Efficacy of Simple Short-Term
            <i>in Vitro</i>
            Assays for Predicting the Potential of Metal Oxide Nanoparticles to Cause Pulmonary Inflammation

Lu, Shengyong; Duffin, Rodger; Poland, Craig A.; Daly, Paul; Murphy, Fiona; Drost, Ellen; MacNee, William; Stone, Vicki; Donaldson, Kenneth

doi:10.1289/ehp.11811

Cited by 238 publications

(187 citation statements)

References 33 publications

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“…With regard to the inflammatory effect of NiO, we carried out an intratracheal instillation study of nanoscale NiO nanoparticles and reported that they caused persistent pulmonary inflammation with a low dose 13,14) . Lu et al 15) also reported that NiO nanoparticles caused pulmonary inflammation in their intratracheal instillation study in mice. On the other hand, with regard to the inflammatory effect of TiO 2 nanoparticles, Warheit et al 16) reported that their intratracheal instillation study showed only transient inflammation in lung tissue.…”

Section: Discussionmentioning

confidence: 94%

Investigation of Gene Expression of MMP-2 and TIMP-2 mRNA in Rat Lung in Inhaled Nickel Oxide and Titanium Dioxide Nanoparticles

et al. 2011

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In order to investigate whether or not dispersed nanoparticles have an effect of inflammation and fibrosis on animals, we developed a nanoparticle generation system and examined the gene expression of matrix metalloproteinase (MMP) and tissue inhibitor matrix proteinase (TIMP) in rat lung containing inhaled nickel oxide (NiO) or titanium dioxide (TiO 2 ) nanoparticles. In both experiments, Wistar male rats were exposed to NiO or TiO 2 nanoparticles for 4 wk (6 h/day). The geometric mean diameters of NiO and TiO 2 in the chamber were 139 ± 12 nm and 51 ± 9 nm, respectively. The average concentration of the particle number of NiO and TiO 2 was 1.0E+05 /cm 3 and 2.8E+05 /cm 3 , respectively. At 4 d, 1 and 3 months after the end of the inhalation, the rats exposed to these particles were sacrificed and the gene expressions of MMP-2, TIMP-2 and type I collagen were measured using RT-PCR. Pathological finding revealed that there was minimum inflammation with nickel oxide only at 4 d and no change with titanium oxide. However, there were no changes of the gene expression of MMP-2, TIMP-2, and type I collagen in either the NiO or TiO 2 exposure groups. In this study, inhalation of nickel oxide and titanium dioxide nanoparticles did not induce the gene expression of MMP-2 and TIMP-2 mRNA in rat lungs.

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Section: Discussionmentioning

confidence: 94%

Investigation of Gene Expression of MMP-2 and TIMP-2 mRNA in Rat Lung in Inhaled Nickel Oxide and Titanium Dioxide Nanoparticles

et al. 2011

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“…26 It was used RBCs from preserved human blood, obtained from the Hemocenter of Campinas at the University of Campinas (Unicamp). A volume of 8 mL of blood was added to 0.8 mL of a 3.8% sodium citrate solution in a 15 mL Falcon tube to prevent coagulation.…”

Section: Hemolysis Assaymentioning

confidence: 99%

Suppression of the hemolytic effect of mesoporous silica nanoparticles after protein corona interaction: independence of the surface microchemical environment

