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Comparison of cellular toxicity caused by ambient ultrafine particles and engineered metal oxide nanoparticles
OBJECTIVE: The development of nanotechnology has spurred concerns about the health effects of exposure to nanoparticles (NPs) and ultrafine particles (UFPs). Toxicological data on NPs and UFPs may provide evidence to support the development of regulations to reduce the risk of particle exposure. We...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4412114/ https://www.ncbi.nlm.nih.gov/pubmed/25888760 http://dx.doi.org/10.1186/s12989-015-0082-8 |
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author | Lu, Senlin Zhang, Wenchao Zhang, Rui Liu, Pinwei Wang, Qiangxiang Shang, Yu Wu, Minghong Donaldson, Ken Wang, Qingyue |
author_facet | Lu, Senlin Zhang, Wenchao Zhang, Rui Liu, Pinwei Wang, Qiangxiang Shang, Yu Wu, Minghong Donaldson, Ken Wang, Qingyue |
author_sort | Lu, Senlin |
collection | PubMed |
description | OBJECTIVE: The development of nanotechnology has spurred concerns about the health effects of exposure to nanoparticles (NPs) and ultrafine particles (UFPs). Toxicological data on NPs and UFPs may provide evidence to support the development of regulations to reduce the risk of particle exposure. We tried to provide fundamental data to determine differences in cytotoxicity induced by ambient UFPs and engineered metal oxide NPs (ZnO, NiO, and CeO(2)). METHODS: UFPs were sampled by using of a nano micro-orifice uniform deposit impactor. Physicochemical characterization of the UFPs and nano metal oxide particles were studied by scanning electron microscopy and transmission electron microscopy. Cellular toxicity induced by the different particles was assessed by using of comprehensive approaches and compared after A549 cells were exposured to the particles. RESULTS: All of the measured particles could damage A549 cells at concentrations ranging from 25 to 200 μg/mL. The lowest survival ratio and the highest lactate dehydrogenase level were caused by nano-ZnO particles, but the highest levels of intracellular reactive oxygen species (ROS) and percentages of apoptosis were observed in cells treated with the soluble fraction of ambient fine particles (PM(1.8)) at 200 μg/mL. Relatively high concentrations of anthropogenic metals, including Zn, Ni, Fe, and Cu, may be responsible for the higher toxicity of fine ambient particles compared with the ambient coarse particles and UFPs. The selected heavy metals (Zn, Ni, Fe, and Cu) were found to be located in the perinuclear and cytoplasmic areas of A549 cells. The distribution pattern of metals from ambient particles showed that distributions of the metals in A549 cells were not uniform and followed the pattern Cu > Zn > Fe > Ni, suggesting that Cu was absorbed by A549 cells more easily than the other metals. CONCLUSIONS: Metal nanoparticles oxides and UFPs at low concentration could damage to cells, but the manufactured metal oxide nanoparticles are not highly toxic to lung cells compared to environmental particles. The local concentration effect of heavy metals in A549 cells, as well as the induction of oxidative stress by the particles, may be responsible for the damage observed to the cells. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12989-015-0082-8) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-4412114 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-44121142015-04-29 Comparison of cellular toxicity caused by ambient ultrafine particles and engineered metal oxide nanoparticles Lu, Senlin Zhang, Wenchao Zhang, Rui Liu, Pinwei Wang, Qiangxiang Shang, Yu Wu, Minghong Donaldson, Ken Wang, Qingyue Part Fibre Toxicol Research OBJECTIVE: The development of nanotechnology has spurred concerns about the health effects of exposure to nanoparticles (NPs) and ultrafine particles (UFPs). Toxicological data on NPs and UFPs may provide evidence to support the development of regulations to reduce the risk of particle exposure. We tried to provide fundamental data to determine differences in cytotoxicity induced by ambient UFPs and engineered metal oxide NPs (ZnO, NiO, and CeO(2)). METHODS: UFPs were sampled by using of a nano micro-orifice uniform deposit impactor. Physicochemical characterization of the UFPs and nano metal oxide particles were studied by scanning electron microscopy and transmission electron microscopy. Cellular toxicity induced by the different particles was assessed by using of comprehensive approaches and compared after A549 cells were exposured to the particles. RESULTS: All of the measured particles could damage A549 cells at concentrations ranging from 25 to 200 μg/mL. The lowest survival ratio and the highest lactate dehydrogenase level were caused by nano-ZnO particles, but the highest levels of intracellular reactive oxygen species (ROS) and percentages of apoptosis were observed in cells treated with the soluble fraction of ambient fine particles (PM(1.8)) at 200 μg/mL. Relatively high concentrations of anthropogenic metals, including Zn, Ni, Fe, and Cu, may be responsible for the higher toxicity of fine ambient particles compared with the ambient coarse particles and UFPs. The selected heavy metals (Zn, Ni, Fe, and Cu) were found to be located in the perinuclear and cytoplasmic areas of A549 cells. The distribution pattern of metals from ambient particles showed that distributions of the metals in A549 cells were not uniform and followed the pattern Cu > Zn > Fe > Ni, suggesting that Cu was absorbed by A549 cells more easily than the other metals. CONCLUSIONS: Metal nanoparticles oxides and UFPs at low concentration could damage to cells, but the manufactured metal oxide nanoparticles are not highly toxic to lung cells compared to environmental particles. The local concentration effect of heavy metals in A549 cells, as well as the induction of oxidative stress by the particles, may be responsible for the damage observed to the cells. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12989-015-0082-8) contains supplementary material, which is available to authorized users. BioMed Central 2015-03-19 /pmc/articles/PMC4412114/ /pubmed/25888760 http://dx.doi.org/10.1186/s12989-015-0082-8 Text en © Lu et al. ; licensee BioMed Central. 2015 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Lu, Senlin Zhang, Wenchao Zhang, Rui Liu, Pinwei Wang, Qiangxiang Shang, Yu Wu, Minghong Donaldson, Ken Wang, Qingyue Comparison of cellular toxicity caused by ambient ultrafine particles and engineered metal oxide nanoparticles |
title | Comparison of cellular toxicity caused by ambient ultrafine particles and engineered metal oxide nanoparticles |
title_full | Comparison of cellular toxicity caused by ambient ultrafine particles and engineered metal oxide nanoparticles |
title_fullStr | Comparison of cellular toxicity caused by ambient ultrafine particles and engineered metal oxide nanoparticles |
title_full_unstemmed | Comparison of cellular toxicity caused by ambient ultrafine particles and engineered metal oxide nanoparticles |
title_short | Comparison of cellular toxicity caused by ambient ultrafine particles and engineered metal oxide nanoparticles |
title_sort | comparison of cellular toxicity caused by ambient ultrafine particles and engineered metal oxide nanoparticles |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4412114/ https://www.ncbi.nlm.nih.gov/pubmed/25888760 http://dx.doi.org/10.1186/s12989-015-0082-8 |
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