MPA-capped CdTe quantum dots exposure causes neurotoxic effects in nematode Caenorhabditis elegans by affecting the transporters and receptors of glutamate, serotonin and dopamine at the genetic level, or by increasing ROS, or both
MPA-capped CdTe quantum dots exposure causes neurotoxic effects in nematode Caenorhabditis elegans by affecting the transporters and receptors of glutamate, serotonin and dopamine at the genetic level, or by increasing ROS, or both
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MPA 封端的 CdTe 量子点暴露通过在基因水平影响谷氨酸、血清素和多巴胺的转运蛋白和受体，或通过增加 ROS，或两者兼而有之，对线虫秀丽隐杆线虫产生神经毒性作用
DOI：
10.1039/c5nr05914c
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发表时间：
2015
期刊：
影响因子：
6.7
通讯作者：
Tang Meng
中科院分区：
文献类型：
--
作者：
Wu Tianshu;He Keyu;Zhan Qinglin;Ang Shengjun;Ying Jiali;Zhang Shihan;Zhang Ting;Xue Yuying;Tang Meng
随着量子点在生物医学领域的广泛应用，对其生物学特性的研究也越来越多。虽然有几项研究试图评估量子点对神经细胞的毒性，但对神经系统的体内毒性作用及其分子机制尚不清楚。本研究的目的是探讨水溶性碲化镉（CdTe）量子点的3-巯基丙酸（MPA）封端对秀丽隐杆线虫（Caelophabditis elegans，C. elegans）。我们的研究结果表明，暴露于MPA帽的CdTe量子点诱导的行为缺陷，包括改变身体弯曲，头部颠簸，咽泵和排便间隔，以及受损的学习和记忆行为的可塑性，基于趋化性或趋热性，在剂量，时间和大小依赖性的方式。进一步的研究表明，MPA-capped CdTe量子点暴露于C. elegans在24 h内在遗传水平上的表达量明显高于elegans，而在72 h后则相反。此外，在CdTe QD处理的蠕虫中观察到过量的活性氧（ROS）产生，这证实了氧化应激损伤的常见纳米毒性机制，并且可能克服C. elegans诱导的长期QD暴露，导致更严重的行为障碍。
As quantum dots (QDs) are widely used in biomedical applications, the number of studies focusing on their biological properties is increasing. While several studies have attempted to evaluate the toxicity of QDs towards neural cells, the in vivo toxic effects on the nervous system and the molecular mechanisms are unclear. The aim of the present study was to investigate the neurotoxic effects and the underlying mechanisms of water-soluble cadmium telluride (CdTe) QDs capped with 3-mercaptopropionic acid (MPA) in Caenorhabditis elegans (C. elegans). Our results showed that exposure to MPA-capped CdTe QDs induced behavioral defects, including alterations to body bending, head thrashing, pharyngeal pumping and defecation intervals, as well as impaired learning and memory behavior plasticity, based on chemotaxis or thermotaxis, in a dose-, time- and size-dependent manner. Further investigations suggested that MPA-capped CdTe QDs exposure inhibited the transporters and receptors of glutamate, serotonin and dopamine in C. elegans at the genetic level within 24 h, while opposite results were observed after 72 h. Additionally, excessive reactive oxygen species (ROS) generation was observed in the CdTe QD-treated worms, which confirmed the common nanotoxicity mechanism of oxidative stress damage, and might overcome the increased gene expression of neurotransmitter transporters and receptors in C. elegans induced by long-term QD exposure, resulting in more severe behavioral impairments.