尼氏体
神经毒性
高磷酸化
神经病理学
细胞凋亡
内科学
磷酸化
化学
医学
内分泌学
锑
病态的
毒性
病理
染色
疾病
生物化学
无机化学
作者
Shenya Xu,Zhongzhen Yang,Yong Zhi,Shali Yu,Tao Zhang,Junkang Jiang,Jun Tang,Huiguang He,Ming Lü,Xiaoke Wang,Qianhui Wu,Xinyuan Zhao
标识
DOI:10.1016/j.scitotenv.2020.143235
摘要
We have previously identified antimony (Sb) as a newly nerve poison which leads to neuronal apoptosis. However, the relationship between Sb exposure and Alzheimer's disease (AD) process lacks direct evidence. HE staining and Nissl staining showed significant nerve damage after Sb exposure. Therefore, we further evaluated Sb-associated AD risk by detecting accumulation of β-amyloid protein (Aβ) and neurofibrillary tangles (NFTs) in the brains of mice exposed to Sb for 4 and 8 weeks, and even 1 year. The results showed that dose of 20 mg/kg induced Aβ accumulation, but not tau hyperphosphorylation after exposure for 4 week. Eight weeks later, both 10 and 20 mg/kg dramatically triggered Aβ accumulation and increased tau phosphorylation at ser199. At the same time, 20 mg/kg could also increase tau phosphorylation at ser396 and number of NFTs. One years later, we found all of AD hallmarks detected in present study showed positive results in the brains of mice exposed to Sb at 10 and 20 mg/kg. In summary, our data provided direct evidence of Sb-associated AD risk, drawing more attention to Sb-triggered neurotoxicity.
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