Apoptosis, rather than neurogenesis, induces significant hippocampal‐dependent learning and memory impairment in chronic low Cd2+ exposure

• DOI: 10.1002/tox.23445
• Publication Date: 2022-01-06T11:40:16Z
• Authors: Tianpeng Li; Shuyan Dong; Chengjian He; Jing Yang; Weiyun Li; Shanshan Li; Jing Li; Xiaoxue Du; Zhaoxia Hou; Luping Li; Songtao Li; Zhihui Huang; Tingting Sun
• Keywords: Neurotoxicity

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 specific mechanism in chronic Cd exposure. To investigate Cd2+ , we traced effects for up to 30 months mice which were exposed by drinking mimicking Cd-polluted water. We found toxicity exposure was process associated transition from autophagy apoptosis, switch autophagy-apoptosis dose-dependent threshold [Cd2+ ] 0.04 mg/L. Furthermore, JNK be hub molecule orchestrated interacting Sirt1 p53. At last, hippocampus-dependent learning memory damaged continuous neuron apoptosis rather than deficit neurogenesis. Therefore, elucidation effect, process, potential molecular important controlling environmental-pollutant Cd.