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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 |
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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 |
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author | Ahamed, Maqusood Khan, M. A. Majeed Akhtar, Mohd Javed Alhadlaq, Hisham A. Alshamsan, Aws |
author_facet | Ahamed, Maqusood Khan, M. A. Majeed Akhtar, Mohd Javed Alhadlaq, Hisham A. Alshamsan, Aws |
author_sort | Ahamed, Maqusood |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-5732217 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-57322172017-12-21 Ag-doping regulates the cytotoxicity of TiO(2) nanoparticles via oxidative stress in human cancer cells Ahamed, Maqusood Khan, M. A. Majeed Akhtar, Mohd Javed Alhadlaq, Hisham A. Alshamsan, Aws Sci Rep Article 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. Nature Publishing Group UK 2017-12-15 /pmc/articles/PMC5732217/ /pubmed/29247182 http://dx.doi.org/10.1038/s41598-017-17559-9 Text en © The Author(s) 2017 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Ahamed, Maqusood Khan, M. A. Majeed Akhtar, Mohd Javed Alhadlaq, Hisham A. Alshamsan, Aws Ag-doping regulates the cytotoxicity of TiO(2) nanoparticles via oxidative stress in human cancer cells |
title | Ag-doping regulates the cytotoxicity of TiO(2) nanoparticles via oxidative stress in human cancer cells |
title_full | Ag-doping regulates the cytotoxicity of TiO(2) nanoparticles via oxidative stress in human cancer cells |
title_fullStr | Ag-doping regulates the cytotoxicity of TiO(2) nanoparticles via oxidative stress in human cancer cells |
title_full_unstemmed | Ag-doping regulates the cytotoxicity of TiO(2) nanoparticles via oxidative stress in human cancer cells |
title_short | Ag-doping regulates the cytotoxicity of TiO(2) nanoparticles via oxidative stress in human cancer cells |
title_sort | ag-doping regulates the cytotoxicity of tio(2) nanoparticles via oxidative stress in human cancer cells |
topic | Article |
url | 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 |
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