AI Article Synopsis
- The study evaluated the nephrotoxic effects of CdSe/ZnS quantum dots (QDs) and explored the mechanisms of toxicity involved.
- The results indicated that CdSe/ZnS QDs reduced cell viability and increased apoptosis in kidney cells, while also elevating oxidative stress markers like MDA and ROS.
- Co-treatment with the antioxidant N-acetylcysteine alleviated some of the oxidative damage, and overall findings linked the nephrotoxicity of QDs to oxidative stress and inflammatory responses mediated by the NRF2/Keap1 pathway.
Article Abstract
Objective: This study aimed to the evaluate the nephrotoxicity of CdSe/ZnS QDs and , as well as investigate the underlying toxicity mechanisms.
Results: experiments showed that compared with control cells, CdSe/ZnS QDs treatment significantly inhibited cell viability and promoted cell apoptosis in dose-dependent manner in NRK cells. Notably, CdSe/ZnS QDs treatment increased the contents of MDA and ROS, and decreased the activities of SOD, CAT and GSH-Px; however, the co-treatment of NAC and QDs relieved the oxidative damage of NRK cells. Moreover, experiments also revealed that CdSe/ZnS QDs treatment obviously increased kidney weight coefficient, damaged the kidney function, as well as induced inflammatory response and inhibited the activation of NRF2/Keap1 pathway in kidney tissues of mice.
Conclusions: CdSe/ZnS QDs exhibited obvious nephrotoxicity by mediating oxidative damage and inflammatory response and via NRF2/Keap1 pathway.
Methods: The characterization of CdSe/ZnS QDs was analyzed by transmission electron microscope, emission spectrum scanning, and dynamic light scattering. Rat kidney cells (NRK) were exposed to different doses of CdSe/ZnS QDs with or without N-acetylcysteine (NAC, antioxidant). Then, cellular uptake of CdSe/ZnS QDs was detected, and cytotoxicity was evaluated by MTT assay and TUNEL assay.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8109115 | PMC |
| http://dx.doi.org/10.18632/aging.103774 | DOI Listing |
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