Oxidative stress induction by nanoparticles in THP-1 cells with 4-HNE production: Stress biomarker or oxidative stress signalling molecule?

Foucaud, Laurent; Goulaouic, S.; Bennasroune, Amar; Laval-Gilly, Philippe; Brown, David M.; Stone, Vicki; Falla, Jaı̈ro

doi:10.1016/j.tiv.2010.07.012

Cited by 24 publications

(18 citation statements)

References 39 publications

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“…1,35 Significant nano toxicity exhibited at 2 mg/mL (P <0.001) and 76 mg/mL (P <0.0001) concentrations of Ag and TiO 2 -NPs signifies that the primary mechanism of NPs induced toxicity is due to oxidative stress, resulting in damage to cellular membranes and biological macromolecules, as reported earlier. 10,24,34 Our previous reported results have also demonstrated that the TiO 2 -NPs induce DNA damage at a critical concentration of 5 mg/mL. 36 The data suggests that the TiO 2 -NPs at lower concentrations up to 5mg/mL modulate the antioxidant enzymes levels, whereas, at higher concentrations, the cellular DNA repair machinery may be adversely affected.…”

Section: Discussionmentioning

confidence: 89%

“…Due to their small aerodynamic diameter, the ultrafine particles (<100 nm) from natural and anthropogenic sources including viruses, biogenic magnetite, ferritin, metal oxides, fullerenes, carbon, polymers and other fumes may contaminate ambient air, penetrate deep into the lungs, and reach different body organs through the blood circulatory system. 10,11,24 The common tendency of TiO 2 -NPs to readily diffuse through the protective cellular barriers may also involve risks to human health, and warrants systematic and indepth investigation of their possible toxicological effects. Therefore, in this study, we have determined the cytotoxicity of crystalline Ag and TiO 2 -NPs using human plasma for understanding the NPs toxicity.…”

Section: Discussionmentioning

confidence: 99%

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In vitro assessment of Ag and TiO2 nanoparticles cytotoxicity

et al. 2014

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Section: Discussionmentioning

confidence: 89%

Section: Discussionmentioning

confidence: 99%

In vitro assessment of Ag and TiO2 nanoparticles cytotoxicity

et al. 2014

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“…Diverse types of nanoparticles have been reported to induce oxidative stress or inflammatory responses. [28][29][30] However, few studies have addressed the mechanism responsible for nanoparticle-induced toxicity. In a previous study, we found that LDH-NPs generated ROS in human alveolar epithelial cancer A549 cells, human osteosarcoma (HOS) cells, and human cervical adenocarcinoma HeLa cells, but not in normal human lung epithelial L-132 cells, and because LDH-NP generated the most ROS and induced the proinflammatory mediator IL-8 in A549 cells, we used this cell line for the present study.…”

Section: Discussionmentioning

confidence: 99%

Oxidative stress by layered double hydroxide nanoparticles via an SFK-JNK and p38-NF-κB signaling pathway mediates induction of interleukin-6 and interleukin-8 in human lung epithelial cells

Choi¹,

Paek²,

Jin³

2015

IJN

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Anionic nanoclays are layered double hydroxide nanoparticles (LDH-NPs) that have been shown to exhibit toxicity by inducing reactive oxidative species and a proinflammatory mediator in human lung epithelial A549 cells. However, the molecular mechanism responsible for this LDH-NP-induced toxicity and the relationship between oxidative stress and inflammatory events remains unclear. In this study, we focused on intracellular signaling pathways and transcription factors induced in response to oxidative stress caused by exposure to LDH-NPs in A549 cells. Mitogen-activated protein kinase (MAPK) cascades, such as extracellular signal-regulated kinase, c-Jun-N-terminal kinase (JNK), and p38, were investigated as potential signaling mechanisms responsible for regulation of oxidative stress and cytokine release. Src family kinases (SFKs), which are known to mediate activation of MAPK, together with redox-sensitive transcription factors, including nuclear factor kappa B and nuclear factor-erythroid 2-related factor-2, were also investigated as downstream events of MAPK signaling. The results obtained suggest that LDH-NP exposure causes oxidative stress, leading to expression of antioxidant enzymes, such as catalase, glucose reductase, superoxide dismutase, and heme oxygenase-1, via a SFK-JNK and p38-nuclear factor kappa B signaling pathway. Further, activation of this signaling was also found to regulate release of inflammatory cytokines, including interleukin-6 and interleukin-8, demonstrating the inflammatory potential of LDH-NP.