Paula¹,

Martinez²,

Júnior³

et al. 2012

J. Braz. Chem. Soc.

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Nanopartículas mesoporosas de sílica são conhecidas por induzirem hemólise de células vermelhas do sangue (RBCs) humano quando ensaios de citotoxicidade são feitos em solução-tampão de fosfato (PBS). Entretanto, em uma abordagem mais realista, a presença de biomoléculas do plasma sanguíneo precisa ser considerada em qualquer avaliação nanotoxicológica de nanopartículas porosas de SiO 2 quando se objetiva a sua utilização em aplicações biomédicas através de administração intravenosa. Nesse contexto, demonstrou-se neste trabalho que nanopartículas porosas de sílica não induzem nenhum efeito citotóxico em células vermelhas do sangue quando ensaios de hemólise são feitos na presença de plasma sanguíneo, independentemente da carga superficial (positiva ou negativa) da nanopartícula. A ausência de hemólise está principalmente associada à adsorção de proteínas do plasma sobre a superfície das nanopartículas, levando à formação de um recobrimento proteico estável (denominado protein corona ou PC) que blinda o ambiente microquímico original das nanopartículas.Mesoporous silica nanoparticles are known to induce the hemolysis of human red blood cells (RBCs) when citotoxicity assays are performed in a phosphate buffer solution (PBS). However, in a more realistic approach, the presence of blood plasma biomolecules must be considered in any nanotoxicological evaluation of porous SiO 2 nanoparticles when biomedical applications through intravenous administration are aimed. In this context, it is demonstrated in this work that porous silica nanoparticles do not induce any cytotoxic effect on RBCs when hemolysis assay is done in the presence of blood plasma, regardless the surface charge (positive or negative) of the nanoparticle. The absence of hemolysis is mainly associated with the adsorption of plasma proteins on the nanoparticle surface, which leads to the formation of a stable protein coating (called protein corona or PC) that shields the original microchemical environment of bare nanoparticles.Keywords: nanoparticles, SiO 2 , mesopores, hemolytic effect, protein corona IntroductionSince porous silica nanoparticles were elected as possible protagonists in a future revolution of several medical processes of theranosis, they have been widely studied during the last decade through the host-guest approach, thus resulting in promising perspectives mainly in the areas of detection 1-3 and treatment of tumors. [4][5][6][7] While part of the scientific community creatively advances towards the engineering of porous silica nanostructures, others are acting in a proactive approach by considering environmental and toxicological effects of nano-based silica materials. In the latter context, several in vitro citotoxicity assays indicated a very high biocompatibility of porous silica nanoparticles. [8][9][10] However, a desirable in vivo biocompatibility is not straightforward. For instance, it is well known that amorphous silica particles induce toxicity on human red blood cells (RBCs) and, consequently, this test is being used as a ke...

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“…Also, lipid peroxidation was observed in cells exposed to metal oxide nanoparticles 30) . In vivo inhalation of NiO induced severe toxic effects such as inflammation and collagen deposition in the lung [31][32][33] . Although some investigations of the toxic effect of nanoparticles in vivo have been performed 34,35) , details of biological responses induced by NiO nanoparticles are still unclear.…”

mentioning

confidence: 99%

Evaluation of Acute Oxidative Stress Induced by NiO Nanoparticles In Vivo and In Vitro

Horie

Fukui

Nishio

et al. 2011

Journal of Occupational Health

100

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Evaluation of Acute Oxidative Stress Induced by NiO Nanoparticles In Vivo and In Vitro:Masanori Horie, et al. Health Research Institute -Objectives: Nickel oxide (NiO) is an important industrial material, and it is also a harmful agent. The toxicity of NiO is size-related: nanoparticles are more toxic than fine-particles. The toxic mechanism induced by NiO nanoparticles remains unexplained, and the relationship between in vitro and in vivo NiO toxicity results is unclear. In the present study, we focused on the oxidative stress caused by NiO nanoparticles by examining and comparing in vitro and in vivo acute responses induced by NiO nanoparticles. Methods: Cellular responses induced by black NiO nanoparticles with a primary particle size of 20 nm, were examined in human lung carcinoma A549 cells. In vivo responses were examined by instillation of NiO nanoparticles into rat trachea. Bronchoalveolar lavage fluid (BALF) was collected after intratracheal instillation at different time points, and concentrations of lipid peroxide heme oxygenase-1 (HO-1), surfactant protein-D (SP-D) and lactate dehydrogenase (LDH) in BALF were measured. Results: The levels of intracellular reactive oxygen species and lipid peroxidation in A549 cells increased with increasing exposure to NiO nanoparticles, and increases in gene expressions of HO-1 and SP-D were observed in A549 cells. The lipid peroxide level in BALF significantly increased after 24 h instillation but decreased three days later. LDH leakage was also observed three days later. Conclusions: NiO nanoparticles induce oxidative stress-related lung injury. In vivo and in vitro oxidative stress was induced resulting in activation of antioxidant systems. Based on these responses, we conclude that the results of the in vivo and in vitro studies tend to correspond. (J Occup Health 2011; 53: 64-74)

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Efficacy of Simple Short-Term in Vitro Assays for Predicting the Potential of Metal Oxide Nanoparticles to Cause Pulmonary Inflammation

Cited by 238 publications

References 33 publications

Investigation of Gene Expression of MMP-2 and TIMP-2 mRNA in Rat Lung in Inhaled Nickel Oxide and Titanium Dioxide Nanoparticles

Investigation of Gene Expression of MMP-2 and TIMP-2 mRNA in Rat Lung in Inhaled Nickel Oxide and Titanium Dioxide Nanoparticles

Suppression of the hemolytic effect of mesoporous silica nanoparticles after protein corona interaction: independence of the surface microchemical environment

Evaluation of Acute Oxidative Stress Induced by NiO Nanoparticles In Vivo and In Vitro

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