Translocation and neurotoxicity of CdTe quantum dots in RMEs motor neurons in nematode Caenorhabditis elegans
Translocation and neurotoxicity of CdTe quantum dots in RMEs motor neurons in nematode Caenorhabditis elegans
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线虫 RME 运动神经元中 CdTe 量子点的易位和神经毒性
DOI：
10.1016/j.jhazmat.2014.09.063
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发表时间：
2015-02-11
影响因子：
13.6
通讯作者：
Wang, Dayong
中科院分区：
文献类型：
--
作者：
Zhao, Yunli;Wang, Xiong;Wang, Dayong
我们采用秀丽隐杆线虫（Caelophabditis elegans）实验系统研究了CdTe量子点（QDs）对RMEs运动神经元的神经毒性作用及其机制。在长时间暴露于0.1-1 μ g/L的CdTe量子点后，观察到异常的觅食行为和RME运动神经元发育的缺陷。观察到的神经毒性从碲化镉量子点对RMEs运动神经元可能不是由于释放镉2+。Mn-SOD编码基因或unc-30基因控制RMEs神经元的细胞特性的过表达阻止了CdTe QDs对RMEs运动神经元的神经毒性作用，表明氧化应激和细胞特性在调节CdTe QDs神经毒性中的关键作用。在线虫体内，CdTe量子点可通过肠屏障转运到RME运动神经元。与此相反，CdTe@ZnS量子点不能转位到RMEs运动神经元，因此，只能适度积累在肠细胞，表明ZnS涂层可能会减少CdTe量子点对RMEs运动神经元的神经毒性。因此，氧化应激，细胞的身份，和生物利用度的组合效应可能会大大有助于对RMEs运动神经元的CdTe量子点的神经毒性的机制。我们的研究结果为了解CdTe量子点对动物神经系统发育和功能的潜在风险提供了见解。2014爱思唯尔有限公司版权所有。
We employed Caenorhabditis elegans assay system to investigate in vivo neurotoxicity of CdTe quantum dots (QDs) on RMEs motor neurons, which are involved in controlling foraging behavior, and the underlying mechanism of such neurotoxicity. After prolonged exposure to 0.1-1 mu g/L of CdTe QDs, abnormal foraging behavior and deficits in development of RMEs motor neurons were observed. The observed neurotoxicity from CdTe QDs on RMEs motor neurons might be not due to released Cd2+. Overexpression of genes encoding Mn-SODs or unc-30 gene controlling cell identity of RMEs neurons prevented neurotoxic effects of CdTe QDs on RMEs motor neurons, suggesting the crucial roles of oxidative stress and cell identity in regulating CdTe QDs neurotoxicity. In nematodes, CdTe QDs could be translocated through intestinal barrier and be deposited in RMEs motor neurons. In contrast, CdTe@ZnS QDs could not be translocated into RMEs motor neurons and therefore, could only moderately accumulated in intestinal cells, suggesting that ZnS coating might reduce neurotoxicity of CdTe QDs on RMEs motor neurons. Therefore, the combinational effects of oxidative stress, cell identity, and bioavailability may contribute greatly to the mechanism of CdTe QDs neurotoxicity on RMEs motor neurons. Our results provide insights into understanding the potential risks of CdTe QDs on the development and function of nervous systems in animals. 2014 Elsevier B.V. All rights reserved.