Lead sulfide nanoparticles (PbS NPs) are semiconductor materials that have been widely applied to light-emitting diodes (LEDs), biological fluorescent probes, infrared detection, solar receivers, ion-selective electrodes, and ion-sensitive materials. However, the effects of PbS NPs on the central nervous system are still unclear. Thus, this study aimed to determine, using rats, the mechanism of action of PbS NPs, exposure to which results in persistent alterations in nervous system function. The results of the Morris water maze test showed that PbS NPs significantly impaired learning and memory. Compared with that in the control group, the lead content in the hippocampal tissue was significantly elevated after PbS NP exposure. Exposure to PbS NPs led to increased oxidative damage in blood and hippocampal tissues, and significantly inhibited the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) while increasing the serum malondialdehyde (MDA) content. In addition, reactive oxygen species triggered the activation of Nrf2 and the antioxidant system, including HO-1, r-GCS, and GSH-Px. Moreover, we observed significant apoptosis in the hippocampi of the rats using the TUNEL assay and transmission electron microscopy. The MOD values from the TUNEL assay of the hippocampi were all significantly higher than those of the control group, which increased as the concentration of the PbS NPs increased. There were also changes in the ultrastructure of the hippocampal neurons and synapses in the PbS-treated rats, including a shorter synaptic active zone, smaller curvature of the synaptic interface, and thicker postsynaptic density. Therefore, PbS NP exposure could lead to increased brain lead content, oxidative damage, and apoptosis.

中文翻译：

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硫化铅纳米颗粒对Nrf2的激活导致学习和记忆受损。

硫化铅纳米颗粒（PbS NPs）是已广泛应用于发光二极管（LED），生物荧光探针，红外检测，太阳能接收器，离子选择电极和离子敏感材料的半导体材料。但是，PbS NPs对中枢神经系统的影响仍不清楚。因此，本研究旨在确定大鼠使用PbS NPs的作用机理，暴露于该作用下会导致神经系统功能的持续改变。莫里斯水迷宫测试的结果表明，PbS NPs严重损害了学习和记忆能力。与对照组相比，PbS NP暴露后海马组织中的铅含量显着升高。暴露于PbS NPs会导致血液和海马组织中的氧化损伤增加，并显着抑制超氧化物歧化酶（SOD），谷胱甘肽过氧化物酶（GSH-Px）和过氧化氢酶（CAT）的活性，同时增加血清丙二醛（MDA）含量。此外，活性氧触发了Nrf2和抗氧化剂系统的活化，包括HO-1，r-GCS和GSH-Px。此外，我们使用TUNEL测定法和透射电子显微镜观察到大鼠海马中明显的细胞凋亡。海马的TUNEL法测得的MOD值均显着高于对照组，随着PbS NPs浓度的增加而增加。在PbS处理的大鼠中，海马神经元和突触的超微结构也发生了变化，包括较短的突触活动区，较小的突触界面弯曲，和较厚的突触后密度。因此，PbS NP暴露可能导致脑铅含量增加，氧化损伤和细胞凋亡。