Comparison of the neurotoxicity associated with cobalt nanoparticles and cobalt chloride in Wistar rats.
Comparison of the neurotoxicity associated with cobalt nanoparticles and cobalt chloride in Wistar rats.
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比较钴纳米颗粒和氯化钴对 Wistar 大鼠的神经毒性。
DOI：
10.1016/j.taap.2019.03.003
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发表时间：
2019
影响因子：
3.8
通讯作者：
Li Huangyuan
中科院分区：
文献类型：
--
作者：
Zheng Fuli;Luo Zhousong;Zheng Chunyan;Li Jing;Zeng Jingwen;Yang Hongyu;Chen Jinfa;Jin Yanqiao;Aschner Michael;Wu Siying;Zhang Qunwei;Li Huangyuan
钴纳米颗粒（CoNPs）具有物理、化学和磁性等特性，在工业上得到了广泛应用，但其毒性机制尚不清楚，可能引起人类神经系统疾病。在这里，我们使用雄性Wistar大鼠来研究与CoNPs和CoCl 2相关的毒性作用的差异。CoCl 2、96 nm和123 nm CoNPs处理后，CoCl 2组脑组织和血液中Co2+含量显著高于CoNPs组，而肝脏中Co2+含量显著低于CoNPs组。在海马和颞叶皮质均观察到显著的神经损伤。CoCl 2和CoNPs处理后MDA含量和Caspase 9蛋白水平均升高，与脂质过氧化和细胞凋亡有关。血红素加氧酶-1和（NF-E2）p45相关因子-2蛋白水平升高，响应于96 nm CoNP暴露。在PC 12细胞中，NRF 2下调导致细胞活力降低和凋亡率增加。总之，CoNPs和CoCl 2都会引起不良的神经效应，其中纳米颗粒显示出更大的神经毒性。此外，NRF 2通过激活下游抗氧化反应保护神经细胞免受CoCl 2和CoNPs诱导的损伤。
Cobalt nanoparticles (CoNPs) have been widely used in industry given their physical, chemical and magnetic properties; however, CoNPs may cause neurological symptoms and diseases in human, yet their mechanisms of toxicity remain unknown. Here, we used male Wistar rats to investigate differences in the toxic effects associated with CoNPs and CoCl2. Upon exposure to CoCl2, and 96 nm or 123 nm CoNPs at the same concentration, the Co2+content in CoCl2group was significantly higher than that in either the CoNPs groups in brain tissues and blood, but lower in liver. Significant neural damage was observed in both hippocampus and cortex of the temporal lobe. Increase malondialdehyde (MDA) content and CASPASE 9 protein level were associated both with CoCl2and CoNPs treatments, consistent with lipid perioxidation and apoptosis. Heme oxygenase-1 and (NF-E2) p45-related factor-2 protein levels were elevated in response to 96 nm CoNPs exposure. In PC12 cells, NRF2 downregulation led to reduced cell viability and increased apoptotic rate. In conclusion, both CoNPs and CoCl2cause adverse neural effects, with nanoparticles showing greater neurotoxic potency. In addition, NRF2 protects neural cells from damage induced by CoCl2and CoNPs by activating downstream antioxidant responses.