A practical approach to assess inhalation toxicity of metal oxide nanoparticles in vitro (original) (raw)
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Comparative effects of metal oxide nanoparticles on human airway epithelial cells and macrophages
Journal of Nanoparticle Research, 2012
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Particle and Fibre Toxicology
Background Acute phase response (APR) is characterized by a change in concentration of different proteins, including C-reactive protein and serum amyloid A (SAA) that can be linked to both exposure to metal oxide nanomaterials and risk of cardiovascular diseases. In this study, we intratracheally exposed mice to ZnO, CuO, Al2O3, SnO2 and TiO2 and carbon black (Printex 90) nanomaterials with a wide range in phagolysosomal solubility. We subsequently assessed neutrophil numbers, protein and lactate dehydrogenase activity in bronchoalveolar lavage fluid, Saa3 and Saa1 mRNA levels in lung and liver tissue, respectively, and SAA3 and SAA1/2 in plasma. Endpoints were analyzed 1 and 28 days after exposure, including histopathology of lung and liver tissues. Results All nanomaterials induced pulmonary inflammation after 1 day, and exposure to ZnO, CuO, SnO2, TiO2 and Printex 90 increased Saa3 mRNA levels in lungs and Saa1 mRNA levels in liver. Additionally, CuO, SnO2, TiO2 and Printex 90 in...
Future Science OA, 2016
Nanoparticles (Nps) can induce toxicity in the lung by accidental or intentional exposure. The main objective of the study reported here was to characterize the effect that four metal oxide Nps (CeO2, TiO2, Al2O3 and ZnO) had at the cellular level on a human lung epithelial cell line. This goal was achieved by studying the capacity of the Nps to activate the main mitogen-activated protein kinases (MAPKs) and the nuclear factor NFκB. Only ZnO Nps were able to activate all of the MAPKs and the release of Zn2+ ions was the main cause of activation. ZnO and Al2O3 Nps activated the NFκB pathway and induced the release of inflammatory cytokines. CeO2 and TiO2 Nps were found to have safer profiles. [Formula: see text] The graphical abstract was obtained using Servier Medical Art.
Metal oxide nanoparticles induce cytotoxic effects on human lung epithelial cells A549
Incerasing in production and exposure to engineered nanoparticles (NPs), make necessary to acquire information about NP potential adverse health effects. Many studies, focused on NP toxicity, highlighted their cytotoxic potential but there is a still a lack of information about the biological mechanisms involved. The aim of this research is the comparison of cytotoxicity between two types of metal nanoxides (CuO and TiO(2)) on A549 cells. After physico-chemical characterization, NPs were administered to cells. Cell-particle interactions, membrane integrity, viability and oxidative stress were investigated. CuO exposure resulted in a significant reduction of cell viability, while no effects were observed after TiO(2) exposure. Both NPs induced cell cycle alteration, with a significant increase in frequency of cells in G1 and G2/M phases for TiO(2) and CuO respectively. Confocal microscopy detected NPs at different cellular levels, and TEM imaging highlighted their ability to be inter...
Metal oxide nanoparticles interact with immune cells and activate different cellular responses
International Journal of Nanomedicine, 2016
Besides cell death, nanoparticles (Nps) can induce other cellular responses such as inflammation. The potential immune response mediated by the exposure of human lymphoid cells to metal oxide Nps (moNps) was characterized using four different moNps (CeO 2 , TiO 2 , Al 2 O 3 , and ZnO) to study the three most relevant mitogen-activated protein kinase subfamilies and the nuclear factor kappa-light-chain-enhancer of the activated B-cell inhibitor, IκBα, as well as the expression of several genes by immune cells incubated with these Nps. The moNps activated different signaling pathways and altered the gene expression in human lymphocyte cells. The ZnO Nps were the most active and the release of Zn 2+ ions was the main mechanism of toxicity. CeO 2 Nps induced the smallest changes in gene expression and in the IκBα protein. The effects of the particles were strongly dependent on the type and concentration of the Nps and on the cell activation status prior to Np exposure.
2013
Background: Hazard identification for risk assessment of nanoparticles (NPs) is mainly composed of in vitro cellbased assays and in vivo animal experimentation. The rapidly increasing number and functionalizations of NPs makes in vivo toxicity tests undesirable on both ethical and financial grounds, creating an urgent need for development of in vitro cell-based assays that accurately predict in vivo toxicity and facilitate safe nanotechnology.
Environmental Health Perspectives, 2006
The mechanisms governing the correlation between exposure to ultrafine particles and the increased incidence of cardiovascular disease remain unknown. Ultrafine particles appear to cross the pulmonary epithelial barrier into the bloodstream, raising the possibility of direct contact with the vascular endothelium. OBJECTIVES: Because endothelial inflammation is critical for the development of cardiovascular pathology, we hypothesized that direct exposure of human aortic endothelial cells (HAECs) to ultrafine particles induces an inflammatory response and that this response depends on particle composition. METHODS: To test the hypothesis, we incubated HAECs for 1-8 hr with different concentrations (0.001-50 µg/mL) of iron oxide (Fe 2 O 3 ), yttrium oxide (Y 2 O 3 ), and zinc oxide (ZnO) nanoparticles and subsequently measured mRNA and protein levels of the three inflammatory markers intracellular cell adhesion molecule-1, interleukin-8, and monocyte chemotactic protein-1. We also determined nanoparticle interactions with HAECs using inductively coupled plasma mass spectrometry and transmission electron microscopy. RESULTS: Our data indicate that nanoparticle delivery to the HAEC surface and uptake within the cells correlate directly with particle concentration in the cell culture medium. All three types of nanoparticles are internalized into HAECs and are often found within intracellular vesicles. Fe 2 O 3 nanoparticles fail to provoke an inflammatory response in HAECs at any of the concentrations tested; however, Y 2 O 3 and ZnO nanoparticles elicit a pronounced inflammatory response above a threshold concentration of 10 µg/mL. At the highest concentration, ZnO nanoparticles are cytotoxic and lead to considerable cell death. CONCLUSIONS: These results demonstrate that inflammation in HAECs following acute exposure to metal oxide nanoparticles depends on particle composition.
Frontiers in Immunology
Copper oxide nanoparticles (CuO NPs) are increasingly used in various industry sectors. Moreover, medical application of CuO NPs as antimicrobials also contributes to human exposure. Their toxicity, including toxicity to the immune system and blood, raises concerns, while information on their immunotoxicity is still very limited. The aim of our work was to evaluate the effects of CuO NPs (number concentration 1.40×106 particles/cm3, geometric mean diameter 20.4 nm) on immune/inflammatory response and antioxidant defense in mice exposed to 32.5 µg CuO/m3 continuously for 6 weeks. After six weeks of CuO NP inhalation, the content of copper in lungs and liver was significantly increased, while in kidneys, spleen, brain, and blood it was similar in exposed and control mice. Inhalation of CuO NPs caused a significant increase in proliferative response of T-lymphocytes after mitogenic stimulation and basal proliferative activity of splenocytes. CuO NPs significantly induced the production...