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首页> 外文期刊>Toxicology Research >Partial protection of N-acetylcysteine against MPA-capped CdTe quantum dot-induced neurotoxicity in rat primary cultured hippocampal neurons
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Partial protection of N-acetylcysteine against MPA-capped CdTe quantum dot-induced neurotoxicity in rat primary cultured hippocampal neurons

机译:N-乙酰半胱氨酸对MPA封端的CdTe量子点诱导的大鼠原代培养海马神经元神经毒性的部分保护

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摘要

As one of the most frequently used quantum dots (QDs), the toxicity of cadmium telluride (CdTe) QDs related to several body systems has been investigated, but the studies on the nervous system are rather limited. It is extremely important to assess QDs' cytotoxicity to neurons by a thorough systematic and quantitative analysis before they are applied in scientific or clinical settings. This study observed that CdTe QDs caused cell death and apoptosis in rat primary cultured hippocampal neurons in a dose-, time-and size-dependent manner. QD-exposed neurons showed an increase in reactive oxygen species (ROS) and intracellular calcium levels that leads to neuron apoptosis and even death, which may be completely or partially protected by a common antioxidant N-acetylcysteine (NAC), respectively. For future research, it is necessary to study the underlying mechanisms by investigating the extrinsic and intrinsic pathways by which CdTe QDs induce neurotoxic effects.
机译:作为最常用的量子点(QD)之一,已经研究了碲化镉(CdTe)量子点与几种人体系统相关的毒性,但对神经系统的研究却十分有限。在将QD用于科学或临床环境之前,通过彻底的系统和定量分析评估QD对神经元的细胞毒性极为重要。这项研究观察到CdTe量子点以剂量,时间和大小依赖的方式引起大鼠原代培养海马神经元的细胞死亡和凋亡。暴露于QD的神经元显示活性氧(ROS)和细胞内钙水平升高,导致神经元凋亡甚至死亡,这可能分别由普通的抗氧化剂N-乙酰半胱氨酸(NAC)完全或部分保护。对于将来的研究,有必要通过研究CdTe QD诱导神经毒性作用的外在和内在途径来研究其潜在机制。

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