Department of Nephrology, Cangzhou Central Hospital, Cangzhou, Hebei Province, China.
Pediatrics Department, Cangzhou Central Hospital, Cangzhou, Hebei Province, China.
Aging (Albany NY). 2020 Nov 16;13(8):12194-12206. doi: 10.18632/aging.103774.
This study aimed to the evaluate the nephrotoxicity of CdSe/ZnS QDs and , as well as investigate the underlying toxicity mechanisms.
experiments showed that compared with control cells, CdSe/ZnS QDs treatment significantly inhibited cell viability and promoted cell apoptosis in dose-dependent manner in NRK cells. Notably, CdSe/ZnS QDs treatment increased the contents of MDA and ROS, and decreased the activities of SOD, CAT and GSH-Px; however, the co-treatment of NAC and QDs relieved the oxidative damage of NRK cells. Moreover, experiments also revealed that CdSe/ZnS QDs treatment obviously increased kidney weight coefficient, damaged the kidney function, as well as induced inflammatory response and inhibited the activation of NRF2/Keap1 pathway in kidney tissues of mice.
CdSe/ZnS QDs exhibited obvious nephrotoxicity by mediating oxidative damage and inflammatory response and via NRF2/Keap1 pathway.
The characterization of CdSe/ZnS QDs was analyzed by transmission electron microscope, emission spectrum scanning, and dynamic light scattering. Rat kidney cells (NRK) were exposed to different doses of CdSe/ZnS QDs with or without N-acetylcysteine (NAC, antioxidant). Then, cellular uptake of CdSe/ZnS QDs was detected, and cytotoxicity was evaluated by MTT assay and TUNEL assay.
本研究旨在评估 CdSe/ZnS QDs 的肾毒性，并探讨其潜在的毒性机制。
实验表明，与对照组细胞相比，CdSe/ZnS QDs 处理以剂量依赖的方式显著抑制 NRK 细胞活力并促进细胞凋亡。值得注意的是，CdSe/ZnS QDs 处理增加了 MDA 和 ROS 的含量，降低了 SOD、CAT 和 GSH-Px 的活性；然而，NAC 和 QDs 的共同处理缓解了 NRK 细胞的氧化损伤。此外，实验还表明，CdSe/ZnS QDs 处理明显增加了肾脏重量系数，损害了肾功能，并在小鼠肾脏组织中诱导了炎症反应和抑制了 NRF2/Keap1 通路的激活。
CdSe/ZnS QDs 通过介导氧化损伤和炎症反应以及通过 NRF2/Keap1 通路表现出明显的肾毒性。
通过透射电子显微镜、发射光谱扫描和动态光散射分析了 CdSe/ZnS QDs 的特性。用不同剂量的 CdSe/ZnS QDs 处理大鼠肾细胞 (NRK)，并加入或不加入 N-乙酰半胱氨酸 (NAC，抗氧化剂)。然后，通过 MTT 测定法和 TUNEL 测定法检测 CdSe/ZnS QDs 的细胞摄取，并评估细胞毒性。
