Abstract：
Ionizing radiation (IR) poses a significant threat to both the natural environment and biological health. Exposure to specific doses of ionizing radiation early in an organism\'s development can lead to developmental toxicity, particularly neurotoxicity. Through experimentation with Xenopus laevis (X. laevis), we examined the effects of radiation on early developmental stage. Our findings revealed that radiation led to developmental abnormalities and mortality in X. laevis embryos in a dose-dependent manner, disrupting redox homeostasis and inducing cell apoptosis. Additionally, radiation caused neurotoxic effects, resulting in abnormal behavior and neuron damage in the embryos. Further investigation into the underlying mechanisms of radiation-induced neurotoxicity indicated the potential involvement of the neuroactive ligand-receptor interaction pathway, which was supported by RNA-Seq analysis. Validation of gene expression associated with this pathway and analysis of neurotransmitter levels confirmed our hypothesis. In addition, we further validated the important role of this signaling pathway in radiation-induced neurotoxicity through edaravone rescue experiments. This research establishes a valuable model for radiation damage studying and provides some insight into radiation-induced neurotoxicity mechanisms.
摘要：
电离辐射（IR）对自然环境和生物健康都构成重大威胁。在生物体发育早期暴露于特定剂量的电离辐射会导致发育毒性，特别是神经毒性。通过对非洲爪狼的实验(X.laevis),我们研究了辐射对早期发育阶段的影响。我们的发现表明，辐射以剂量依赖的方式导致X.laevis胚胎的发育异常和死亡，破坏氧化还原稳态并诱导细胞凋亡。此外,辐射引起神经毒性作用，导致胚胎中的异常行为和神经元损伤。对辐射诱导的神经毒性的潜在机制的进一步研究表明神经活性配体-受体相互作用途径的潜在参与，这得到了RNA-Seq分析的支持。与该途径相关的基因表达的验证和神经递质水平的分析证实了我们的假设。此外,我们通过依达拉奉抢救实验进一步验证了该信号通路在辐射诱导的神经毒性中的重要作用.本研究为辐射损伤研究建立了一个有价值的模型，并为辐射诱导的神经毒性机制提供了一些见解。
