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Synthesis of Cd-free InP/ZnS Quantum Dots Suitable for Biomedical Applications
Published on: February 6, 2016
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CdSe/ZnS quantum dots exhibited nephrotoxicity through mediating oxidative damage and inflammatory response
Xiuli Li1, Huiwu Zhang2, Fuyun Sun1
1Department of Nephrology, Cangzhou Central Hospital, Cangzhou, Hebei Province, China.
Aging
|November 17, 2020
Summary
Cadmium selenide/zinc sulfide quantum dots (CdSe/ZnS QDs) cause kidney damage through oxidative stress and inflammation. Antioxidant treatment with N-acetylcysteine (NAC) mitigated these toxic effects in rat kidney cells.
Area of Science:
- Nanotechnology
- Toxicology
- Biomedical Engineering
Background:
- Quantum dots (QDs) offer unique optical and electronic properties for various applications.
- Understanding the potential toxicity of nanomaterials like CdSe/ZnS QDs is crucial for safe implementation.
- Nephrotoxicity of QDs requires thorough investigation to establish safety profiles.
Purpose of the Study:
- To evaluate the nephrotoxicity of Cadmium Selenide/Zinc Sulfide Quantum Dots (CdSe/ZnS QDs) both in vitro and in vivo.
- To elucidate the underlying mechanisms of CdSe/ZnS QDs-induced kidney toxicity.
- To assess the protective effects of antioxidants against QD-induced renal damage.
Main Methods:
- Characterization of CdSe/ZnS QDs using electron microscopy, spectroscopy, and dynamic light scattering.
- In vitro cytotoxicity assays (MTT, TUNEL) on rat kidney (NRK) cells exposed to QDs with/without N-acetylcysteine (NAC).
- In vivo assessment of kidney function, weight, and NRF2/Keap1 pathway activation in mice exposed to QDs.
Main Results:
- CdSe/ZnS QDs significantly reduced NRK cell viability and induced apoptosis in a dose-dependent manner.
- QD exposure increased oxidative stress markers (MDA, ROS) and decreased antioxidant enzyme activities (SOD, CAT, GSH-Px).
- In vivo studies showed increased kidney weight, impaired kidney function, inflammation, and NRF2/Keap1 pathway inhibition in mice treated with QDs.
Conclusions:
- CdSe/ZnS QDs demonstrate significant nephrotoxicity through oxidative damage and inflammatory responses.
- The NRF2/Keap1 pathway is implicated in the toxicity mechanisms of CdSe/ZnS QDs.
- Co-administration with NAC effectively ameliorated QD-induced oxidative stress and cytotoxicity in vitro.

