Roles of ROS and cell cycle arrest in the genotoxicity induced by gold nanorod core/silver shell nanostructure

To understand the genotoxicity induced in the liver by silver nanoparticles (AgNPs) and silver ions, an engineered gold nanorod core/silver shell nanostructure (Au@Ag NR) and humanized hepatocyte HepaRG cells were used in this study. The involvement of oxidative stress and cell cycle arrest in the D...

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Published inNanoscale research letters Vol. 15; no. 1; pp. 224 - 13
Main Authors Wang, Dan, Dan, Mo, Ji, Yinglu, Wu, Xiaochun, Wang, Xue, Wen, Hairuo
Format Journal Article
LanguageEnglish
Published New York Springer US 07.12.2020
Springer Nature B.V
SpringerOpen
Subjects
Bioassays
Cell cycle
Cell cycle arrest
Chemistry and Materials Science
Chromosomes
Clastogenicity
Comet assay
Comet nuclei
Damage detection
Deoxyribonucleic acid
DNA
DNA damage
Genotoxicity
Gold
Gold nanorod core/silver shell nanostructures
HepaRG cells
Materials Science
Molecular Medicine
Nano Express
Nanochemistry
Nanoparticles
Nanorods
Nanoscale Science and Technology
Nanostructure
Nanotechnology
Nanotechnology and Microengineering
Oxidative stress
Silver
Silver ions
Cell cycle arrest
Oxidative stress
Gold nanorod core/silver shell nanostructures
HepaRG cells
Genotoxicity
Silver ions
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Abstract To understand the genotoxicity induced in the liver by silver nanoparticles (AgNPs) and silver ions, an engineered gold nanorod core/silver shell nanostructure (Au@Ag NR) and humanized hepatocyte HepaRG cells were used in this study. The involvement of oxidative stress and cell cycle arrest in the DNA and chromosome damage induced by 0.4–20 µg mL −1 Au@Ag NR were investigated by comet assay, γ-H2AX assay and micronucleus test. Further, the distribution of Au@Ag NR was analyzed. Our results demonstrated that both Ag + and Au@Ag NR led to DNA cleavage and chromosome damage (clastogenicity) in HepaRG cells and that the Au@Ag NR retained in the nucleus may further release Ag + , aggravating the damages, which are mainly caused by cell cycle arrest and ROS formation. The results reveal the correlation between the intracellular accumulation, Ag + ion release and the potential genotoxicity of AgNPs.
AbstractList To understand the genotoxicity induced in the liver by silver nanoparticles (AgNPs) and silver ions, an engineered gold nanorod core/silver shell nanostructure (Au@Ag NR) and humanized hepatocyte HepaRG cells were used in this study. The involvement of oxidative stress and cell cycle arrest in the DNA and chromosome damage induced by 0.4–20 µg mL −1 Au@Ag NR were investigated by comet assay, γ-H2AX assay and micronucleus test. Further, the distribution of Au@Ag NR was analyzed. Our results demonstrated that both Ag + and Au@Ag NR led to DNA cleavage and chromosome damage (clastogenicity) in HepaRG cells and that the Au@Ag NR retained in the nucleus may further release Ag + , aggravating the damages, which are mainly caused by cell cycle arrest and ROS formation. The results reveal the correlation between the intracellular accumulation, Ag + ion release and the potential genotoxicity of AgNPs.
Abstract To understand the genotoxicity induced in the liver by silver nanoparticles (AgNPs) and silver ions, an engineered gold nanorod core/silver shell nanostructure (Au@Ag NR) and humanized hepatocyte HepaRG cells were used in this study. The involvement of oxidative stress and cell cycle arrest in the DNA and chromosome damage induced by 0.4–20 µg mL−1 Au@Ag NR were investigated by comet assay, γ-H2AX assay and micronucleus test. Further, the distribution of Au@Ag NR was analyzed. Our results demonstrated that both Ag+ and Au@Ag NR led to DNA cleavage and chromosome damage (clastogenicity) in HepaRG cells and that the Au@Ag NR retained in the nucleus may further release Ag+, aggravating the damages, which are mainly caused by cell cycle arrest and ROS formation. The results reveal the correlation between the intracellular accumulation, Ag+ ion release and the potential genotoxicity of AgNPs.
