Biological safety and tissue distribution of (16-mercaptohexadecyl)trimethylammonium bromide-modified cationic gold nanorods
Language English Country Netherlands Media print-electronic
Document type Journal Article
PubMed
29149721
DOI
10.1016/j.biomaterials.2017.10.044
PII: S0142-9612(17)30703-2
Knihovny.cz E-resources
- Keywords
- Autophagy, Genotoxicity, Lysosomal stress, Plasmonic photothermal effect, Spleen, Thrombocytes,
- MeSH
- Autophagy drug effects MeSH
- Quaternary Ammonium Compounds metabolism MeSH
- Humans MeSH
- Lysosomes drug effects metabolism MeSH
- Mesenchymal Stem Cells cytology drug effects MeSH
- Actin Cytoskeleton drug effects metabolism MeSH
- Mutagens toxicity MeSH
- Mice, Inbred C57BL MeSH
- Cell Line, Tumor MeSH
- Nanotubes chemistry toxicity ultrastructure MeSH
- Podocytes drug effects metabolism MeSH
- Cell Movement drug effects MeSH
- DNA Damage MeSH
- Spleen drug effects pathology MeSH
- Sulfhydryl Compounds metabolism MeSH
- Tissue Distribution MeSH
- Blood Platelets drug effects pathology ultrastructure MeSH
- Gold metabolism MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- (16-mercaptohexadecyl)trimethylammonium bromide MeSH Browser
- Quaternary Ammonium Compounds MeSH
- Mutagens MeSH
- Sulfhydryl Compounds MeSH
- Gold MeSH
The exceptionally high cellular uptake of gold nanorods (GNRs) bearing cationic surfactants makes them a promising tool for biomedical applications. Given the known specific toxic and stress effects of some preparations of cationic nanoparticles, the purpose of this study was to evaluate, in an in vitro and in vivo in mouse, the potential harmful effects of GNRs coated with (16-mercaptohexadecyl)trimethylammonium bromide (MTABGNRs). Interestingly, even after cellular accumulation of high amounts of MTABGNRs sufficient for induction of photothermal effect, no genotoxicity (even after longer-term accumulation), induction of autophagy, destabilization of lysosomes (dominant organelles of their cellular destination), alterations of actin cytoskeleton, or in cell migration could be detected in vitro. In vivo, after intravenous administration, the majority of GNRs accumulated in mouse spleen followed by lungs and liver. Microscopic examination of the blood and spleen showed that GNRs interacted with white blood cells (mononuclear and polymorphonuclear leukocytes) and thrombocytes, and were delivered to the spleen red pulp mainly as GNR-thrombocyte complexes. Importantly, no acute toxic effects of MTABGNRs administered as 10 or 50 μg of gold per mice, as well as no pathological changes after their high accumulation in the spleen were observed, indicating good tolerance of MTABGNRs by living systems.
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