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The toxicity of nanoparticles and their interaction with cells: an in vitro metabolomic perspective

Awashra, Mohammad, Młynarz, Piotr·2023·Nanoscale Advances
DOI 10.1039/d2na00534dPMC PMC10186990
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Abstract

The interaction of nanoparticles (NPs) with cells depends on their physicochemical properties and can lead to cytotoxic events. Metabolomics reveals the molecular mechanisms of this nanotoxicity and avoids the misleading interferences with NPs.

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Figures

Fig. 1 Nanoparticle internalization via phagocytoses.
Fig. 1 Nanoparticle internalization via phagocytoses.CC BY · PubMed Central
Fig. 2 Pinocytosis internalization mechanisms. (1) Macropinocytosis. (2) Clathrin-mediated endocytosis. (3) Caveolae-mediated endocytosis.
Fig. 2 Pinocytosis internalization mechanisms. (1) Macropinocytosis. (2) Clathrin-mediated endocytosis. (3) Caveolae-mediated endocytosis.CC BY · PubMed Central
Fig. 3 Physicochemical properties of NPs.
Fig. 3 Physicochemical properties of NPs.CC BY · PubMed Central
Fig. 4 Schematic representation of the mitochondrial membrane: different NP surface charges induce different mechanisms of cell death.77 The neutrally charged NP (*) does not disrupt the mitochondrial membrane potential, and therefore apoptosis is not activated. The positively charged NP (+) disrupts the slight negative charge on the cytosolic side of the outer membrane, leading to a disruption in the mitochondrial membrane potential. The disruption damages the membrane and proteins, such as caspase activators, leak into the cytosol. The negatively charged NP (−) increases the negative charge on the outer membrane, which leads to a disruption in the mitochondrial membrane potential. The mitochondria compensate by releasing calcium ions that were stored in the matrix of the mitochondria. The spike in calcium induced apoptosis.77
Fig. 4 Schematic representation of the mitochondrial membrane: different NP surface charges induce different mechanisms of cell death.77 The neutrally charged NP (*) does not disrupt the mitochondrial membrane potential, and therefore apoptosis is not activated. The positively charged NP (+) disrupts the slight negative charge on the cytosolic side of the outer membrane, leading to a disruption in the mitochondrial membrane potential. The disruption damages the membrane and proteins, such as caspase activators, leak into the cytosol. The negatively charged NP (−) increases the negative charge on the outer membrane, which leads to a disruption in the mitochondrial membrane potential. The mitochondria compensate by releasing calcium ions that were stored in the matrix of the mitochondria. The spike in calcium induced apoptosis.77CC BY · PubMed Central
Fig. 5 Various modes of action of NPs on cells.
Fig. 5 Various modes of action of NPs on cells.CC BY · PubMed Central
Fig. 6 Three ways of NPs interference with MTT cell viability test. (a) NPs in the absence of cells showed light absorbance at the same wavelength of MTT assay (525 nm in this study). The absorbance of the 5 NPs was measured at a concentration of 32 μg mL−1. Data was obtained from ref. 100 (b) NPs can catalyze the reduction of the MTT (or another test agent) to its colored (or fluorescent) form without the existence of cell enzymes. (c) NPs may adsorb and denature the cell enzymes that reduce the MTT dye to its colored form, giving false results.
Fig. 6 Three ways of NPs interference with MTT cell viability test. (a) NPs in the absence of cells showed light absorbance at the same wavelength of MTT assay (525 nm in this study). The absorbance of the 5 NPs was measured at a concentration of 32 μg mL−1. Data was obtained from ref. 100 (b) NPs can catalyze the reduction of the MTT (or another test agent) to its colored (or fluorescent) form without the existence of cell enzymes. (c) NPs may adsorb and denature the cell enzymes that reduce the MTT dye to its colored form, giving false results.CC BY · PubMed Central
