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Ag-doping regulates the cytotoxicity of TiO(2) nanoparticles via oxidative stress in human cancer cells
We investigated the anticancer potential of Ag-doped (0.5–5%) anatase TiO(2) NPs. Characterization study showed that dopant Ag was well-distributed on the surface of host TiO(2) NPs. Size (15 nm to 9 nm) and band gap energy (3.32 eV to 3.15 eV) of TiO(2) NPs were decreases with increasing the concen...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5732217/ https://www.ncbi.nlm.nih.gov/pubmed/29247182 http://dx.doi.org/10.1038/s41598-017-17559-9 |
Sumario: | We investigated the anticancer potential of Ag-doped (0.5–5%) anatase TiO(2) NPs. Characterization study showed that dopant Ag was well-distributed on the surface of host TiO(2) NPs. Size (15 nm to 9 nm) and band gap energy (3.32 eV to 3.15 eV) of TiO(2) NPs were decreases with increasing the concentration of Ag dopant. Biological studies demonstrated that Ag-doped TiO(2) NP-induced cytotoxicity and apoptosis in human liver cancer (HepG2) cells. The toxic intensity of TiO(2) NPs was increases with increasing the amount of Ag-doping. The Ag-doped TiO(2) NPs further found to provoke reactive oxygen species (ROS) generation and antioxidants depletion. Toxicity induced by Ag-doped TiO(2) NPs in HepG2 cells was efficiently abrogated by antioxidant N-acetyl-cysteine (ROS scavenger). We also found that Ag-doped TiO(2) NPs induced cytotoxicity and oxidative stress in human lung (A549) and breast (MCF-7) cancer cells. Interestingly, Ag-doped TiO(2) NPs did not cause much toxicity to normal cells such as primary rat hepatocytes and human lung fibroblasts. Overall, we found that Ag-doped TiO(2) NPs have potential to selectively kill cancer cells while sparing normal cells. This study warranted further research on anticancer potential of Ag-doped TiO(2) NPs in various types of cancer cells and in vivo models. |
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