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首页> 外文期刊>Journal of applied toxicology >Transcriptome analysis of different sizes of 3-mercaptopropionic acid-modified cadmium telluride quantum dot-induced toxic effects reveals immune response in rat hippocampus
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Transcriptome analysis of different sizes of 3-mercaptopropionic acid-modified cadmium telluride quantum dot-induced toxic effects reveals immune response in rat hippocampus

机译:三维巯基酸改性碲化镉量子点诱导的毒性作用的不同尺寸的转录组分析显示大鼠海马的免疫应答

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摘要

Recently, the increasing number of bio-safety assessments on cadmium-containing quantum dots (QDs) suggested that they could lead to detrimental effects on the central nervous system (CNS) of living organisms, but the underlying action mechanisms are still rarely reported. In this study, whole-transcriptome sequencing was performed to analyze the changes in genome-wide gene expression pattern of rat hippocampus after treatments of cadmium telluride (CdTe) QDs with two sizes to understand better the mechanisms of CdTe QDs causing toxic effects in the CNS. We identified 2095 differentially expressed genes (DEGs). Fifty-five DEGs were between the control and 2.2 nm CdTe QDs, 1180 were between the control and 3.5 nm CdTe QDs and 860 were between the two kinds of CdTe QDs. It seemed that the 3.5 nm CdTe QD exposure might elicit severe effects in the rat hippocampus than 2.2 nm CdTe QDs at the transcriptome level. After bioinformatics analysis, we found that most DEG-enriched Gene Ontology subcategories and Kyoto Encyclopedia of Genes and Genomes pathways were related with the immune system process. For example, the Gene Ontology subcategories included immune response, inflammatory response and T-cell proliferation; Kyoto Encyclopedia of Genes and Genomes pathways included NOD/Toll-like receptor signaling pathway, nuclear factor-κB signaling pathway, tumor necrosis factor signaling pathway, natural killer cell-mediated cytotoxicity and T/B-cell receptor signaling pathway. The traditional toxicological examinations confirmed the systemic immune response and CNS inflammation in rats exposed to CdTe QDs. This transcriptome analysis not only revealed the probably molecular mechanisms of CdTe QDs causing neurotoxicity, but also provided references for the further related studies. Copyright ? 2018 John Wiley & Sons, Ltd.
机译:最近,越来越多的含镉的量子点(QDS)的生物安全评估表明它们可能导致对生物体的中枢神经系统(CNS)的有害影响,但仍然很少报告潜在的行动机制。在该研究中,进行全转录组测序,以分析大鼠海马在治疗碲化镉(CdTe)QDs的大鼠海马的基因组基因表达模式的变化,以了解更好的CdTe QD机制导致CNS中的毒性效应。我们鉴定了2095个差异表达基因(DEGS)。在对照和2.2nm Cdte QDS之间,在对照和2.2nm cdte qds之间,在控制和3.5nm cdte qd和860之间,在两种CdTe Qds之间进行了380。似乎3.5nm cdte qd暴露可能在转录组水平下在大鼠海马中引起大鼠海马的严重影响。在生物信息学分析后,我们发现最富集的基因本体论亚类别和基因和基因组途径的京都百科全书与免疫系统过程有关。例如,基因本体亚类别包括免疫应答,炎症反应和T细胞增殖;基因和基因组的京都百科全书包括点/收费的受体信号通路,核因子-κB信号通路,肿瘤坏死因子信号通路,天然杀伤细胞介导的细胞毒性和T / B细胞受体信号传导途径。传统的毒理学检查证实了暴露于CdTe QDS的大鼠的全身免疫应答和CNS炎症。该转录组分析不仅揭示了CDTE QD的可能性,导致神经毒性,而且还提供了对进一步相关研究的参考。版权? 2018 John Wiley&Sons,Ltd。

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