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“…Toxicity and cellular responses to nanosilver particles are a serious concern. It has been reported that nanoparticles mediate their toxicity by induction of reactive oxygen species (ROS; Foucaud et al, 2010;Chairuangkitti et al, 2013). This increase in the cellular ROS levels was associated with induction of reduced cell growth, apoptotic and necrotic cell death (Zanette et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

In vitro effect of nanosilver on gene expression of superoxide dismutases and nitric oxide synthases in chicken sertoli cells

Hassanpour

Mirshokraei

Sadrabad

et al. 2015

Animal

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To evaluate effects of different concentrations of nanosilver colloid on the cell culture of Sertoli cells, the proportion of lipid peroxidation, antioxidant capacity, nitric oxide (NO) production and genes expression of superoxide dismutases (SOD1 and SOD2) and nitric oxide synthases (eNOS and iNOS) were measured. Sertoli cells were incubated at concentrations of 25, 75 and 125 ppm nanosilver for 48 h. There was progressive lipid peroxidation in treatments according to increasing of nanosilver. Lipid peroxidation, as indicated by malondialdehyde levels, was significantly elevated by the highest concentration of silver colloid (125 ppm), although antioxidant capacity, as measured by ferric ion reduction, was unaffected. Nitrite, as an index of NO production was reduced only in 125 ppm of nanosilver. Expression of SOD1 gene was reduced in nanosilver-treated cells at all concentrations, whereas expression of SOD2 gene was reduced only in cells treated with 125 ppm nanosilver. Expression of iNOS gene was progressively increased with higher concentrations of nanosilver. Expression of eNOS gene was also increased in 125 ppm of nanosilver. In conclusion, toxic effects of nanosilver could be due to high lipid peroxidation and suppression of antioxidant mechanisms via reduced expression of SOD genes and increased expression of NOS genes.

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Oxidative stress induction by nanoparticles in THP-1 cells with 4-HNE production: Stress biomarker or oxidative stress signalling molecule?

Cited by 24 publications

References 39 publications

In vitro assessment of Ag and TiO2 nanoparticles cytotoxicity

In vitro assessment of Ag and TiO2 nanoparticles cytotoxicity

Oxidative stress by layered double hydroxide nanoparticles via an SFK-JNK and p38-NF-κB signaling pathway mediates induction of interleukin-6 and interleukin-8 in human lung epithelial cells

In vitro effect of nanosilver on gene expression of superoxide dismutases and nitric oxide synthases in chicken sertoli cells

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Oxidative stress induction by nanoparticles in THP-1 cells with 4-HNE production: Stress biomarker or oxidative stress signalling molecule?

Cited by 24 publications

References 39 publications

In vitro assessment of Ag and TiO2 nanoparticles cytotoxicity

In vitro assessment of Ag and TiO2 nanoparticles cytotoxicity

Oxidative stress by layered double hydroxide nanoparticles via an SFK-JNK and p38-NF-&kappa;B signaling pathway mediates induction of interleukin-6 and interleukin-8 in human lung epithelial cells

In vitro effect of nanosilver on gene expression of superoxide dismutases and nitric oxide synthases in chicken sertoli cells

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Oxidative stress by layered double hydroxide nanoparticles via an SFK-JNK and p38-NF-κB signaling pathway mediates induction of interleukin-6 and interleukin-8 in human lung epithelial cells