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In vivo degeneration and the fate of inorganic nanoparticles

Feliu, Neus, Docter, Dominic, Heine, Markus, del Pino, Pablo, Ashraf, Sumaira, Kolosnjaj-Tabi, Jelena, Macchiarini, Paolo, Nielsen, Peter, Alloyeau, Damien, Gazeau, Florence, Stauber, Roland H., Parak, Wolfgang J.·2016·Chemical Society Reviews
DOI 10.1039/c5cs00699f
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Abstract

Nanoparticles comprise of a core, a surface coating, and a corona of adsorbed biomolecules, of which all parts can have a different fate.

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Image 1
CC-BY-NC · From the PDF
Fig. 1 The in vivo pathway and fate of NPs through the human body. While accidental exposure of humans to NPs and their entry into the body most likely occur through inhalation and the oral route, biomedical applications mainly focus on intravenous injection or oral application routes. Upon inhalation, ingestion, or injection of pristine NPs, they come into contact with various complex physiological environments, leading to the covering of NPs with various biomolecules. Upon the formation of such a corona made of biomolecules, the in vivo transformation of pristine NPs is rapidly initiated. During their passage through different compartments of the body, the in vivo degeneration and fate of NPs differ significantly, which is indicated by the different symbols for the NPs. While NP-biomolecule corona complexes are quite stable in plasma, their uptake into organs, such as the liver can trigger corona and NP degradation. Likewise, the conditions in the digestive tract, such as low pH and the presence of surfactants, may lead to similar degradation processes. Such in vivo transformation of nanomaterials should be considered in nanotoxicology and nanomedicine.
Fig. 1 The in vivo pathway and fate of NPs through the human body. While accidental exposure of humans to NPs and their entry into the body most likely occur through inhalation and the oral route, biomedical applications mainly focus on intravenous injection or oral application routes. Upon inhalation, ingestion, or injection of pristine NPs, they come into contact with various complex physiological environments, leading to the covering of NPs with various biomolecules. Upon the formation of such a corona made of biomolecules, the in vivo transformation of pristine NPs is rapidly initiated. During their passage through different compartments of the body, the in vivo degeneration and fate of NPs differ significantly, which is indicated by the different symbols for the NPs. While NP-biomolecule corona complexes are quite stable in plasma, their uptake into organs, such as the liver can trigger corona and NP degradation. Likewise, the conditions in the digestive tract, such as low pH and the presence of surfactants, may lead to similar degradation processes. Such in vivo transformation of nanomaterials should be considered in nanotoxicology and nanomedicine.CC-BY-NC · From the PDF
Image 3
CC-BY-NC · From the PDF
Image 4
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Fig. 4 Fate of two double-labeled NPs in vivo . The upper lane displays polymer-coated 59 Fe-labeled FeO x NPs. The carboxyl groups of the surface were covalently coupled to a 14 C-labeled peptide (11-As, myelin basic protein). After i.v. injection in groups of mice ( n = 3-4), the 59 Fe and 14 C-labels disappeared synchronously from blood following a first order kinetics due to the fast uptake mainly into liver and spleen. 89 In the bottom lane, polymer-coated 59 Fe-labeled FeO x NPs were covalently labeled with 125 I-labeled mouse-transferrin. The blood half-life and organ distribution were followed in groups of mice after i.v. injection. Again, a synchronous removal of both labels from the blood was found, probably indicating the uptake of intact NPs into the liver, without separation of the protein covered shell/polymer from the core already in the bloodstream. 80
Fig. 4 Fate of two double-labeled NPs in vivo . The upper lane displays polymer-coated 59 Fe-labeled FeO x NPs. The carboxyl groups of the surface were covalently coupled to a 14 C-labeled peptide (11-As, myelin basic protein). After i.v. injection in groups of mice ( n = 3-4), the 59 Fe and 14 C-labels disappeared synchronously from blood following a first order kinetics due to the fast uptake mainly into liver and spleen. 89 In the bottom lane, polymer-coated 59 Fe-labeled FeO x NPs were covalently labeled with 125 I-labeled mouse-transferrin. The blood half-life and organ distribution were followed in groups of mice after i.v. injection. Again, a synchronous removal of both labels from the blood was found, probably indicating the uptake of intact NPs into the liver, without separation of the protein covered shell/polymer from the core already in the bloodstream. 80CC-BY-NC · From the PDF
Fig. 5 (A) Au cores were coated with an amphiphilic polymer. Cores and polymer shells were labelled with 198 Au and 111 In, respectively. The question was whether in vivo the polymer shells would remain around the cores or whether they would separate. (B) The ratio of radioactivities originating from 111 In and 198 Au is shown for different organs 24 hours after retention. In case this ratio is higher than one, the polymer must have come off the NP cores. A figure adopted from Kreyling et al. , 125 GIT = gastrointestinal tract.
Fig. 5 (A) Au cores were coated with an amphiphilic polymer. Cores and polymer shells were labelled with 198 Au and 111 In, respectively. The question was whether in vivo the polymer shells would remain around the cores or whether they would separate. (B) The ratio of radioactivities originating from 111 In and 198 Au is shown for different organs 24 hours after retention. In case this ratio is higher than one, the polymer must have come off the NP cores. A figure adopted from Kreyling et al. , 125 GIT = gastrointestinal tract.CC-BY-NC · From the PDF
Image 7
CC-BY-NC · From the PDF
Fig. 6 Intralysosomal degradation of FeO x nanospheres, nanocubes and gold/FeO x heterostructures in murine splenic macrophages. At day 1 (D1) postinjection, FeO x NPs are concentrated within lysosomes of macrophages. After one week (D7), a fair share of NPs arranges on the margins of lysosomes or appears to be more isolated. Red arrows point to NP-adjacent to monodisperse iron-rich ferritin proteins. Some parts of gold/FeO x heterostructures have been locally degraded leaving gold remnants (yellow arrows). Scanning transmission electron microscopy (STEM) - high-angle annular dark field (HAADF) and elemental nanoanalysis by STEM-EDX confirm the partial or total disappearance of iron oxidesurrounding the resilient gold core. The Fourier transformation (FT) of the degraded and resilient nanocubes at day 14 (D14, white square on the high resolution TEM micrograph) shows that nanocubes maintain their initial lattice structure (spinel inverse or vacancy-ordered g -Fe2O3 structures). The FT of the ferritin protein core (red square) shows a hematite structure, suggesting local transfer of iron from degraded NPs to the storage protein. An image adapted from a previously published work. 50,110,163
Fig. 6 Intralysosomal degradation of FeO x nanospheres, nanocubes and gold/FeO x heterostructures in murine splenic macrophages. At day 1 (D1) postinjection, FeO x NPs are concentrated within lysosomes of macrophages. After one week (D7), a fair share of NPs arranges on the margins of lysosomes or appears to be more isolated. Red arrows point to NP-adjacent to monodisperse iron-rich ferritin proteins. Some parts of gold/FeO x heterostructures have been locally degraded leaving gold remnants (yellow arrows). Scanning transmission electron microscopy (STEM) - high-angle annular dark field (HAADF) and elemental nanoanalysis by STEM-EDX confirm the partial or total disappearance of iron oxidesurrounding the resilient gold core. The Fourier transformation (FT) of the degraded and resilient nanocubes at day 14 (D14, white square on the high resolution TEM micrograph) shows that nanocubes maintain their initial lattice structure (spinel inverse or vacancy-ordered g -Fe2O3 structures). The FT of the ferritin protein core (red square) shows a hematite structure, suggesting local transfer of iron from degraded NPs to the storage protein. An image adapted from a previously published work. 50,110,163CC-BY-NC · From the PDF
Fig. 7 Progressive erosion of different FeO x NPs in lysosome-like medium. An image adopted from a previously published work. 50,163,169
Fig. 7 Progressive erosion of different FeO x NPs in lysosome-like medium. An image adopted from a previously published work. 50,163,169CC-BY-NC · From the PDF
Fig. 8 Protective role of coating on NP degradation. (A) Carbon mapping obtained by energy filtered TEM (EFTEM) evidences the uneven coverage of the amphiphilic polymer layer surrounding the cubes. White arrows point to polymer-poor regions where the degradation begins. An image adapted from Lartigue et al. 163 (B) Step-by-step degradation of nanocubes showing faster degradation in zones with poor polymer coating (black arrows) and the protective effect of dense coating areas (blue arrows). (C) The coverage of multicore FeO x NPs with a 3 nm gold layer (iron featured in red and gold in green on the Bragg filtered high-resolution micrograph on the left) protects the NPs from degradation. The EDX quantitative measurement of the Fe/Au ratio shows that the thickest gold layer efficiently delays NP degradation and iron release in lysosome-like medium.
Fig. 8 Protective role of coating on NP degradation. (A) Carbon mapping obtained by energy filtered TEM (EFTEM) evidences the uneven coverage of the amphiphilic polymer layer surrounding the cubes. White arrows point to polymer-poor regions where the degradation begins. An image adapted from Lartigue et al. 163 (B) Step-by-step degradation of nanocubes showing faster degradation in zones with poor polymer coating (black arrows) and the protective effect of dense coating areas (blue arrows). (C) The coverage of multicore FeO x NPs with a 3 nm gold layer (iron featured in red and gold in green on the Bragg filtered high-resolution micrograph on the left) protects the NPs from degradation. The EDX quantitative measurement of the Fe/Au ratio shows that the thickest gold layer efficiently delays NP degradation and iron release in lysosome-like medium.CC-BY-NC · From the PDF