Fig. 7 Interference of NPs with ELISA assay. (a) NPs can adsorb different cytokines on their surface. (b) IL-8 were quantified by ELISA after 24 h of incubation with NPs at 75 μg cm−2 after elimination of particles by centrifugation. Results (n = 6) are expressed as % of control (cytokine incubated in the absence of NPs). *Significantly different from the control (p < 0.05 ANOVA followed by Dunnett's test). (b) Is reproduced from ref. 122 with permission from Taylor & Francis. Copyright 2015.
Fig. 7 Interference of NPs with ELISA assay. (a) NPs can adsorb different cytokines on their surface. (b) IL-8 were quantified by ELISA after 24 h of incubation with NPs at 75 μg cm−2 after elimination of particles by centrifugation. Results (n = 6) are expressed as % of control (cytokine incubated in the absence of NPs). *Significantly different from the control (p < 0.05 ANOVA followed by Dunnett's test). (b) Is reproduced from ref. 122 with permission from Taylor & Francis. Copyright 2015.CC BY · PubMed Central
Fig. 8 Evaluation of apoptosis and necrosis activities in MCF-7 cells using Annexin-V/PI staining. (Left) Untreated cells (control) and (Right) cells treated with ZnPNPs. Reproduced from ref. 135, with permission. Copyright © 2020, Springer Science Business Media, LLC, part of Springer Nature.
Fig. 8 Evaluation of apoptosis and necrosis activities in MCF-7 cells using Annexin-V/PI staining. (Left) Untreated cells (control) and (Right) cells treated with ZnPNPs. Reproduced from ref. 135, with permission. Copyright © 2020, Springer Science Business Media, LLC, part of Springer Nature.CC BY · PubMed Central
Fig. 9 Overview of the connection of the main omics-sciences: genomics, transcriptomics, proteomics, and metabolomics. Metabolomics represents the final output of cellular processes.
Fig. 9 Overview of the connection of the main omics-sciences: genomics, transcriptomics, proteomics, and metabolomics. Metabolomics represents the final output of cellular processes.CC BY · PubMed Central
Fig. 10 Metabolomics workflow for NMR- or MS-based metabolomics. DA: discriminant analysis; PCA: principal component analysis; PLS: partial least squares; and OPLS: orthogonal partial least squares.
Fig. 10 Metabolomics workflow for NMR- or MS-based metabolomics. DA: discriminant analysis; PCA: principal component analysis; PLS: partial least squares; and OPLS: orthogonal partial least squares.CC BY · PubMed Central
Fig. 11 Summary of various metabolic responses of A549 (Right) and 16HBE (Left) cells to AuNR exposure. Metabolites in red or blue represent a significant increase or decrease in their levels, respectively, in the AuNR-treated groups compared with the non-treated groups. (This figure has been reprinted from ref. 169 with permission. Copyright © 2013, Elsevier Ltd).
Fig. 11 Summary of various metabolic responses of A549 (Right) and 16HBE (Left) cells to AuNR exposure. Metabolites in red or blue represent a significant increase or decrease in their levels, respectively, in the AuNR-treated groups compared with the non-treated groups. (This figure has been reprinted from ref. 169 with permission. Copyright © 2013, Elsevier Ltd).CC BY · PubMed Central
Fig. 12 Comparison of the metabolic changes induced due to the interactions between AuNPs or AgNPs with HDFs cells. While AgNPs (Right) induced cytotoxicity in the HDF cells, the effect of AuNPs (Left) was suppressed by an antioxidant mechanism.172
Fig. 12 Comparison of the metabolic changes induced due to the interactions between AuNPs or AgNPs with HDFs cells. While AgNPs (Right) induced cytotoxicity in the HDF cells, the effect of AuNPs (Left) was suppressed by an antioxidant mechanism.172CC BY · PubMed Central
