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Cellular Toxicity of Nanoparticles

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Toxicology".

Deadline for manuscript submissions: closed (29 February 2016) | Viewed by 62454

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Special Issue Editors

Dr. Michael N. Routledge

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Guest Editor

1. Leeds Institute of Cardiovascular and Metabolic Medicine, School of Medicine, University of Leeds, LS2 9JT Leeds, UK
2. School of Food and Biological Engineering, Jiangsu University, Zhenjiang, China
Interests: environmental toxicology; biomarkers of exposure; aflatoxin exposure and health; mycotoxins; nanoparticle toxicity; air pollution particulate toxicit

Prof. Dr. Bing Yan

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Guest Editor

Key Laboratory for Water Quality and Conservation of the Pearl River Delta, Institute of Environmental Research at Greater Bay, Ministry of Education, Guangzhou University, Guangzhou 510006, China
Interests: nanomedicine; nanotoxicology; environmental safety; environmental toxicology; theranostics; imaging; nanoparticle library; nanoparticle modification; surface modification; chemical biology
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Special Issue Information

Dear Colleagues,

The realization that the properties of nano-sized materials provide many advantages over existing materials with the same chemical composition has led to a nanotechnology revolution, with the development, manufacture, and application of engineered nanoparticles across a range of commercial products, including textiles, detergents, food packaging, paints, and cosmetics. With increasing potential exposure to humans and the environment, which result from the widespread use of nanoparticles in a range of products, it has become recognized that there needs to be a greater understanding of the toxicity of these nanoparticles so as to inform risk assessments and regulations. Underpinning this need for greater understanding is the evidence that environmental exposures to ultrafine particles (in the nanoparticle size range) from the combustion of fossil fuels, including traffic exhaust emissions, are associated with a number of human diseases. Fundamental to understanding the toxicity of nanoparticles from all sources is the study of how nanoparticles interact with, enter, and damage cells. Research papers in this field have increased exponentially over the last decade and there is increasing recognition of the need for an integrated approach between toxicologists, cell biologists, and microscopists, so as to maximize the understanding of how nanoparticles interact with cells, enter cells, and damage cells. The scope of this Special Issue brings together papers from international experts in the cellular toxicity of nanoparticles, who are working in areas of both human toxicology and ecotoxicology, so as to explore the mechanisms of uptake and toxicity of different types of nanoparticles from a range of sources.

Dr. Michael Routledge
Prof. Dr. Bing Yan
Guest Editors

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Keywords

nanotoxicity
engineered nanoparticles
ultrafine particles
environmental exposure
cellular uptake of nanoparticles
nanoparticle cytotoxicity
nanoparticle genotoxicity
ecotoxicology
nanoparticle microscopy

Published Papers (7 papers)

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Research

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10352 KiB

Open AccessArticle

Toxicological Effects of Caco-2 Cells Following Short-Term and Long-Term Exposure to Ag Nanoparticles

by Ni Chen, Zheng-Mei Song, Huan Tang, Wen-Song Xi, Aoneng Cao, Yuanfang Liu and Haifang Wang

Int. J. Mol. Sci. 2016, 17(6), 974; https://doi.org/10.3390/ijms17060974 - 21 Jun 2016

