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Dose-dependent genotoxicity of ammonia-modified graphene oxide particles in lung cancer cells
Graphene oxide (GO), the water soluble form of 2D graphene, has received much attention because of its attractive properties for a wide range of applications and products. Surface modification with different functional groups can improve GO biocompatibility for further biomedical applications. In th...
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Published in: | Journal of physics. Conference series 2019-03, Vol.1186 (1), p.12009 |
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Main Authors: | , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Graphene oxide (GO), the water soluble form of 2D graphene, has received much attention because of its attractive properties for a wide range of applications and products. Surface modification with different functional groups can improve GO biocompatibility for further biomedical applications. In the present study we have evaluated genotoxicity of pristine and ammonia-modified graphene oxide (GO-NH2) nanoparticles (NPs) in a human lung epithelial cell line, A549, exposed for 24 h to different concentrations of NPs (0.1, 1, 10, 20 and 50 μg/ml). Quantification of reactive oxygen species (ROS) indicated that exposure to higher concentrations of both types of NPs resulted in enhanced ROS generation. The observed comet tail migration in the method of Single Cell Gel Electrophoresis in the cells treated with 20 and 50 μg/ml GO and GO-NH2 indicated presence of damages in DNA. Cell cycle analysis showed that after treatment of A549 cells with increasing concentrations of NPs for 24h the percentage of cells in G0/G1 phase of the cell cycle decreased while the percentage of cells in G2/M increased. The presented results suggest that ammonia-modified GO NPs applied at concentrations higher than 20 μg/ml induced stronger toxicity effect in A549 cells compared to pristine GO and that the use of low concentrations of GO and GO-NH2 NPs is important to avoide adverse biological effects. |
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ISSN: | 1742-6588 1742-6596 |
DOI: | 10.1088/1742-6596/1186/1/012009 |