EPR spin trapping evaluation of ROS production in human fibroblasts exposed to cerium oxide nanoparticles: Evidence for NADPH oxidase and mitochondrial stimulation

Culcasi, Marcel; Benameur, Laı̈la; Mercier, Anne; Lucchesi, Céline; Rahmouni, Hidayat; Asteian, Alice; Casano, Gilles; Botta, A.; Kovacic, Hervé; Pietri, Sylvia

doi:10.1016/j.cbi.2012.08.007

Cited by 69 publications

(55 citation statements)

References 61 publications

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“…Notably, NPs can induce genotoxic damage to the cell when present alone in the cell culture medium but can, conversely, protect the cells from oxidative stress when another genotoxic compound is also present. However, more studies are also necessary to distinguish between specific hypotheses regarding the mechanism of interaction between CeO 2 –NPs and cells [28–30]. The cyto- and genotoxicity of CeO 2 –NPs are safety concerns for in vivo applications.…”

Section: Discussionmentioning

confidence: 99%

Cytotoxicity and Genotoxicity of Ceria Nanoparticles on Different Cell Lines in Vitro

Marzi

Monaco

Lapuente

et al. 2013

IJMS

149

100

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Owing to their radical scavenging and UV-filtering properties, ceria nanoparticles (CeO2-NPs) are currently used for various applications, including as catalysts in diesel particulate filters. Because of their ability to filter UV light, CeO2-NPs have garnered significant interest in the medical field and, consequently, are poised for use in various applications. The aim of this work was to investigate the effects of short-term (24 h) and long-term (10 days) CeO2-NP exposure to A549, CaCo2 and HepG2 cell lines. Cytotoxicity assays tested CeO2-NPs over a concentration range of 0.5 μg/mL to 5000 μg/mL, whereas genotoxicity assays tested CeO2-NPs over a concentration range of 0.5 μg/mL to 5000 μg/mL. In vitro assays showed almost no short-term exposure toxicity on any of the tested cell lines. Conversely, long-term CeO2-NP exposure proved toxic for all tested cell lines. NP genotoxicity was detectable even at 24-h exposure. HepG2 was the most sensitive cell line overall; however, the A549 line was most sensitive to the lowest concentration tested. Moreover, the results confirmed the ceria nanoparticles’ capacity to protect cells when they are exposed to well-known oxidants such as H2O2. A Comet assay was performed in the presence of both H2O2 and CeO2-NPs. When hydrogen peroxide was maintained at 25 μM, NPs at 0.5 μg/mL, 50 μg/mL, and 500 μg/mL protected the cells from oxidative damage. Thus, the NPs prevented H2O2-induced genotoxic damage.

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Section: Discussionmentioning

confidence: 99%

Cytotoxicity and Genotoxicity of Ceria Nanoparticles on Different Cell Lines in Vitro

Marzi

Monaco

Lapuente

et al. 2013

IJMS

149

100

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“…NADPH oxidase is abundant in “professional” phagocytes but this protein is also present in non inflammatory cells where it contributes to cell signaling. Involvement of NADPH oxidase in CeO 2 and CoCr NP toxicity has for instance been demonstrated in fibroblasts (Culcasi et al, 2012, Raghunathan et al, 2013). Other enzymes also generate ROS as by-products of their activity such as cytochrome P450, xanthine oxidase, lipoxygenase, cyclooxygenase as well as enzymes within the peroxisome complex.…”

Section: 2 Hierarchical Oxidative Stress Modelmentioning

confidence: 99%

Intracellular Signal Modulation by Nanomaterials

Hussain

Garantziotis

Rodrigues‐Lima

et al. 2014

Advances in Experimental Medicine and Biology

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A thorough understanding of the interactions of nanomaterials with biological systems and the resulting activation of signal transduction pathways is essential for the development of safe and consumer friendly nanotechnology. Here we present an overview of signaling pathways induced by nanomaterial exposures and describe the possible correlation of their physicochemical characteristics with biological outcomes. In addition to the hierarchical oxidative stress model and a review of the intrinsic and cell-mediated mechanisms of reactive Oxygen species (ROS) generating capacities of nanomaterials, we also discuss other oxidative stress dependent and independent cellular signaling pathways. Induction of the inflammasome, calcium signaling, and endoplasmic reticulum stress are reviewed. Furthermore, the uptake mechanisms can crucially affect the cytotoxicity of nanomaterials and membrane-dependent signaling pathways can be responsible for cellular effects of nanomaterials. Epigenetic regulation by nanomaterials effects of nanoparticle-protein interactions on cell signaling pathways, and the induction of various cell death modalities by nanomaterials are described. We describe the common trigger mechanisms shared by various nanomaterials to induce cell death pathways and describe the interplay of different modalities in orchestrating the final outcome after nanomaterial exposures. A better understanding of signal modulations induced by nanomaterials is not only essential for the synthesis and design of safer nanomaterials but will also help to discover potential nanomedical applications of these materials. Several biomedical applications based on the different signaling pathways induced by nanomaterials are already proposed and will certainly gain a great deal of attraction in the near future.

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“…Interestingly, in Culcasi et al 77 after micromolar doses of nano-CeO 2 were applied to human fibroblasts, the membrane NADPH oxidase activation occurred. The cytotoxic effects may be caused by the activation of both the mitochondrial and Nox2-and Nox4-dependent NADPH oxidase complexes.…”

mentioning

confidence: 99%

Central nervous system toxicity of metallic nanoparticles

Feng¹,

Chen²,

Zhang³

et al. 2015

IJN

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Nanomaterials (NMs) are increasingly used for the therapy, diagnosis, and monitoring of disease- or drug-induced mechanisms in the human biological system. In view of their small size, after certain modifications, NMs have the capacity to bypass or cross the blood–brain barrier. Nanotechnology is particularly advantageous in the field of neurology. Examples may include the utilization of nanoparticle (NP)-based drug carriers to readily cross the blood–brain barrier to treat central nervous system (CNS) diseases, nanoscaffolds for axonal regeneration, nanoelectromechanical systems in neurological operations, and NPs in molecular imaging and CNS imaging. However, NPs can also be potentially hazardous to the CNS in terms of nano-neurotoxicity via several possible mechanisms, such as oxidative stress, autophagy, and lysosome dysfunction, and the activation of certain signaling pathways. In this review, we discuss the dual effect of NMs on the CNS and the mechanisms involved. The limitations of the current research are also discussed.

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EPR spin trapping evaluation of ROS production in human fibroblasts exposed to cerium oxide nanoparticles: Evidence for NADPH oxidase and mitochondrial stimulation

Cited by 69 publications

References 61 publications

Cytotoxicity and Genotoxicity of Ceria Nanoparticles on Different Cell Lines in Vitro

Cytotoxicity and Genotoxicity of Ceria Nanoparticles on Different Cell Lines in Vitro

Intracellular Signal Modulation by Nanomaterials

Central nervous system toxicity of metallic nanoparticles

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