Cited by 47 | Viewed by 8329

Abstract

Extensive utilization increases the exposure of humans to Ag nanoparticles (NPs) via the oral pathway. To comprehensively address the action of Ag NPs to the gastrointestinal systems in real situations, i.e., the long-term low-dose exposure, we evaluated and compared the toxicity of three Ag NPs (20–30 nm with different surface coatings) to the human intestine cell Caco-2 after 1-day and 21-day exposures, using various biological assays. In both the short- and long-term exposures, the variety of surface coating predominated the toxicity of Ag NPs in a descending order of citrate-coated Ag NP (Ag-CIT), bare Ag NP (Ag-B), and poly (N-vinyl-2-pyrrolidone)-coated Ag NP (Ag-PVP). The short-term exposure induced cell growth inhibition and death. The cell viability loss appeared after cells were exposed to 0.7 μg/mL Ag-CIT, 0.9 μg/mL Ag-B or >1.0 μg/mL Ag-PVP for 24 h. The short-term and higher-dose exposure also induced reactive oxygen species (ROS) generation, mitochondrial damage, cell membrane leakage, apoptosis, and inflammation (IL-8 level). The long-term exposure only inhibited the cell proliferation. After 21-day exposure to 0.4 μg/mL Ag-CIT, the cell viability dropped to less than 50%, while cells exposed to 0.5 μg/mL Ag-PVP remained normal as the control. Generally, 0.3 μg/mL is the non-toxic dose for the long-term exposure of Caco-2 cells to Ag NPs in this study. However, cells presented inflammation after exposure to Ag NPs with the non-toxic dose in the long-term exposure. Full article

(This article belongs to the Special Issue Cellular Toxicity of Nanoparticles)

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Inhaled Cadmium Oxide Nanoparticles: Their in Vivo Fate and Effect on Target Organs

by Jana Dumkova, Lucie Vrlikova, Zbynek Vecera, Barbora Putnova, Bohumil Docekal, Pavel Mikuska, Petr Fictum, Ales Hampl and Marcela Buchtova

Int. J. Mol. Sci. 2016, 17(6), 874; https://doi.org/10.3390/ijms17060874 - 03 Jun 2016

Cited by 31 | Viewed by 6674

Abstract

The increasing amount of heavy metals used in manufacturing equivalently increases hazards of environmental pollution by industrial products such as cadmium oxide (CdO) nanoparticles. Here, we aimed to unravel the CdO nanoparticle destiny upon their entry into lungs by inhalations, with the main focus on the ultrastructural changes that the nanoparticles may cause to tissues of the primary and secondary target organs. We indeed found the CdO nanoparticles to be transported from the lungs into secondary target organs by blood. In lungs, inhaled CdO nanoparticles caused significant alterations in parenchyma tissue including hyperemia, enlarged pulmonary septa, congested capillaries, alveolar emphysema and small areas of atelectasis. Nanoparticles were observed in the cytoplasm of cells lining bronchioles, in the alveolar spaces as well as inside the membranous pneumocytes and in phagosomes of lung macrophages. Nanoparticles even penetrated through the membrane into some organelles including mitochondria and they also accumulated in the cytoplasmic vesicles. In livers, inhalation caused periportal inflammation and local hepatic necrosis. Only minor changes such as diffusely thickened filtration membrane with intramembranous electron dense deposits were observed in kidney. Taken together, inhaled CdO nanoparticles not only accumulated in lungs but they were also transported to other organs causing serious damage at tissue as well as cellular level. Full article

(This article belongs to the Special Issue Cellular Toxicity of Nanoparticles)

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1844 KiB

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Titanium Dioxide Particle Type and Concentration Influence the Inflammatory Response in Caco-2 Cells

by Saeko Tada-Oikawa, Gaku Ichihara, Hitomi Fukatsu, Yuka Shimanuki, Natsuki Tanaka, Eri Watanabe, Yuka Suzuki, Masahiko Murakami, Kiyora Izuoka, Jie Chang, Wenting Wu, Yoshiji Yamada and Sahoko Ichihara

Int. J. Mol. Sci. 2016, 17(4), 576; https://doi.org/10.3390/ijms17040576 - 16 Apr 2016