To understand the genotoxicity induced in the liver by silver nanoparticles (AgNPs) and silver ions, an engineered gold nanorod core/silver shell nanostructure (Au@Ag NR) and humanized hepatocyte HepaRG cells were used in this study. The involvement of oxidative stress and cell cycle arrest in the DNA and chromosome damage induced by 0.4–20 µg mL−1 Au@Ag NR were investigated by comet assay, γ-H2AX assay and micronucleus test. Further, the distribution of Au@Ag NR was analyzed. Our results demonstrated that both Ag+ and Au@Ag NR led to DNA cleavage and chromosome damage (clastogenicity) in HepaRG cells and that the Au@Ag NR retained in the nucleus may further release Ag+, aggravating the damages, which are mainly caused by cell cycle arrest and ROS formation. The results reveal the correlation between the intracellular accumulation, Ag+ ion release and the potential genotoxicity of AgNPs.
To understand the genotoxicity induced in the liver by silver nanoparticles (AgNPs) and silver ions, an engineered gold nanorod core/silver shell nanostructure (Au@Ag NR) and humanized hepatocyte HepaRG cells were used in this study. The involvement of oxidative stress and cell cycle arrest in the DNA and chromosome damage induced by 0.4-20 µg mL-1 Au@Ag NR were investigated by comet assay, γ-H2AX assay and micronucleus test. Further, the distribution of Au@Ag NR was analyzed. Our results demonstrated that both Ag+ and Au@Ag NR led to DNA cleavage and chromosome damage (clastogenicity) in HepaRG cells and that the Au@Ag NR retained in the nucleus may further release Ag+, aggravating the damages, which are mainly caused by cell cycle arrest and ROS formation. The results reveal the correlation between the intracellular accumulation, Ag+ ion release and the potential genotoxicity of AgNPs.To understand the genotoxicity induced in the liver by silver nanoparticles (AgNPs) and silver ions, an engineered gold nanorod core/silver shell nanostructure (Au@Ag NR) and humanized hepatocyte HepaRG cells were used in this study. The involvement of oxidative stress and cell cycle arrest in the DNA and chromosome damage induced by 0.4-20 µg mL-1 Au@Ag NR were investigated by comet assay, γ-H2AX assay and micronucleus test. Further, the distribution of Au@Ag NR was analyzed. Our results demonstrated that both Ag+ and Au@Ag NR led to DNA cleavage and chromosome damage (clastogenicity) in HepaRG cells and that the Au@Ag NR retained in the nucleus may further release Ag+, aggravating the damages, which are mainly caused by cell cycle arrest and ROS formation. The results reveal the correlation between the intracellular accumulation, Ag+ ion release and the potential genotoxicity of AgNPs.
ArticleNumber 224
Author Wang, Xue
Wen, Hairuo
Ji, Yinglu
Wang, Dan
Dan, Mo
Wu, Xiaochun
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Issue 1
Keywords Cell cycle arrest
Oxidative stress
Gold nanorod core/silver shell nanostructures
HepaRG cells
Genotoxicity
Silver ions
Language English
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SSID ssj0047076
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Snippet To understand the genotoxicity induced in the liver by silver nanoparticles (AgNPs) and silver ions, an engineered gold nanorod core/silver shell nanostructure...
Abstract To understand the genotoxicity induced in the liver by silver nanoparticles (AgNPs) and silver ions, an engineered gold nanorod core/silver shell...
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pubmedcentral
proquest
crossref
springer
SourceType Open Website
Open Access Repository
Aggregation Database
Enrichment Source
Index Database
Publisher
StartPage 224
SubjectTerms Bioassays
Cell cycle
Cell cycle arrest
Chemistry and Materials Science
Chromosomes
Clastogenicity
Comet assay
Comet nuclei
Damage detection
Deoxyribonucleic acid
DNA
DNA damage
Genotoxicity
Gold
Gold nanorod core/silver shell nanostructures
HepaRG cells
Materials Science
Molecular Medicine
Nano Express
Nanochemistry
Nanoparticles
Nanorods
Nanoscale Science and Technology
Nanostructure
Nanotechnology
Nanotechnology and Microengineering
Oxidative stress
Silver
Silver ions
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Title Roles of ROS and cell cycle arrest in the genotoxicity induced by gold nanorod core/silver shell nanostructure
URI https://link.springer.com/article/10.1186/s11671-020-03455-1
https://www.proquest.com/docview/2473377971
https://www.proquest.com/docview/2467840692
https://pubmed.ncbi.nlm.nih.gov/PMC7721938
https://doaj.org/article/e8bd13565b0647de9211ce7201af555e
Volume 15
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