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      Nanomaterials: health effects and legislation Translated title: Efectos de los nanomateriales en la salud y su normatividad

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          Abstract

          The mechanisms by which nanomaterials interact with biological systems is not well understood and although the benefits of some nanomaterials are evident, some offset effects on health and the environment may occur; however, scientific information is scarce. This document gives a brief description of the effects of nanomaterials on health and the current tendencies in developing the pertinent regulations.

          Translated abstract

          La forma como los materiales nanométricos interactúan con sistemas biológicos es poco conocida, y aunque los beneficios de algunos nanomateriales son evidentes también existe la posibilidad de que algunos puedan ser nocivos para la salud y el medio ambiente; sin embargo, la información científica sobre los efectos de los nanomateriales en estos ámbitos es escasa. Este documento hace una breve descripción de los efectos en la salud de los nanomateriales y los desarrollos legislativos concernientes a su regulación.

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          Most cited references94

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          In vitro cytotoxicity testing of polycations: influence of polymer structure on cell viability and hemolysis.

          A comparative in vitro cytotoxicity study with different water-soluble, cationic macromolecules which have been described as gene delivery systems was performed. Cytotoxicity in L929 mouse fibroblasts was monitored using the MTT assay and the release of the cytosolic enzyme lactate dehydrogenase (LDH). Microscopic observations were carried out as indicators for cell viability. Furthermore, hemolysis of erythrocytes was quantified spectrophotometrically. To determine the nature of cell death induced by the polycations, the nuclear morphology after DAPI staining and the inhibition of the toxic effects by the caspase inhibitor zVAD.fmk were investigated. All assays yielded comparable results and allowed the following ranking of the polymers with regard to cytotoxicity: Poly(ethylenimine)=poly(L-lysine)>poly(diallyl-dimethyl-ammonium chloride)>diethylaminoethyl-dextran>poly(vinyl pyridinium bromide)>Starburst dendrimer>cationized albumin>native albumin. The magnitude of the cytotoxic effects of all polymers were found to be time- and concentration dependent. The molecular weight as well as the cationic charge density of the polycations were confirmed as key parameters for the interaction with the cell membranes and consequently, the cell damage. Evaluating the nature of cell death induced by poly(ethylenimine), we did not detect any indication for apoptosis suggesting that the polymer induced a necrotic cell reaction. Cell nuclei retained their size, chromatin was homogenously distributed and cell membranes lost their integrity very rapidly at an early stage. Furthermore, the broad spectrum caspase inhibitor zVAD.fmk did not inhibit poly(ethylenimine)-induced cell damage. Insights into the structure-toxicity relationship are necessary to optimize the cytotoxicity and biocompatibility of non-viral gene delivery systems.
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            Acute toxicity and biodistribution of different sized titanium dioxide particles in mice after oral administration.

            In order to evaluate the toxicity of TiO(2) particles, the acute toxicity of nano-sized TiO(2) particles (25 and 80nm) on adult mice was investigated compared with fine TiO(2) particles (155nm). Due to the low toxicity, a fixed large dose of 5g/kg body weight of TiO(2) suspensions was administrated by a single oral gavage according to the OECD procedure. In 2 weeks, TiO(2) particles showed no obvious acute toxicity. However, the female mice showed high coefficients of liver in the nano-sized (25 and 80nm) groups. The changes of serum biochemical parameters (ALT/AST, LDH) and pathology (hydropic degeneration around the central vein and the spotty necrosis of hepatocytes) of liver indicated that the hepatic injury was induced after exposure to mass different-sized TiO(2) particles. In addition, the nephrotoxicity like increased BUN level and pathology change of kidneys was also observed in the experimental groups. The significant change of serum LDH and alpha-HBDH in 25 and 80nm groups showed the myocardial damage compared with the control group. However, there are no abnormal pathology changes in the heart, lung, testicle (ovary), and spleen tissues. Biodistribution experiment showed that TiO(2) mainly retained in the liver, spleen, kidneys, and lung tissues, which indicated that TiO(2) particles could be transported to other tissues and organs after uptake by gastrointestinal tract.
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              Titanium dioxide nanoparticles induce DNA damage and genetic instability in vivo in mice.

              Titanium dioxide (TiO(2)) nanoparticles are manufactured worldwide in large quantities for use in a wide range of applications including pigment and cosmetic manufacturing. Although TiO(2) is chemically inert, TiO(2) nanoparticles can cause negative health effects, such as respiratory tract cancer in rats. However, the mechanisms involved in TiO(2)-induced genotoxicity and carcinogenicity have not been clearly defined and are poorly studied in vivo. The present study investigates TiO(2) nanoparticles-induced genotoxicity, oxidative DNA damage, and inflammation in a mice model. We treated wild-type mice with TiO(2) nanoparticles in drinking water and determined the extent of DNA damage using the comet assay, the micronuclei assay, and the gamma-H2AX immunostaining assay and by measuring 8-hydroxy-2'-deoxyguanosine levels and, as a genetic instability endpoint, DNA deletions. We also determined mRNA levels of inflammatory cytokines in the peripheral blood. Our results show that TiO(2) nanoparticles induced 8-hydroxy-2'-deoxyguanosine, gamma-H2AX foci, micronuclei, and DNA deletions. The formation of gamma-H2AX foci, indicative of DNA double-strand breaks, was the most sensitive parameter. Inflammation was also present as characterized by a moderate inflammatory response. Together, these results describe the first comprehensive study of TiO(2) nanoparticles-induced genotoxicity in vivo in mice possibly caused by a secondary genotoxic mechanism associated with inflammation and/or oxidative stress. Given the growing use of TiO(2) nanoparticles, these findings raise concern about potential health hazards associated with TiO(2) nanoparticles exposure.
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                Author and article information

                Journal
                iei
                Ingeniería e Investigación
                Ing. Investig.
                Facultad de Ingeniería, Universidad Nacional de Colombia. (Bogotá, Distrito Capital, Colombia )
                0120-5609
                January 2012
                : 32
                : 1
                : 36-41
                Affiliations
                [01] orgnameUniversidad Nacional de Colombia hrzear@ 123456unal.edu.co
                Article
                S0120-56092012000100007 S0120-5609(12)03200107
                464095cc-6d62-45cd-87e2-85966af343b0

                This work is licensed under a Creative Commons Attribution 4.0 International License.

                History
                : 27 February 2012
                : 06 September 2011
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 60, Pages: 6
                Product

                SciELO Colombia

                Categories
                New knowledge papers

                legislation,health effects,Nanomaterials,legislación,efectos sobre la salud,nanomateriales

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