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Investigation of Cytotoxicity, Apoptosis, and Oxidative Stress Response of Fe(3)O(4)-RGO Nanocomposites in Human Liver HepG2 cells
Iron oxide–reduced graphene oxide (Fe(3)O(4)-RGO) nanocomposites have attracted enormous interest in the biomedical field. However, studies on biological response of Fe(3)O(4)-RGO nanocomposites at the cellular and molecular level are scarce. This study was designed to synthesize, characterize, and...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7040707/ https://www.ncbi.nlm.nih.gov/pubmed/32024252 http://dx.doi.org/10.3390/ma13030660 |
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author | Ahamed, Maqusood Akhtar, Mohd Javed Khan, M. A. Majeed |
author_facet | Ahamed, Maqusood Akhtar, Mohd Javed Khan, M. A. Majeed |
author_sort | Ahamed, Maqusood |
collection | PubMed |
description | Iron oxide–reduced graphene oxide (Fe(3)O(4)-RGO) nanocomposites have attracted enormous interest in the biomedical field. However, studies on biological response of Fe(3)O(4)-RGO nanocomposites at the cellular and molecular level are scarce. This study was designed to synthesize, characterize, and explore the cytotoxicity of Fe(3)O(4)-RGO nanocomposites in human liver (HepG2) cells. Potential mechanisms of cytotoxicity of Fe(3)O(4)-RGO nanocomposites were further explored through oxidative stress. Prepared samples were characterized by UV-visible spectrophotometer, X-ray diffraction, scanning electron microscopy, transmission electron microscopy, and energy dispersive spectroscopy. The results demonstrated that RGO induce dose-dependent cytotoxicity in HepG2 cells. However, Fe(3)O(4)-RGO nanocomposites were not toxic. We further noted that RGO induce apoptosis in HepG2 cells, as evidenced by mitochondrial membrane potential loss, higher caspase-3 enzyme activity, and cell cycle arrest. On the other hand, Fe(3)O(4)-RGO nanocomposites did not alter these apoptotic parameters. Moreover, we observed that RGO increases intracellular reactive oxygen species and hydrogen peroxide while decrease antioxidant glutathione. Again, Fe(3)O(4)-RGO nanocomposites did not exert oxidative stress. Altogether, we found that RGO significantly induced cytotoxicity, apoptosis and oxidative stress. However, Fe(3)O(4)-RGO nanocomposites showed good biocompatibility to HepG2 cells. This study warrants further research to investigate the biological response of Fe(3)O(4)-RGO nanocomposites at the gene and molecular level. |
format | Online Article Text |
id | pubmed-7040707 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-70407072020-03-09 Investigation of Cytotoxicity, Apoptosis, and Oxidative Stress Response of Fe(3)O(4)-RGO Nanocomposites in Human Liver HepG2 cells Ahamed, Maqusood Akhtar, Mohd Javed Khan, M. A. Majeed Materials (Basel) Article Iron oxide–reduced graphene oxide (Fe(3)O(4)-RGO) nanocomposites have attracted enormous interest in the biomedical field. However, studies on biological response of Fe(3)O(4)-RGO nanocomposites at the cellular and molecular level are scarce. This study was designed to synthesize, characterize, and explore the cytotoxicity of Fe(3)O(4)-RGO nanocomposites in human liver (HepG2) cells. Potential mechanisms of cytotoxicity of Fe(3)O(4)-RGO nanocomposites were further explored through oxidative stress. Prepared samples were characterized by UV-visible spectrophotometer, X-ray diffraction, scanning electron microscopy, transmission electron microscopy, and energy dispersive spectroscopy. The results demonstrated that RGO induce dose-dependent cytotoxicity in HepG2 cells. However, Fe(3)O(4)-RGO nanocomposites were not toxic. We further noted that RGO induce apoptosis in HepG2 cells, as evidenced by mitochondrial membrane potential loss, higher caspase-3 enzyme activity, and cell cycle arrest. On the other hand, Fe(3)O(4)-RGO nanocomposites did not alter these apoptotic parameters. Moreover, we observed that RGO increases intracellular reactive oxygen species and hydrogen peroxide while decrease antioxidant glutathione. Again, Fe(3)O(4)-RGO nanocomposites did not exert oxidative stress. Altogether, we found that RGO significantly induced cytotoxicity, apoptosis and oxidative stress. However, Fe(3)O(4)-RGO nanocomposites showed good biocompatibility to HepG2 cells. This study warrants further research to investigate the biological response of Fe(3)O(4)-RGO nanocomposites at the gene and molecular level. MDPI 2020-02-02 /pmc/articles/PMC7040707/ /pubmed/32024252 http://dx.doi.org/10.3390/ma13030660 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Ahamed, Maqusood Akhtar, Mohd Javed Khan, M. A. Majeed Investigation of Cytotoxicity, Apoptosis, and Oxidative Stress Response of Fe(3)O(4)-RGO Nanocomposites in Human Liver HepG2 cells |
title | Investigation of Cytotoxicity, Apoptosis, and Oxidative Stress Response of Fe(3)O(4)-RGO Nanocomposites in Human Liver HepG2 cells |
title_full | Investigation of Cytotoxicity, Apoptosis, and Oxidative Stress Response of Fe(3)O(4)-RGO Nanocomposites in Human Liver HepG2 cells |
title_fullStr | Investigation of Cytotoxicity, Apoptosis, and Oxidative Stress Response of Fe(3)O(4)-RGO Nanocomposites in Human Liver HepG2 cells |
title_full_unstemmed | Investigation of Cytotoxicity, Apoptosis, and Oxidative Stress Response of Fe(3)O(4)-RGO Nanocomposites in Human Liver HepG2 cells |
title_short | Investigation of Cytotoxicity, Apoptosis, and Oxidative Stress Response of Fe(3)O(4)-RGO Nanocomposites in Human Liver HepG2 cells |
title_sort | investigation of cytotoxicity, apoptosis, and oxidative stress response of fe(3)o(4)-rgo nanocomposites in human liver hepg2 cells |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7040707/ https://www.ncbi.nlm.nih.gov/pubmed/32024252 http://dx.doi.org/10.3390/ma13030660 |
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