Fig. 13 Untargeted metabolomic analysis was used to reveal the effect of exposure of two different doses (12.5 and 25 μg mL−1) of ZnO, SiO2, TiO2, and CeO2 NPs on the metabolism of human bronchial epithelial cells (BEAS-2B). (a) Schematic diagram of the study workflow. (b) Hierarchical cellular stress responses based on metabolomics and functional assays. The cells were maintained in the healthy state at the tier 1 stage. At an intermediate level of cellular stress (tier 2), the exposure to SiO2, TiO2, and CeO2 NPs altered several metabolic pathways and induced inflammation. At a high level of cellular stress (tier 3), ZnO NPs significantly affected toxicity and DNA damage related metabolic pathways. Only a short list of significantly altered pathways is presented due to the limited space. Adapted with permission from ref. 217 Copyright 2019, the American Chemical Society.
Fig. 13 Untargeted metabolomic analysis was used to reveal the effect of exposure of two different doses (12.5 and 25 μg mL−1) of ZnO, SiO2, TiO2, and CeO2 NPs on the metabolism of human bronchial epithelial cells (BEAS-2B). (a) Schematic diagram of the study workflow. (b) Hierarchical cellular stress responses based on metabolomics and functional assays. The cells were maintained in the healthy state at the tier 1 stage. At an intermediate level of cellular stress (tier 2), the exposure to SiO2, TiO2, and CeO2 NPs altered several metabolic pathways and induced inflammation. At a high level of cellular stress (tier 3), ZnO NPs significantly affected toxicity and DNA damage related metabolic pathways. Only a short list of significantly altered pathways is presented due to the limited space. Adapted with permission from ref. 217 Copyright 2019, the American Chemical Society.CC BY · PubMed Central
Fig. 14 Global metabolomics and pathway analysis in aSiO2 NP-exposed HepG2 cells (a–c) and Institute for Cancer Research (ICR) mice (d–f). OPLS-DA score plot from the NMR spectra of metabolomes from HepG2 cells treated with 100 mg L−1 aSiO2 NPs for 24 h (a) and from ICR mice liver treated with 50 mg kg−1 aSiO2 NPs for 24 h. Selected significantly altered global metabolites level in HepG2 cells (b) and in ICR mice liver (e) after treatment with the NPs. Pathway-based enrichment analysis performed by MetaboAnalyst 3.0 with significant altered metabolites (>1.5 fold) in HepG2 cells (c) and ICR mice liver (f) after treatment with the NPs. This figure has been reproduced from ref. 240 with permission from Elsevier B.V., Copyright 2018.
Fig. 14 Global metabolomics and pathway analysis in aSiO2 NP-exposed HepG2 cells (a–c) and Institute for Cancer Research (ICR) mice (d–f). OPLS-DA score plot from the NMR spectra of metabolomes from HepG2 cells treated with 100 mg L−1 aSiO2 NPs for 24 h (a) and from ICR mice liver treated with 50 mg kg−1 aSiO2 NPs for 24 h. Selected significantly altered global metabolites level in HepG2 cells (b) and in ICR mice liver (e) after treatment with the NPs. Pathway-based enrichment analysis performed by MetaboAnalyst 3.0 with significant altered metabolites (>1.5 fold) in HepG2 cells (c) and ICR mice liver (f) after treatment with the NPs. This figure has been reproduced from ref. 240 with permission from Elsevier B.V., Copyright 2018.CC BY · PubMed Central
Fig. 15 [(a) Comparison of ZnO NPs with PS NPs].247 (a) Summary comparing the relevant metabolic responses of BEAS-2B cells to ZnO and PS_LD NP exposure. Arrow in orange or blue represents a significant increase or decrease in the ZnO or PS_LD NP exposure, respectively, compared with the non-treated groups. This figure is adapted with permission from ref. 247 Copyright 2019, Taylor & Francis. [(b and c) Comparison of ZnO NPs with Zn2+].254 (b) Proportion of significantly changed metabolites in different categories after 2 (2 d) and 7 (7 d) days exposure to ZnO NPs and ZnCl2. (c) Edwards–Venn diagram of the total number of significantly