Silver nanoparticles induce toxicity in A549 cells via ROS-dependent and ROS-independent pathways

Chairuangkitti, Porntipa; Lawanprasert, Somsong; Roytrakul, Sittiruk; Aueviriyavit, Sasitorn; Phummiratch, Duangkamol; Kulthong, Kornphimol; Chanvorachote, Pithi; Maniratanachote, Rawiwan

doi:10.1016/j.tiv.2012.08.021

Cited by 251 publications

(171 citation statements)

References 25 publications

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“…Some researchers reported that AgNPs can act as free radical scavengers. 19,20 In contrast, Chairuankitti et al 21 found that the toxic effects of AgNPs on A549 cells are mediated via both ROS-dependent and ROS-independent mechanisms. Moreover, AshaRani et al 16 showed that AgNPs caused mitochondrial dysfunction, namely the induction of ROS, which in turn set off DNA damage and chromosomal aberrations in normal human lung fibroblast cells.…”

Section: Discussionmentioning

confidence: 98%

Pharmacological and toxicological effects of co-exposure of human gingival fibroblasts to silver nanoparticles and sodium fluoride

Inkielewicz‐Stępniak¹,

Santos-Martínez²,

Medina³

et al. 2014

IJN

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Background Silver nanoparticles (AgNPs) and fluoride (F) are pharmacological agents widely used in oral medicine and dental practice due to their anti-microbial/anti-cavity properties. However, risks associated with the co-exposure of local cells and tissues to these xenobiotics are not clear. Therefore, we have evaluated the effects of AgNPs and F co-exposure on human gingival fibroblast cells. Methods Human gingival fibroblast cells (CRL-2014) were exposed to AgNPs and/or F at different concentrations for up to 24 hours. Cellular uptake of AgNPs was examined by transmission electron microscopy. Downstream inflammatory effects and oxidative stress were measured by real-time quantitative polymerase chain reaction (PCR) and reactive oxygen species (ROS) generation. Cytotoxicity and apoptosis were measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and real-time quantitative PCR and flow cytometry, respectively. Finally, the involvement of mitogen-activated protein kinases (MAPK) was studied using Western blot. Results We found that AgNPs penetrated the cell membrane and localized inside the mitochondria. Co-incubation experiments resulted in increased oxidative stress, inflammation, and apoptosis. In addition, we found that co-exposure to both xenobiotics phosphorylated MAPK, particularly p42/44 MAPK. Conclusion A combined exposure of human fibroblasts to AgNPs and F results in increased cellular damage. Further studies are needed in order to evaluate pharmacological and potentially toxicological effects of AgNPs and F on oral health.

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Section: Discussionmentioning

confidence: 98%

Pharmacological and toxicological effects of co-exposure of human gingival fibroblasts to silver nanoparticles and sodium fluoride

Inkielewicz‐Stępniak¹,

Santos-Martínez²,

Medina³

et al. 2014

IJN

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“…8,19 However, ROS-independent mechanisms were also involved in NPs' toxicity. 20,21 Recently, SiNPs have been reported to protect pea seedings against Cr(VI) phytotoxicity via reducing oxidative stress, and enhancing antioxidant defense system. 22 These data of agreement and discordance with regard to NPs' toxicity and its mechanisms indicate that hazards and exact mechanisms have not been clearly defined.…”

Section: Discussionmentioning

confidence: 99%

Amorphous silica nanoparticles trigger vascular endothelial cell injury through apoptosis and autophagy via reactive oxygen species-mediated MAPK/Bcl-2 and PI3K/Akt/mTOR signaling

Guo¹,

Yang²,

Li³

et al. 2016

IJN

192

111

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Environmental exposure to silica nanoparticles (SiNPs) is inevitable due to their widespread application in industrial, commercial, and biomedical fields. In recent years, most investigators focus on the evaluation of cardiovascular effects of SiNPs in vivo and in vitro. Endothelial injury and dysfunction is now hypothesized to be a dominant mechanism in the development of cardiovascular diseases. This study aimed to explore interaction of SiNPs with endothelial cells, and extensively investigate the exact effects of reactive oxygen species (ROS) on the signaling molecules and cytotoxicity involved in SiNPs-induced endothelial injury. Significant induction of cytotoxicity as well as oxidative stress, apoptosis, and autophagy was observed in human umbilical vein endothelial cells following the SiNPs exposure ( P <0.05). The oxidative stress was induced by ROS generation, leading to redox imbalance and lipid peroxidation. SiNPs induced mitochondrial dysfunction, characterized by membrane potential collapse, and elevated Bax and declined bcl-2 expression, ultimately leading to apoptosis, and also increased number of autophagosomes and autophagy marker proteins, such as LC3 and p62. Phosphorylated ERK, PI3K, Akt, and mTOR were significantly decreased, but phosphorylated JNK and p38 MAPK were increased in SiNPs-exposed endothelial cells. In contrast, all of these stimulation phenomena were effectively inhibited by N -acetylcysteine. The N -acetylcysteine supplement attenuated SiNPs-induced endothelial toxicity through inhibition of apoptosis and autophagy via MAPK/Bcl-2 and PI3K/Akt/mTOR signaling, as well as suppression of intracellular ROS property via activating antioxidant enzyme and Nrf2 signaling. In summary, the results demonstrated that SiNPs triggered autophagy and apoptosis via ROS-mediated MAPK/Bcl-2 and PI3K/Akt/mTOR signaling in endothelial cells, and subsequently disturbed the endothelial homeostasis and impaired endothelium. Our findings may provide experimental evidence and explanation for cardiovascular diseases triggered by SiNPs. Furthermore, results hint that the application of antioxidant may provide a novel way for safer use of nanomaterials.

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“…Mitochondrial depolarization associated with AgNP exposure could instead be part of one or more signaling cascades involving crosstalk between the mitochondrion and other cellular components, since exposure to AgNPs results in calcium-induced opening of the mitochondrial permeability transition pore 88 and induction of mitochondrially-mediated apoptotic mechanisms. 74 This suggests that mitochondrial effects, such as loss of membrane potential, may be a primary effect in AgNP exposure only in certain cell types, or that mitochondrial depolarization is a secondary effect and arises concurrently with cell death in other cell types. This conclusion, however, is dependent upon the measured parameters within the few studies listed (differing sizes, types, and concentrations of AgNPs used, differing in vitro conditions, etc.)…”

Section: Mitochondrial Depolarizationmentioning

confidence: 99%

A systematic review of evidence for silver nanoparticle-induced mitochondrial toxicity

Maurer

Meyer

2016

Environ. Sci.: Nano

102

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Silver nanoparticles induce toxicity in A549 cells via ROS-dependent and ROS-independent pathways

Cited by 251 publications

References 25 publications

Pharmacological and toxicological effects of co-exposure of human gingival fibroblasts to silver nanoparticles and sodium fluoride

Pharmacological and toxicological effects of co-exposure of human gingival fibroblasts to silver nanoparticles and sodium fluoride

Amorphous silica nanoparticles trigger vascular endothelial cell injury through apoptosis and autophagy via reactive oxygen species-mediated MAPK/Bcl-2 and PI3K/Akt/mTOR signaling

A systematic review of evidence for silver nanoparticle-induced mitochondrial toxicity

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