Toxicology in vitro : an international journal published in association with BIBRA · 2009
Intracellular oxidative stress and cadmium ions release induce cytotoxicity of unmodified cadmium sulfide quantum dots.
Сравнительное исследованиеСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Li K G, Chen J T, Bai S S, Wen X, Song S Y, Yu Q, Li J, Wang Y Q
Аннотация
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 microg/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 microg/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 24h, 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.
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 microg/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 microg/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 24h, 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.