Increased oxidative stress and activated heat shock proteins in human cell lines by silver nanoparticles

Xin, Lili; J, Wang; Wu, Yanhu; Guo, Sifan; Tong, Jian

doi:10.1177/0960327114538988

Cited by 42 publications

(28 citation statements)

References 39 publications

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“…The AgNPs with < 100 nm particle size were characterized by TEM and DLS analysis as described previously (Xin et al , ). The TEM analysis showed that the primary particles of AgNPs were spherical and approximately 20–50 nm in diameter.…”

Section: Resultsmentioning

confidence: 69%

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Comparative genotoxicity of silver nanoparticles in human liver HepG2 and lung epithelial A549 cells

Wang¹,

Che

Zhang

et al. 2016

J of Applied Toxicology

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With the rapid expanding of human exposure to silver nanoparticles (AgNPs), genotoxicity screening of nanosilver is necessary to ensure consumer safety. Here, we assessed one key DNA damage responsive pathway activated by GADD45a gene after 24 h of AgNPs exposure in stable luciferase reporter cell systems based on two widely used in vitro cell models, human liver HepG2 and lung epithelial A549 cells. The comet assay and micronucleus test were also conducted to confirm the genetic damage induced by AgNPs. Our results showed that AgNPs produced a strong dose-dependent increase in transcriptional activation of GADD45a promoter indicated by luciferase activity accompanying by the significant decreases in cell viability. Surprisingly, in HepG2-luciferase cells, the relative luciferase activity was greater than 4.5× the control level after being treated with 200 μg ml AgNPs. These results were generally in line with the positive and dose-dependent responses in cytotoxicity, DNA strand breaks indicated by Olive tail moment, tail DNA (%) and tail length, and chromosome damage indicated by induction of micronuclei, nucleoplasmic bridges, and nuclear buds. Additionally, compared with the A549-luciferase cells, the HepG2-luciferase cells seemed to be more susceptible to AgNPs as higher levels of genotoxicity were induced. We concluded that our GADD45a promoter-driven luciferase reporter gene cell system, together with the comet assay and micronucleus test, can be used as valuable tools for rapid screening of genotoxic potential of nanosilver. Copyright © 2016 John Wiley & Sons, Ltd.

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Section: Resultsmentioning

confidence: 69%

“…No.576832) AgNPs, with < 100 nm particle size, were purchased from Sigma‐Aldrich. The AgNPs were characterized by transmission electron microscope (TEM; HITACHI H‐600, Tokyo, Japan) and Dynamic light scattering (DLS) as described previously (Xin et al , ). Zeta potential analysis was also conducted in this study.…”

Section: Methodsmentioning

confidence: 99%

Comparative genotoxicity of silver nanoparticles in human liver HepG2 and lung epithelial A549 cells

Wang¹,

Che

Zhang

et al. 2016

J of Applied Toxicology

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“…However, the use of Ag NP is debated because of their toxicity in vivo and in many cell types in vitro [6,7,8,9,10,11], even though in several cases the underlying mechanisms have not been elucidated. Initially, we focused on human osteoblast-like cells and found a dose dependent toxic effect of Ag NP, with an IC 50 around 25 µg/mL.…”

Section: Discussionmentioning

confidence: 99%

“…Ag NP cause abnormalities in zebrafish development in a dose-dependent manner [6] and are toxic for a variety of normal and neoplastic cells [7,8,9,10,11] mainly by generating oxidative and nitrosative stresses [9,10]. Since nanoparticulate silver coatings for orthopedic implants represent a promising approach to prevent infections, the effects of Ag NP have been studied on bone cells.…”

Section: Introductionmentioning

confidence: 99%

Silver Nanoparticles in Orthopedic Applications: New Insights on Their Effects on Osteogenic Cells

et al. 2017

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Infections of orthopedic implants are associated with high morbidity. The emergence of antibiotic resistant strains and the tendency of microbes to form biofilms on orthopedic devices prompt the individuation of novel antimicrobial agents. Silver nanoparticles represent an interesting alternative, but their effects on bone cells need to be clarified. We focused on osteoblast-like cells and on bone marrow-mesenchymal stem cells and found that these cells are rather resistant to the cytotoxic effects of silver nanoparticles, with a half maximal inhibitory concentration around 25 µg/mL as detected by MTT assay. Within a month of treatment, osteoblast-like cells adapt to the presence of the nanoparticles by upregulating hsp70 as shown by western blot. Hsp70 overexpression correlates with the restoration of normal cell proliferation. No alterations in the extent and time requirements were detected in mesenchymal stem cell induced to differentiate in osteoblasts in the presence of silver nanoparticles. Because the concentrations of silver nanoparticles which show antimicrobial activity are lower than those exerting toxic effects on bone-forming cells in vitro, we suggest that silver nanoparticles might represent a challenging tool to fight infections in orthopedic implants.

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“…17 In addition, AT-III activity is a plasma coagulation inhibitor, which is significantly lower under exposure to endosulfan. 23 vWF is one of the most important biomarkers for endothelial cell injury. The above results indicated that endosulfan may cause the hypercoagulability of blood by promoting platelet aggregation and the transformation of fibrinogen into fibrin on the one hand, and by depressing AT-III activity on the other hand.…”

Section: Discussionmentioning

confidence: 99%

Endosulfan inducing blood hypercoagulability and endothelial cells apoptosis via the death receptor pathway in Wistar rats

et al. 2015

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To investigate the effects of endosulfan on coagulation status and its mechanism, 32 male Wistar rats were randomly divided into four groups, including a control solution and three concentrations of endosulfan groups (1, 5, 10 mg kg −1 per day). The results showed that endosulfan significantly promoted platelet aggregation, prolonged the thrombin time and increased the D-dimer level, and decreased antithrombin III activity and the fibrinogen level. It also significantly enhanced the plasma levels of ROS and vWF, increased the expressions of 8-OHdG and apoptosis positive cells in the endothelial cells and promoted the expressions of Fas, FasL, caspase-8, and caspase-3 in vascular endothelial cells. The results suggested that endosulfan could cause the hypercoagulability of blood by promoting both platelet aggregation and the transformation of fibrinogen into fibrin, as well as depressing antithrombin III activity.Furthermore, endosulfan could induce the dysfunction of endothelial cells by causing apoptosis via a death receptor pathway, resulting from oxidative stress, which could be one of the key mechanisms behind hypercoagulability induced by endosulfan.

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Increased oxidative stress and activated heat shock proteins in human cell lines by silver nanoparticles

Cited by 42 publications

References 39 publications

Comparative genotoxicity of silver nanoparticles in human liver HepG2 and lung epithelial A549 cells

Comparative genotoxicity of silver nanoparticles in human liver HepG2 and lung epithelial A549 cells

Silver Nanoparticles in Orthopedic Applications: New Insights on Their Effects on Osteogenic Cells

Endosulfan inducing blood hypercoagulability and endothelial cells apoptosis via the death receptor pathway in Wistar rats

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