Effects of CdTe quantum dot exposure on the calcium signaling pathway in rat dorsal root ganglion cells ND7/23

Previous study has shown that CdTe QDs exposure reduced ND7/23 cells activity and induced cell Apoptosis in a time-dependent manner. The mitochondrial pathway was involved in CdTe QDs-induced ND7/23 cell Apoptosis. The toxic effects at the subcellular level of ND7/23 cells after CdTe QDs exposure was still unclear. Whether the two classical mechanisms, endoplasmic reticulum stress and calcium ion imbalance, were involved in the subcellular structural and functional dysfunction of ND7/23 cells induced by CdTe QDs, and whether the CA²⁺-calpain2 pathway played a significant role in the CdTe QDs-induced ND7/23 cell Apoptosis remained to be validated. Therefore, this research focused on the study of CdTe QDs exposure-induced endoplasmic reticulum stress, organelle damage, and calcium homeostasis imbalance in ND7/23 cells. The Apoptosis signaling pathway mediated by calpain2 and endoplasmic reticulum stress were also investigated. The results showed that exposure to 10μM CdTe QDs for 0-24h resulted in an increase in intracellular and mitochondrial CA²⁺ concentration, accompanied by swelling of the endoplasmic reticulum and mitochondria and loss of mitochondrial cristae. CdTe QDs exposure also led to an increase in the expression of endoplasmic reticulum stress-related Bip protein. CdTe QDs exposure also initiated the up-regulation of calpain2 and cleaved-caspase7 protein expression, as well as cleavage of caspase12 and PARP proteins in ND7/23 cells. Addition of the calcium chelator BAPTA-AM and the calpeptin 2 inhibitor calpeptin significantly inhibited CdTe QDs-induced Apoptosis and reversed the expression of these proteins. This study confirmed that exposure to CdTe QDs triggered endoplasmic reticulum stress in ND7/23 cells, along with the activation of the calpain2-caspase12 signaling pathway, resulting in mitochondria-independent Apoptosis.

Ca(2+) signaling; CdTe QDs; Endoplasmic reticulum stress; ND7/23 cell; Neurotoxicity; mitochondria-independent apoptosis.