The study aims to investigate the effects of nano-alumina (AlNPs) on the early development and neurobehavior of zebrafish and the role of mTOR in this process. After embryos and grown-up larvae exposed to AlNPs from 0 to 200 μg/mL, we examined the development, neurobehavior, AlNPs content, and mTOR pathway genes. Moreover, embryos were randomly administered with control, negative control, mTOR knockdown, AlNPs, and mTOR knockdown + AlNPs, then examined for development, neurobehavior, oxidative stress, neurotransmitters, and development genes. As AlNPs increased, swimming speed and distance initially increased and then decreased; thigmotaxis and panic-avoidance reflex substantially decreased in the high-dose AlNPs group; aluminum and nanoparticles considerably accumulated in the 100 μg/mL AlNPs group; AlNPs at high dose decreased mTOR gene and protein levels, stimulating autophagy via increasing ULK1 and ULK2. mTOR knockdown exacerbated the harm to normal development rate, eye and body length, and neurobehavior induced by AlNPs through raising ROS, SOD, and ACH levels but decreasing AchE activity and development genes. Therefore, AlNPs suppress neurobehavior through downregulating mTOR, and mTOR knockdown further aggravates their early development and neurobehavior loss, suggesting mTOR could be a potential target for the toxicity of AlNPs.

中文翻译：

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纳米氧化铝诱导斑马鱼早期发育和神经行为毒性，与 mTOR 相关


该研究旨在探讨纳米氧化铝 （AlNPs） 对斑马鱼早期发育和神经行为的影响以及 mTOR 在此过程中的作用。胚胎和成年幼虫暴露于 0 至 200 μg/mL 的 AlNPs 后，我们检查了发育、神经行为、AlNPs 含量和 mTOR 通路基因。此外，胚胎随机施用对照、阴性对照、mTOR 敲低、AlNPs 和 mTOR 敲除 + AlNPs，然后检查发育、神经行为、氧化应激、神经递质和发育基因。随着 AlNPs 的增加，游泳速度和距离最初增加后减少;高剂量 AlNPs 组的触觉性和恐慌回避反射显着降低;铝和纳米颗粒在 100 μg/mL AlNPs 组中大量积累;高剂量的 AlNPs 降低 mTOR 基因和蛋白质水平，通过增加 ULK1 和 ULK2 刺激自噬。mTOR 敲除通过提高 ROS 、 SOD 和 ACH 水平，但降低 AchE 活性和发育基因，加剧了 AlNPs 诱导的正常发育速度、眼长和体长以及神经行为的危害。因此，AlNPs 通过下调 mTOR 来抑制神经行为，而 mTOR 敲除进一步加剧了它们的早期发育和神经行为丧失，表明 mTOR 可能是 AlNPs 毒性的潜在靶点。