Toxic Effects of CdTe Quantum Dots on Locomotor Behavior, Neurodevelopment, and Axon Growth in Zebrafish Larvae.

IF 2.7 4区 医学 Q3 TOXICOLOGY
Changcun Bai, Meng Tang
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Abstract

The nervous system is very sensitive to CdTe quantum dots (CdTe QDs), and an understanding of the effects of CdTe QDs on the nervous system is indispensable for their use in biomedical applications, especially in clinical medicine. This research explored the possible neurotoxic effects of CdTe QDs on the peripheral nervous system of zebrafish, including motor neuron damage, altered mobility and motor behavior of zebrafish larvae. The mechanism of peripheral neurotoxicity induced by CdTe QDs was also investigated by qRT-PCR in this study. The experimental results showed that 100 nM and above quantum dot exposure induced shortening of axon length of motor neurons and reduced the length and number of neurogenesis as well as motor nerve branching in 24-120-hpf zebrafish. The toxic effects of 100 nM and above CdTe QDs on motor neurons were further manifested as a decrease in the overall activity level of the 144-hpf zebrafish larvae including decreased locomotor velocity and shortened movement time. The average swimming velocity and total movement time of zebrafish in the 400-nM CdTe QDs-treated group were 24.7% and 17.1% of those of the control group, respectively. Molecular toxicology studies showed that genes related to neurogenesis (nrd) and axonal growth (mbp, gfap, and gap43) were significantly affected by CdTe QDs exposure. Their expressions all tended to decrease in zebrafish larvae at 72 hpf after exposure to 400-nM CdTe QDs. In conclusion, the present study demonstrates that exposure of zebrafish to CdTe QDs at early life stages leads to adverse neural outcomes through inhibition of neural development and motor neuron axon growth.

CdTe量子点对斑马鱼幼体运动行为、神经发育和轴突生长的毒性作用。
神经系统对CdTe量子点(CdTe QDs)非常敏感,了解CdTe量子点对神经系统的影响对于其在生物医学应用,特别是临床医学中的应用是必不可少的。本研究探讨了CdTe量子点对斑马鱼周围神经系统可能的神经毒性作用,包括运动神经元损伤、斑马鱼幼鱼运动能力和运动行为的改变。本研究还采用qRT-PCR方法探讨了CdTe量子点诱导周围神经毒性的机制。实验结果表明,100 nM及以上量子点暴露诱导24-120-hpf斑马鱼运动神经元轴突长度缩短,神经发生的长度和数量减少,运动神经分支减少。100 nM及以上CdTe量子点对运动神经元的毒性作用进一步表现为144-hpf斑马鱼幼鱼的整体活动水平下降,包括运动速度下降和运动时间缩短。400 nm CdTe qds处理组斑马鱼的平均游泳速度和总运动时间分别为对照组的24.7%和17.1%。分子毒理学研究表明,与神经发生(nrd)和轴突生长相关的基因(mbp、gfap和gap43)受到CdTe量子点暴露的显著影响。在暴露于400 nm CdTe量子点后,72 hpf时斑马鱼幼体中它们的表达均有降低的趋势。总之,本研究表明,斑马鱼在生命早期暴露于CdTe量子点会通过抑制神经发育和运动神经元轴突生长而导致不良的神经结局。
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来源期刊
CiteScore
7.00
自引率
6.10%
发文量
145
审稿时长
1 months
期刊介绍: Journal of Applied Toxicology publishes peer-reviewed original reviews and hypothesis-driven research articles on mechanistic, fundamental and applied research relating to the toxicity of drugs and chemicals at the molecular, cellular, tissue, target organ and whole body level in vivo (by all relevant routes of exposure) and in vitro / ex vivo. All aspects of toxicology are covered (including but not limited to nanotoxicology, genomics and proteomics, teratogenesis, carcinogenesis, mutagenesis, reproductive and endocrine toxicology, toxicopathology, target organ toxicity, systems toxicity (eg immunotoxicity), neurobehavioral toxicology, mechanistic studies, biochemical and molecular toxicology, novel biomarkers, pharmacokinetics/PBPK, risk assessment and environmental health studies) and emphasis is given to papers of clear application to human health, and/or advance mechanistic understanding and/or provide significant contributions and impact to their field.
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