CdTe quantum dots induce apoptosis in RSC96 cells by disrupting calcium homeostasis and triggering subcellular structural dysfunction

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 CA²⁺ 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 CA²⁺ 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 CA²⁺ chelator BAPTA-AM partially restored the cellular mitochondrial membrane potential, while decreasing the Apoptosis rate of RSC96 cells.

Calcium homeostasis; CdTe quantum dots; Cell apoptosis; Mitochondrial dysfunction; Oxidative stress; RSC96 cells.