Cited by 43 | Viewed by 6868

Abstract

Titanium dioxide (TiO₂) nanoparticles are widely used in cosmetics, sunscreens, biomedicine, and food products. When used as a food additive, TiO₂ nanoparticles are used in significant amounts as white food-coloring agents. However, the effects of TiO₂ nanoparticles on the gastrointestinal tract remain unclear. The present study was designed to determine the effects of five TiO₂ particles of different crystal structures and sizes in human epithelial colorectal adenocarcinoma (Caco-2) cells and THP-1 monocyte-derived macrophages. Twenty-four-hour exposure to anatase (primary particle size: 50 and 100 nm) and rutile (50 nm) TiO₂ particles reduced cellular viability in a dose-dependent manner in THP-1 macrophages, but in not Caco-2 cells. However, 72-h exposure of Caco-2 cells to anatase (50 nm) TiO₂ particles reduced cellular viability in a dose-dependent manner. The highest dose (50 µg/mL) of anatase (100 nm), rutile (50 nm), and P25 TiO₂ particles also reduced cellular viability in Caco-2 cells. The production of reactive oxygen species tended to increase in both types of cells, irrespective of the type of TiO₂ particle. Exposure of THP-1 macrophages to 50 µg/mL of anatase (50 nm) TiO₂ particles increased interleukin (IL)-1β expression level, and exposure of Caco-2 cells to 50 µg/mL of anatase (50 nm) TiO₂ particles also increased IL-8 expression. The results indicated that anatase TiO₂ nanoparticles induced inflammatory responses compared with other TiO₂ particles. Further studies are required to determine the in vivo relevance of these findings to avoid the hazards of ingested particles. Full article

(This article belongs to the Special Issue Cellular Toxicity of Nanoparticles)

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Review

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941 KiB

Open AccessReview

Toxicological Considerations, Toxicity Assessment, and Risk Management of Inhaled Nanoparticles

by Shahnaz Bakand and Amanda Hayes

Int. J. Mol. Sci. 2016, 17(6), 929; https://doi.org/10.3390/ijms17060929 - 14 Jun 2016

Cited by 146 | Viewed by 10802

Abstract

Novel engineered nanoparticles (NPs), nanomaterial (NM) products and composites, are continually emerging worldwide. Many potential benefits are expected from their commercial applications; however, these benefits should always be balanced against risks. Potential toxic effects of NM exposure have been highlighted, but, as there is a lack of understanding about potential interactions of nanomaterials (NMs) with biological systems, these side effects are often ignored. NPs are able to translocate to the bloodstream, cross body membrane barriers effectively, and affect organs and tissues at cellular and molecular levels. NPs may pass the blood–brain barrier (BBB) and gain access to the brain. The interactions of NPs with biological milieu and resulted toxic effects are significantly associated with their small size distribution, large surface area to mass ratio (SA/MR), and surface characteristics. NMs are able to cross tissue and cell membranes, enter into cellular compartments, and cause cellular injury as well as toxicity. The extremely large SA/MR of NPs is also available to undergo reactions. An increased surface area of the identical chemical will increase surface reactivity, adsorption properties, and potential toxicity. This review explores biological pathways of NPs, their toxic potential, and underlying mechanisms responsible for such toxic effects. The necessity of toxicological risk assessment to human health should be emphasised as an integral part of NM design and manufacture. Full article

(This article belongs to the Special Issue Cellular Toxicity of Nanoparticles)

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238 KiB

Open AccessReview

Adverse Biological Effect of TiO₂ and Hydroxyapatite Nanoparticles Used in Bone Repair and Replacement

by Jiangxue Wang, Liting Wang and Yubo Fan

Int. J. Mol. Sci. 2016, 17(6), 798; https://doi.org/10.3390/ijms17060798 - 24 May 2016

