Bai Changcun, Tang Meng
School of Public Health, Bengbu Medical University, Bengbu 233000, PR China.
Key Laboratory of Environmental Medicine and Engineering, Ministry of Education, School of Public Health, Southeast University, Nanjing 210009, PR China.
NanoImpact. 2025 Jun 15;39:100572. doi: 10.1016/j.impact.2025.100572.
The toxic effects at the subcellular level of RSC96 cells after CdTe QDs exposure was still unclear. Meanwhile, whether the two classical mechanisms, oxidative stress and calcium ion overload, were involved in CdTe QDs-induced subcellular structural and functional dysfunction of RSC96 cells, which ultimately triggered cell death, remained to be verified. This research focused on the study of CdTe QDs exposure-induced oxidative stress in RSC96 cells, as well as the changes in intracellular calcium ion levels and intra-mitochondrial calcium ion levels. The subcellular structural and functional impairments of RSC96 cells induced by CdTe QDs exposure and the correlation of these impairments were further explored. In addition, the role of antioxidants and calcium chelators in maintaining RSC96 cell homeostasis under CdTe QDs exposure was also investigated. The results showed that 0-80 μM CdTe QDs exposure for 24 h induced oxidative stress and elevated Ca concentration in RSC96 cells, which further caused endoplasmic reticulum expansion and mitochondria structural damage such as rupture of mitochondrial cristae and disappearance of cristae. Exposure to CdTe QDs in RSC96 cells induced endoplasmic reticulum stress and mitochondrial impairment, characterized by enhanced production of mtROS and a notable reduction in mitochondrial membrane potential. Intracellular Ca overload and elevated mtROS concentration in mitochondria were closely associated with mitochondrial dysfunction and cell death triggered by exposure to CdTe QDs. Preincorporation of Mito-TEMPO mitigated the apoptosis rate of RSC96 cells and up-regulated the cellular ATP synthesizing capacity. Preincorporation of the Ca chelator BAPTA-AM partially restored the cellular mitochondrial membrane potential, while decreasing the apoptosis rate of RSC96 cells.
碲化镉量子点（CdTe QDs）暴露后对RSC96细胞亚细胞水平的毒性作用仍不清楚。同时，氧化应激和钙离子超载这两种经典机制是否参与了CdTe QDs诱导的RSC96细胞亚细胞结构和功能障碍（最终引发细胞死亡）仍有待验证。本研究聚焦于CdTe QDs暴露诱导RSC96细胞氧化应激的研究，以及细胞内钙离子水平和线粒体内钙离子水平的变化。进一步探讨了CdTe QDs暴露诱导的RSC96细胞亚细胞结构和功能损伤以及这些损伤之间的相关性。此外，还研究了抗氧化剂和钙螯合剂在CdTe QDs暴露下维持RSC96细胞稳态中的作用。结果表明，0 - 80 μM CdTe QDs暴露24小时可诱导RSC96细胞氧化应激并升高钙离子浓度，进而导致内质网扩张和线粒体结构损伤，如线粒体嵴破裂和嵴消失。RSC96细胞暴露于CdTe QDs会诱导内质网应激和线粒体损伤，其特征是线粒体活性氧（mtROS）生成增加以及线粒体膜电位显著降低。细胞内钙离子超载和线粒体内mtROS浓度升高与CdTe QDs暴露引发的线粒体功能障碍和细胞死亡密切相关。预先加入Mito-TEMPO可降低RSC96细胞的凋亡率并上调细胞ATP合成能力。预先加入钙螯合剂BAPTA-AM可部分恢复细胞线粒体膜电位，同时降低RSC96细胞的凋亡率。