changed metabolites. The total numbers of significantly changed metabolites in ZnO_2 d (d = days), ZnO_7 d, ZnCl2_2 d, and ZnCl2_7 d groups were 99, 121, 128, and 183, respectively. The altered metabolites were obtained by conducting PLS-DA analyses for each Zn-exposed group vs. the matched control group (VIP > 1 and p < 0.05). Note: the metabolites identified from the positive ion mode and negative ion mode were merged together. (b and c) Are reprinted with permission from ref. 254 Copyright 2020, the American Chemical Society. [(d–f) Comparison of ZnO NPs solo exposure to their co-exposure with GO].257 (d) Schematic illustration of A549 cells ZnO NPs solo exposure vs. co-exposure with GO. The GO sheets reduce the cytotoxicity of ZnO NPs by blocking their internalization into the A549 cells. (e) Influence of GO on the bioavailability of ZnO NPs. The Zn concentrations were normalized by the protein concentrations. All data expressed as the mean ± SD. All differences were identified by one-way ANOVA followed by Tukey post hoc test. * Indicates p-value. (f) Interaction network of metabolites in ZnO NPs solo and co-exposure groups. (d–f) Are reproduced from ref. 257 with permission from The Royal Society of Chemistry, Copyright 2019.
Fig. 15 [(a) Comparison of ZnO NPs with PS NPs].247 (a) Summary comparing the relevant metabolic responses of BEAS-2B cells to ZnO and PS_LD NP exposure. Arrow in orange or blue represents a significant increase or decrease in the ZnO or PS_LD NP exposure, respectively, compared with the non-treated groups. This figure is adapted with permission from ref. 247 Copyright 2019, Taylor & Francis. [(b and c) Comparison of ZnO NPs with Zn2+].254 (b) Proportion of significantly changed metabolites in different categories after 2 (2 d) and 7 (7 d) days exposure to ZnO NPs and ZnCl2. (c) Edwards–Venn diagram of the total number of significantly changed metabolites. The total numbers of significantly changed metabolites in ZnO_2 d (d = days), ZnO_7 d, ZnCl2_2 d, and ZnCl2_7 d groups were 99, 121, 128, and 183, respectively. The altered metabolites were obtained by conducting PLS-DA analyses for each Zn-exposed group vs. the matched control group (VIP > 1 and p < 0.05). Note: the metabolites identified from the positive ion mode and negative ion mode were merged together. (b and c) Are reprinted with permission from ref. 254 Copyright 2020, the American Chemical Society. [(d–f) Comparison of ZnO NPs solo exposure to their co-exposure with GO].257 (d) Schematic illustration of A549 cells ZnO NPs solo exposure vs. co-exposure with GO. The GO sheets reduce the cytotoxicity of ZnO NPs by blocking their internalization into the A549 cells. (e) Influence of GO on the bioavailability of ZnO NPs. The Zn concentrations were normalized by the protein concentrations. All data expressed as the mean ± SD. All differences were identified by one-way ANOVA followed by Tukey post hoc test. * Indicates p-value. (f) Interaction network of metabolites in ZnO NPs solo and co-exposure groups. (d–f) Are reproduced from ref. 257 with permission from The Royal Society of Chemistry, Copyright 2019.CC BY · PubMed Central
Mohammad Awashra
Mohammad AwashraCC BY · PubMed Central
Piotr Młynarz
Piotr MłynarzCC BY · PubMed Central

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Metadata

Authors
Awashra, M., & Młynarz, P.
Venue
Nanoscale Advances
Publisher
Royal Society of Chemistry (RSC)
Published
2023
Volume
5
Issue
10
Pages
2674-2723
ISSN
2516-0230
DOI
10.1039/d2na00534d
PMC
PMC10186990
Cited by
319
References
6
Language
en
Licence
creativecommons.org/licenses/by/3.0/ (vor, 29 d)
Funders
Politechnika Wrocławska ((Wrocław University of Science and Technology), Wydział Chemiczny (Faculty of Chemistry))

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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

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