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Skoglund, Sara
Publications (3 of 3) Show all publications
Di Bucchianico, S., Gliga, A. R., Åkerlund, E., Skoglund, S., Odnevall Wallinder, I., Fadeel, B. & Karlsson, H. L. (2018). Calcium-dependent cyto- and genotoxicity of nickel metal and nickel oxide nanoparticles in human lung cells. Particle and Fibre Toxicology, 15, Article ID 32.
Open this publication in new window or tab >>Calcium-dependent cyto- and genotoxicity of nickel metal and nickel oxide nanoparticles in human lung cells
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2018 (English)In: Particle and Fibre Toxicology, ISSN 1743-8977, E-ISSN 1743-8977, Vol. 15, article id 32Article in journal (Refereed) Published
Abstract [en]

Background: Genotoxicity is an important toxicological endpoint due to the link to diseases such as cancer. Therefore, an increased understanding regarding genotoxicity and underlying mechanisms is needed for assessing the risk with exposure to nanoparticles (NPs). The aim of this study was to perform an in-depth investigation regarding the genotoxicity of well-characterized Ni and NiO NPs in human bronchial epithelial BEAS-2B cells and to discern possible mechanisms. Comparisons were made with NiCl2 in order to elucidate effects of ionic Ni. Methods: BEAS-2B cells were exposed to Ni and NiO NPs, as well as NiCl2, and uptake and cellular dose were investigated by transmission electron microscopy (TEM) and inductively coupled plasma mass spectrometry (ICP-MS). The NPs were characterized in terms of surface composition (X-ray photoelectron spectroscopy), agglomeration (photon cross correlation spectroscopy) and nickel release in cell medium (ICP-MS). Cell death (necrosis/apoptosis) was investigated by Annexin VFITC/PI staining and genotoxicity by cytokinesis-block micronucleus (cytome) assay (OECD 487), chromosomal aberration (OECD 473) and comet assay. The involvement of intracellular reactive oxygen species (ROS) and calcium was explored using the fluorescent probes, DCFH-DA and Fluo-4. Results: NPs were efficiently taken up by the BEAS-2B cells. In contrast, no or minor uptake was observed for ionic Ni from NiCl2. Despite differences in uptake, all exposures (NiO, Ni NPs and NiCl2) caused chromosomal damage. Furthermore, NiO NPs were most potent in causing DNA strand breaks and generating intracellular ROS. An increase in intracellular calcium was observed and modulation of intracellular calcium by using inhibitors and chelators clearly prevented the chromosomal damage. Chelation of iron also protected against induced damage, particularly for NiO and NiCl2. Conclusions: This study has revealed chromosomal damage by Ni and NiO NPs as well as Ni ionic species and provides novel evidence for a calcium-dependent mechanism of cyto- and genotoxicity.

Place, publisher, year, edition, pages
BMC, 2018
Keywords
Nickel/nickel oxide nanoparticles, Chromosomal aberrations, Endoreduplication, Calcium homeostasis, Carcinogenic potential
National Category
Pharmacology and Toxicology
Identifiers
urn:nbn:se:kth:diva-232767 (URN)10.1186/s12989-018-0268-y (DOI)000439340800001 ()30016969 (PubMedID)2-s2.0-85050147056 (Scopus ID)
Funder
Forte, Swedish Research Council for Health, Working Life and Welfare, 2011-0832Swedish Research Council, 2014-4598 2017-03931
Note

QC 20180803

Available from: 2018-08-03 Created: 2018-08-03 Last updated: 2019-08-20Bibliographically approved
Åkerlund, E., Cappellini, F., Di Bucchianico, S., Islam, S., Skoglund, S., Derr, R., . . . Karlsson, H. L. (2018). Genotoxic and mutagenic properties of Ni and NiO nanoparticles investigated by comet assay,-H2AX staining, Hprt mutation assay and ToxTracker reporter cell lines. Environmental and Molecular Mutagenesis, 59(3), 211-222
Open this publication in new window or tab >>Genotoxic and mutagenic properties of Ni and NiO nanoparticles investigated by comet assay,-H2AX staining, Hprt mutation assay and ToxTracker reporter cell lines
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2018 (English)In: Environmental and Molecular Mutagenesis, ISSN 0893-6692, E-ISSN 1098-2280, Vol. 59, no 3, p. 211-222Article in journal (Refereed) Published
Abstract [en]

