0.04 mg/L. Furthermore, JNK was found to be a hub molecule orchestrated the switch of autophagy-apoptosis by interacting with Sirt1 and p53. At last, the hippocampus-dependent learning and memory was damaged by continuous neuron apoptosis rather than deficit of neurogenesis. Therefore, elucidation of the effect, process, and potential molecular mechanism of the chronic low Cd2+ exposure is important for controlling of the environmental-pollutant Cd.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Cadmio
/
Neurogénesis
Límite:
Animals
Idioma:
En
Revista:
Environ Toxicol
Asunto de la revista:
SAUDE AMBIENTAL
/
TOXICOLOGIA
Año:
2022
Tipo del documento:
Article
País de afiliación:
China