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      Nanoparticles and Neurotoxicity

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          Abstract

          Humans are exposed to nanoparticles (NPs; diameter < 100 nm) from ambient air and certain workplaces. There are two main types of NPs; combustion-derived NPs (e.g., particulate matters, diesel exhaust particles, welding fumes) and manufactured or engineered NPs (e.g., titanium dioxide, carbon black, carbon nanotubes, silver, zinc oxide, copper oxide). Recently, there have been increasing reports indicating that inhaled NPs can reach the brain and may be associated with neurodegeneration. It is necessary to evaluate the potential toxic effects of NPs on brain because most of the neurobehavioral disorders may be of environmental origin. This review highlights studies on both combustion-derived NP- and manufactured or engineered NP-induced neuroinflammation, oxidative stress, and gene expression, as well as the possible mechanism of these effects in animal models and in humans.

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          Probing the Cytotoxicity of Semiconductor Quantum Dots

          Austin M. Derfus, Warren C W Chan, Sangeeta N. Bhatia (2004)
          With their bright, photostable fluorescence, semiconductor quantum dots show promise as alternatives to organic dyes for biological labeling. Questions about their potential cytotoxicity, however, remain unanswered. While cytotoxicity of bulk cadmium selenide (CdSe) is well documented, a number of groups have suggested that CdSe QDs are cytocompatible, at least with some immortalized cell lines. Using primary hepatocytes as a liver model, we found that CdSe-core QDs were indeed acutely toxic under certain conditions. Specifically, we found that the cytotoxicity of QDs was modulated by processing parameters during synthesis, exposure to ultraviolet light, and surface coatings. Our data further suggests that cytotoxicity correlates with the liberation of free Cd2+ ions due to deterioration of the CdSe lattice. When appropriately coated, CdSe-core QDs can be rendered non-toxic and used to track cell migration and reorganization in vitro. Our results inform design criteria for the use of QDs in vitro and especially in vivo where deterioration over time may occur.
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            Size-dependent proinflammatory effects of ultrafine polystyrene particles: a role for surface area and oxidative stress in the enhanced activity of ultrafines.

            D. Brown, M. Wilson, W MacNee … (2001)
            Studies into the effects of ultrafine particles in the lung have shown adverse effects considered to be due in part to the particle size. Air pollution particles (PM(10)) are associated with exacerbations of respiratory disease and deaths from cardiovascular causes in epidemiological studies and the ultrafine fraction of PM(10) has been hypothesized to play an important role. The aim of the present study was to investigate proinflammatory responses to various sizes of polystyrene particles as a simple model of particles of varying size including ultrafine. In the animal model, we demonstrated that there was a significantly greater neutrophil influx into the rat lung after instillation of 64-nm polystyrene particles compared with 202- and 535-nm particles and this was mirrored in other parameters of lung inflammation, such as increased protein and lactate dehydrogenase in bronchoalveolar lavage. When surface area instilled was plotted against inflammation, these two variables were directly proportional and the line passed through zero. This suggests that surface area drives inflammation in the short term and that ultrafine particles cause a greater inflammatory response because of the greater surface area they possess. In vitro, we measured the changes in intracellular calcium concentration in mono mac 6 cells in view of the potential role of calcium as a signaling molecule. Calcium changes after particle exposure may be important in leading to proinflammatory gene expression such as chemokines. We demonstrated that only ultrafine polystyrene particles induced a significant increase in cytosolic calcium ion concentration. Experiments using dichlorofluorescin diacetate demonstrated greater oxidant activity of the ultrafine particles, which may explain their activity in these assays. There were significant increases in IL-8 gene expression in A549 epithelial cells after treatment with the ultrafine particles but not particles of other sizes. These findings suggest that ultrafine particles composed of low-toxicity material such as polystyrene have proinflammatory activity as a consequence of their large surface area. This supports a role for such particles in the adverse health effects of PM(10). Copyright 2001 Academic Press.
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              Manufactured Nanomaterials (Fullerenes, C60) Induce Oxidative Stress in the Brain of Juvenile Largemouth Bass

              Eva Oberdörster (2004)
              Although nanotechnology has vast potential in uses such as fuel cells, microreactors, drug delivery devices, and personal care products, it is prudent to determine possible toxicity of nanotechnology-derived products before widespread use. It is likely that nanomaterials can affect wildlife if they are accidentally released into the environment. The fullerenes are one type of manufactured nanoparticle that is being produced by tons each year, and initially uncoated fullerenes can be modified with biocompatible coatings. Fullerenes are lipophilic and localize into lipid-rich regions such as cell membranes in vitro, and they are redox active. Other nano-sized particles and soluble metals have been shown to selectively translocate into the brain via the olfactory bulb in mammals and fish. Fullerenes (C60) can form aqueous suspended colloids (nC60); the question arises of whether a redox-active, lipophilic molecule could cause oxidative damage in an aquatic species. The goal of this study was to investigate oxyradical-induced lipid and protein damage, as well as impacts on total glutathione (GSH) levels, in largemouth bass exposed to nC60. Significant lipid peroxidation was found in brains of largemouth bass after 48 hr of exposure to 0.5 ppm uncoated nC60. GSH was also marginally depleted in gills of fish, and nC60 increased water clarity, possibly due to bactericidal activity. This is the first study showing that uncoated fullerenes can cause oxidative damage and depletion of GSH in vivo in an aquatic species. Further research needs to be done to evaluate the potential toxicity of manufactured nanomaterials, especially with respect to translocation into the brain.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Mol Sci
                Journal ID (publisher-id): ijms
                Title: International Journal of Molecular Sciences
                Publisher: Molecular Diversity Preservation International (MDPI)
                ISSN (Electronic): 1422-0067
                Publication date Collection: 2011
                Publication date (Electronic): 23 September 2011
                Volume: 12
                Issue: 9
                Pages: 6267-6280
                Affiliations
                [1 ]Center for Environmental Health Sciences, National Institute for Environmental Studies, 16-2 Onogawa, Tsukuba, Ibaraki 305-8506, Japan
                [2 ]Center for Environmental Risk Research, National Institute for Environmental Studies, 16-2 Onogawa, Tsukuba, Ibaraki 305-8506, Japan; E-Mail: fujimaki@ 123456nies.go.jp
                Author notes
                [* ]Author to whom correspondence should be addressed; E-Mail: tin.tin.win.shwe@ 123456nies.go.jp ; Tel.: +81-29-850-2334 (ext. 2542); Fax: +81-29-850-2334.
                Article
                Publisher ID: ijms-12-06267
                DOI: 10.3390/ijms12096267
                PMC ID: 3189781
                PubMed ID: 22016657
                SO-VID: 38e18c68-34a3-432e-b024-87b296f2064c
                Copyright © © 2011 by the authors; licensee MDPI, Basel, Switzerland.
                License:

                This article is an open-access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/3.0/).

                History
                Date received : 8 August 2011
                Date revision received : 12 September 2011
                Date accepted : 19 September 2011
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular biology
                Keywords: brain,neurotoxicity,nanoparticles,oxidative stress,neuroinflammation
                Data availability:
                ScienceOpen disciplines: Molecular biology
                Keywords: brain, neurotoxicity, nanoparticles, oxidative stress, neuroinflammation

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