Cited by 56 | Viewed by 5982

Abstract

The adverse biological effect of nanoparticles is an unavoidable scientific problem because of their small size and high surface activity. In this review, we focus on nano-hydroxyapatite and TiO₂ nanoparticles (NPs) to clarify the potential systemic toxicological effect and cytotoxic response of wear nanoparticles because they are attractive materials for bone implants and are widely investigated to promote the repair and reconstruction of bone. The wear nanoparticles would be prone to binding with proteins to form protein-particle complexes, to interacting with visible components in the blood including erythrocytes, leukocytes, and platelets, and to being phagocytosed by macrophages or fibroblasts to deposit in the local tissue, leading to the formation of fibrous local pseudocapsules. These particles would also be translocated to and disseminated into the main organs such as the lung, liver and spleen via blood circulation. The inflammatory response, oxidative stress, and signaling pathway are elaborated to analyze the potential toxicological mechanism. Inhibition of the oxidative stress response and signaling transduction may be a new therapeutic strategy for wear debris–mediated osteolysis. Developing biomimetic materials with better biocompatibility is our goal for orthopedic implants. Full article

(This article belongs to the Special Issue Cellular Toxicity of Nanoparticles)

1045 KiB

Open AccessReview

Cytotoxicity of Nanoparticles Contained in Food on Intestinal Cells and the Gut Microbiota

by Esther E. Fröhlich and Eleonore Fröhlich

Int. J. Mol. Sci. 2016, 17(4), 509; https://doi.org/10.3390/ijms17040509 - 06 Apr 2016

Cited by 170 | Viewed by 15871

Abstract

Toxicity of nanoparticles (NPs) upon oral exposure has been studied in animals using physiological changes, behavior, histology, and blood analysis for evaluation. The effects recorded include the combination of the action on cells of the exposed animal and the reaction of the microorganisms that populate the external and internal surfaces of the body. The importance of these microorganisms, collectively termed as microbiota, for the health of the host has been widely recognized. They may also influence toxicity of NPs but these effects are difficult to differentiate from toxicity on cells of the gastrointestinal tract. To estimate the likelihood of preferential damage of the microbiota by NPs the relative sensitivity of enterocytes and bacteria was compared. For this comparison NPs with antimicrobial action present in consumer products were chosen. The comparison of cytotoxicity with Escherichia coli as representative for intestinal bacteria and on gastrointestinal cells revealed that silver NPs damaged bacteria at lower concentrations than enterocytes, while the opposite was true for zinc oxide NPs. These results indicate that silver NPs may cause adverse effects by selectively affecting the gut microbiota. Fecal transplantation from NP-exposed animals to unexposed ones offers the possibility to verify this hypothesis. Full article

(This article belongs to the Special Issue Cellular Toxicity of Nanoparticles)

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224 KiB

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Drosophotoxicology: An Emerging Research Area for Assessing Nanoparticles Interaction with Living Organisms

by Mariana Carmen Chifiriuc, Attila Cristian Ratiu, Marcela Popa and Alexandru Al. Ecovoiu

Int. J. Mol. Sci. 2016, 17(2), 36; https://doi.org/10.3390/ijms17020036 - 14 Feb 2016

Cited by 68 | Viewed by 6944

Abstract

The rapid development of nanotechnology allowed the fabrication of a wide range of different nanomaterials, raising many questions about their safety and potential risks for the human health and environment. Most of the current nanotoxicology research is not standardized, hampering any comparison or reproducibility of the obtained results. Drosophotoxicology encompasses the plethora of methodological approaches addressing the use of Drosophila melanogaster as a choice organism in toxicology studies. Drosophila melanogaster model offers several important advantages, such as a relatively simple genome structure, short lifespan, low maintenance cost, readiness of experimental manipulation comparative to vertebrate models from both ethical and technical points of view, relevant gene homology with higher organisms, and ease of obtaining mutant phenotypes. The molecular pathways, as well as multiple behavioral and developmental parameters, can be evaluated using this model in lower, medium or high throughput type assays, allowing a systematic classification of the toxicity levels of different nanomaterials. The purpose of this paper is to review the current research on the applications of Drosophila melanogaster model for the in vivo assessment of nanoparticles toxicity and to reveal the huge potential of this model system to provide results that could enable a proper selection of different nanostructures for a certain biomedical application. Full article

(This article belongs to the Special Issue Cellular Toxicity of Nanoparticles)

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