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Metadata

Authors
Feliu, N., Docter, D., Heine, M., del Pino, P., Ashraf, S., Kolosnjaj-Tabi, J., Macchiarini, P., Nielsen, P., Alloyeau, D., Gazeau, F., Stauber, R. H., & Parak, W. J.
Venue
Chemical Society Reviews
Publisher
Royal Society of Chemistry (RSC)
Published
2016
Volume
45
Issue
9
Pages
2440-2457
ISSN
  • 0306-0012
  • 1460-4744
DOI
10.1039/c5cs00699f
Cited by
423
References
7
Language
en
Funders
  • Bundesministerium für Bildung und Forschung (MRCyte/NanoBEL)
  • European Commission (FutureNanoNeeds)
  • Alexander von Humboldt-Stiftung

About these checks

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.

What counts as a claim ›How we measure confidence ›How we check this ›

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How to cite

Cite CoChat for the checks on this page, and the paper for its own findings.

This page
CoChat. (2026). Citation check: In vivo degeneration and the fate of inorganic nanoparticles. https://app.cochat.ai/papers/10.1039/c5cs00699f
The paper
Feliu, N., Docter, D., Heine, M., del Pino, P., Ashraf, S., Kolosnjaj-Tabi, J., Macchiarini, P., Nielsen, P., Alloyeau, D., Gazeau, F., Stauber, R. H., & Parak, W. J. (2016). In vivo degeneration and the fate of inorganic nanoparticles. Chemical Society Reviews. https://doi.org/10.1039/c5cs00699f