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

Area of Science:

• Cell Biology
• Toxicology
• Nanotechnology

Background:

• The subcellular toxic effects of Cadmium Telluride Quantum Dots (CdTe QDs) on RSC96 cells remain largely unknown.
• The involvement of oxidative stress and calcium ion overload in CdTe QDs-induced cellular dysfunction and death requires verification.

Purpose of the Study:

• To investigate CdTe QDs-induced oxidative stress and changes in intracellular and mitochondrial calcium levels in RSC96 cells.
• To explore the correlation between subcellular structural and functional impairments and cell death.
• To assess the protective roles of antioxidants and calcium chelators against CdTe QDs toxicity.

Main Methods:

• Exposure of RSC96 cells to varying concentrations of CdTe QDs (0-80 μM) for 24 hours.
• Measurement of intracellular and mitochondrial calcium ion levels.
• Assessment of oxidative stress markers, including mitochondrial reactive oxygen species (mtROS).
• Evaluation of endoplasmic reticulum and mitochondrial structural integrity.
• Analysis of cell apoptosis rates and cellular ATP synthesis capacity.
• Treatment with antioxidants (Mito-TEMPO) and calcium chelators (BAPTA-AM).

Main Results:

• CdTe QDs exposure led to oxidative stress, elevated intracellular Ca2+ concentration, endoplasmic reticulum expansion, and mitochondrial damage (cristae rupture/disappearance).
• CdTe QDs induced endoplasmic reticulum stress, mitochondrial impairment (increased mtROS, reduced mitochondrial membrane potential), and cell death.
• Intracellular Ca2+ overload and elevated mtROS were closely linked to mitochondrial dysfunction and cell death.
• Mito-TEMPO mitigated apoptosis and enhanced ATP synthesis, while BAPTA-AM partially restored mitochondrial membrane potential and reduced apoptosis.

Conclusions:

• CdTe QDs induce RSC96 cell death through oxidative stress and calcium overload, leading to endoplasmic reticulum and mitochondrial dysfunction.
• Antioxidants and calcium chelators demonstrate protective effects against CdTe QDs-induced cellular damage, highlighting potential therapeutic strategies.