A review of mammalian toxicity of ZnO nanoparticles

Rob J Vandebriel, Wim H De JongLaboratory for Health Protection Research, National Institute for Public Health and the Environment, Bilthoven, The NetherlandsAbstract: This review summarizes the literature on mammalian toxicity of ZnO nanoparticles (NPs) published between 2009 and 2011. The toxic ef...

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Autores principales:	Vandebriel RJ, De Jong WH
Formato:	article
Lenguaje:	EN
Publicado:	Dove Medical Press 2012
Materias:	Medical technology R855-855.5 Chemical technology TP1-1185
Acceso en línea:	https://doaj.org/article/a582d71a5a9d41a3bc279038cf280691
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spelling	oai:doaj.org-article:a582d71a5a9d41a3bc279038cf2806912021-12-02T02:50:25ZA review of mammalian toxicity of ZnO nanoparticles1177-8903https://doaj.org/article/a582d71a5a9d41a3bc279038cf2806912012-08-01T00:00:00Zhttp://www.dovepress.com/a-review-of-mammalian-toxicity-of-zno-nanoparticles-a10711https://doaj.org/toc/1177-8903Rob J Vandebriel, Wim H De JongLaboratory for Health Protection Research, National Institute for Public Health and the Environment, Bilthoven, The NetherlandsAbstract: This review summarizes the literature on mammalian toxicity of ZnO nanoparticles (NPs) published between 2009 and 2011. The toxic effects of ZnO NPs are due to the compound&#39;s solubility. Whether the increased intracellular [Zn2+] is due to the NPs being taken up by cells or to NP dissolution in medium is still unclear. In vivo airway exposure poses an important hazard. Inhalation or instillation of the NPs results in lung inflammation and systemic toxicity. Reactive oxygen species (ROS) generation likely plays an important role in the inflammatory response. The NPs do not, or only to a minimal extent, cross the skin; this also holds for sunburned skin. Intraperitoneal administration induces neurological effects. The NPs show systemic distribution; target organs are liver, spleen, lung, and kidney and, in some cases, the heart. In vitro exposure of BEAS-2B bronchial epithelial cells and A549 alveolar adenocarcinoma cells results in cytotoxicity, increased oxidative stress, increased intracellular [Ca2+], decreased mitochondrial membrane potential, and interleukin (IL)-8 production. Decreased contractility of airway smooth muscle cells poses an additional hazard. In contrast to the results for BEAS-2B and A549 cells, in RKO colon carcinoma cells ZnO NPs and not Zn2+ induce cytotoxicity and mitochondrial dysfunction. Short-term exposure of skin cells results in apoptosis but not in an inflammatory response, while long-term exposure leads to increased ROS generation, decreased mitochondrial activity, and formation of tubular intercellular structures. Macrophages, monocytes, and dendritic cells are affected; exposure results in cytotoxicity, oxidative stress, intracellular Ca2+ flux, decreased mitochondrial membrane potential, and production of IL-1&beta; and chemokine CXCL9. The NPs are phagocytosed by macrophages and dissolved in lysosomes. In vitro the Comet assay and the cytokinesis-blocked micronucleus assay show genotoxicity, whereas the Ames test does not. This is, however, not confirmed by in vivo genotoxicity assays. Protein binding results in increased stability.Keywords: solubility, inflammation, reactive oxygen species, intracellular calcium, mitochondrial membrane potential, lysosomesVandebriel RJDe Jong WHDove Medical PressarticleMedical technologyR855-855.5Chemical technologyTP1-1185ENNanotechnology, Science and Applications, Vol 2012, Iss default, Pp 61-71 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medical technology R855-855.5 Chemical technology TP1-1185
spellingShingle	Medical technology R855-855.5 Chemical technology TP1-1185 Vandebriel RJ De Jong WH A review of mammalian toxicity of ZnO nanoparticles
description	Rob J Vandebriel, Wim H De JongLaboratory for Health Protection Research, National Institute for Public Health and the Environment, Bilthoven, The NetherlandsAbstract: This review summarizes the literature on mammalian toxicity of ZnO nanoparticles (NPs) published between 2009 and 2011. The toxic effects of ZnO NPs are due to the compound&#39;s solubility. Whether the increased intracellular [Zn2+] is due to the NPs being taken up by cells or to NP dissolution in medium is still unclear. In vivo airway exposure poses an important hazard. Inhalation or instillation of the NPs results in lung inflammation and systemic toxicity. Reactive oxygen species (ROS) generation likely plays an important role in the inflammatory response. The NPs do not, or only to a minimal extent, cross the skin; this also holds for sunburned skin. Intraperitoneal administration induces neurological effects. The NPs show systemic distribution; target organs are liver, spleen, lung, and kidney and, in some cases, the heart. In vitro exposure of BEAS-2B bronchial epithelial cells and A549 alveolar adenocarcinoma cells results in cytotoxicity, increased oxidative stress, increased intracellular [Ca2+], decreased mitochondrial membrane potential, and interleukin (IL)-8 production. Decreased contractility of airway smooth muscle cells poses an additional hazard. In contrast to the results for BEAS-2B and A549 cells, in RKO colon carcinoma cells ZnO NPs and not Zn2+ induce cytotoxicity and mitochondrial dysfunction. Short-term exposure of skin cells results in apoptosis but not in an inflammatory response, while long-term exposure leads to increased ROS generation, decreased mitochondrial activity, and formation of tubular intercellular structures. Macrophages, monocytes, and dendritic cells are affected; exposure results in cytotoxicity, oxidative stress, intracellular Ca2+ flux, decreased mitochondrial membrane potential, and production of IL-1&beta; and chemokine CXCL9. The NPs are phagocytosed by macrophages and dissolved in lysosomes. In vitro the Comet assay and the cytokinesis-blocked micronucleus assay show genotoxicity, whereas the Ames test does not. This is, however, not confirmed by in vivo genotoxicity assays. Protein binding results in increased stability.Keywords: solubility, inflammation, reactive oxygen species, intracellular calcium, mitochondrial membrane potential, lysosomes
format	article
author	Vandebriel RJ De Jong WH
author_facet	Vandebriel RJ De Jong WH
author_sort	Vandebriel RJ
title	A review of mammalian toxicity of ZnO nanoparticles
title_short	A review of mammalian toxicity of ZnO nanoparticles
title_full	A review of mammalian toxicity of ZnO nanoparticles
title_fullStr	A review of mammalian toxicity of ZnO nanoparticles
title_full_unstemmed	A review of mammalian toxicity of ZnO nanoparticles
title_sort	review of mammalian toxicity of zno nanoparticles
publisher	Dove Medical Press
publishDate	2012
url	https://doaj.org/article/a582d71a5a9d41a3bc279038cf280691
work_keys_str_mv	AT vandebrielrj areviewofmammaliantoxicityofznonanoparticles AT dejongwh areviewofmammaliantoxicityofznonanoparticles AT vandebrielrj reviewofmammaliantoxicityofznonanoparticles AT dejongwh reviewofmammaliantoxicityofznonanoparticles
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A review of mammalian toxicity of ZnO nanoparticles

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