Intracellular oxidative stress and cadmium ions release induce cytotoxicity of unmodified cadmium sulfide quantum dots

摘要

Objective: To fully understand the cytotoxicity of after-degradation QDs, we synthesized CdS QDs and investigated its toxicity mechanism. Methods: Biomimetic method was proposed to synthesize cadmium sulfide (CdS) QDs. Thereafter MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide) assay was conducted to evaluate their cytotoxicity. To investigate the toxicity mechanism, we subsequently conducted intracellular reactive oxygen species (ROS) measurement with DCFH-DA, glutathione (GSH) measurement with DTNB, and cellular cadmium assay using atomic absorption spectrometer. Microsized CdS were simultaneously tested as a comparison. Results: MTT assay results indicated that CdS QDs are more toxic than microsized CdS especially at concentrations below 40 mu g/ml. While microsized CdS did not trigger ROS elevation, CdS QDs increase ROS by 20-30% over control levels. However, they both deplete cellular GSH significantly at the medium concentration of 20 mu g/ml. In the presence of NAC, cells are partially protected from CdS QDs, but not from microsized particles. Additionally, nearly 20% of cadmium was released from CdS nanoparticles within 24 h, which also accounts for QDs' toxicity. Conclusion: Intracellular ROS production, GSH depletion. and cadmium ions (Cd(2+)) release are possible mechanisms for CdS QDs' cytotoxicity. We also suggested that with QD concentration increasing, the principal toxicity mechanism changes from intracellular oxidative stress to Cd(2+) release. Crown Copyright (C) 2009 Published by Elsevier Ltd. All rights reserved.