Nickel (Ni) compounds are classified as carcinogenic to humans but the underlying mechanisms are still poorly understood. Furthermore, effects related to nanoparticles (NPs) of Ni have not been fully elucidated. The aim of this study was to investigate genotoxicity and mutagenicity of Ni and NiO NPs and compare the effect to soluble Ni from NiCl2. We employed different models; i.e., exposure of (1) human bronchial epithelial cells (HBEC) followed by DNA strand break analysis (comet assay and -H2AX staining); (2) six different mouse embryonic stem (mES) reporter cell lines (ToxTracker) that are constructed to exhibit fluorescence upon the induction of various pathways of relevance for (geno)toxicity and cancer; and (3) mES cells followed by mutagenicity testing (Hprt assay). The results showed increased DNA strand breaks (comet assay) for the NiO NPs and at higher doses also for the Ni NPs whereas no effects were observed for Ni ions/complexes from NiCl2. By employing the reporter cell lines, oxidative stress was observed as the main toxic mechanism and protein unfolding occurred at cytotoxic doses for all three Ni-containing materials. Oxidative stress was also detected in the HBEC cells following NP-exposure. None of these materials induced the reporter related to direct DNA damage and stalled replication forks. A small but statistically significant increase in Hprt mutations was observed for NiO but only at one dose. We conclude that Ni and NiO NPs show more pronounced (geno)toxic effects compared to Ni ions/complexes, indicating more serious health concerns. Environ. Mol. Mutagen. 59:211-222, 2018.

Place, publisher, year, edition, pages
Wiley, 2018
Keywords
genotoxicity, lung cells, nanomaterials, nickel, reporter cell lines
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:kth:diva-225174 (URN)10.1002/em.22163 (DOI)000427564000004 ()29243303 (PubMedID)2-s2.0-85041238601 (Scopus ID)
Funder
Swedish Research Council, 2013-5621 2014-4598Forte, Swedish Research Council for Health, Working Life and Welfare, 2011-0832
Note

QC 20180404

Available from: 2018-04-04 Created: 2018-04-04 Last updated: 2018-04-04Bibliographically approved
Skoglund, S., Blomberg, E., Odnevall Wallinder, I., Grillo, I., Pedersen, J. S. & Bergström, L. M. (2017). A novel explanation for the enhanced colloidal stability of silver nanoparticles in the presence of an oppositely charged surfactant. Physical Chemistry, Chemical Physics - PCCP, 19(41), 28037-28043
Open this publication in new window or tab >>A novel explanation for the enhanced colloidal stability of silver nanoparticles in the presence of an oppositely charged surfactant
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2017 (English)In: Physical Chemistry, Chemical Physics - PCCP, ISSN 1463-9076, E-ISSN 1463-9084, Vol. 19, no 41, p. 28037-28043Article in journal (Refereed) Published
Abstract [en]

The structural behavior in aqueous mixtures of negatively charged silver nanoparticles (Ag NPs) together with the cationic surfactants cetyltrimethylammonium bromide (CTAB) and dodecyltrimethylammonium chloride (DTAC), respectively, has been investigated using SANS and SAXS. From our SANS data analysis we are able to conclude that the surfactants self-assemble into micellar clusters surrounding the Ag NPs. We are able to quantify our results by means of fitting experimental SANS data with a model based on cluster formation of micelles with very good agreement. Based on our experimental results, we propose a novel mechanism for the stabilization of negatively charged Ag NPs in a solution of positively charged surfactants in which cluster formation of micelles in the vicinity of the particles prevents the particles from aggregating. Complementary SAXS and DLS measurements further support this novel way of explaining stabilization of small hydrophilic nanoparticles in surfactant-containing solutions.

Place, publisher, year, edition, pages
ROYAL SOC CHEMISTRY, 2017
National Category
Chemical Sciences
Identifiers
urn:nbn:se:kth:diva-217409 (URN)10.1039/c7cp04662f (DOI)000413778800015 ()28994441 (PubMedID)2-s2.0-85032624124 (Scopus ID)
Note

QC 20171121

Available from: 2017-11-21 Created: 2017-11-21 Last updated: 2017-11-21Bibliographically approved
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