Quantum dots (QDs) have been proposed as novel luminescent markers for research applications, but a recent study showed that oxidation of CdSe-core QDs could release cadmium ions and trigger cell death. Here, we sought to elucidate the precise apoptotic mechanisms governing this effect. Our results revealed that CdSe-core QDs induced apoptotic biochemical changes, including activation of c-Jun N-terminal kinase (JNK), caspase-3 and p21-activated protein kinase 2 (PAK2), in a human osteoblast cell line. Treatment of osteoblasts with a JNK-specific inhibitor (SP600125) reduced CdSe-core QD-induced activation of both JNK and caspase-3, indicating that JNK activity is required for CdSe-core QD-induced caspase activation. Experiments using caspase-3 inhibitors and antisense oligonucleotides against PAK2 showed that caspase-3 activation is required for PAK2 activation, and both of these activations are required for CdSe QD-induced apoptosis in osteoblasts. Interestingly, ZnS surface-modified CdSe QDs were not cytotoxic to osteoblasts at any tested concentration. These findings provide important new insights into the apoptotic mechanisms triggered by CdSe QDs in a human osteoblast cell line, and suggest that surface modification might be a useful strategy for minimizing the cytotoxicity of CdSe QDs for research applications.
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