Tight junction between endothelial cells: the interaction between nanoparticles and blood vessels

• Yue Zhang and
• Wan-Xi Yang

Beilstein J. Nanotechnol. 2016, 7, 675–684, doi:10.3762/bjnano.7.60

• blood vessels, which are the sites of phosphorylation of tight junction proteins (claudins, occludins, and ZO (Zonula occludens)) proteins, oxidative stress and shear stress. We propose a connection between the presence of nanoparticles and the regulation of the tight junction, which might be the key

• approach for nanoparticles to penetrate endothelial layers and then have an impact on other tissues and organs. Keywords: blood vessels; endothelial cells; nanoparticles; oxidative stress; tight junction; Introduction Products related to nanoparticles (NPs) are increasingly growing in number. We can

• their diameter, that is, NPs are particles between 1 and 100 nanometers in size. Generally, the toxicity of NPs is based on the following mechanisms: oxidative stress, disruption of cell membranes, and unknown effects when they enter organs (Table 1). For instance, gold NPs can cause serious damage in

Unraveling the neurotoxicity of titanium dioxide nanoparticles: focusing on molecular mechanisms

• Bin Song,
• Yanli Zhang,
• Jia Liu,
• Xiaoli Feng,
• Ting Zhou and
• Longquan Shao

Beilstein J. Nanotechnol. 2016, 7, 645–654, doi:10.3762/bjnano.7.57

• remain unclear. However, we have concluded from previous studies that these mechanisms mainly consist of oxidative stress (OS), apoptosis, inflammatory response, genotoxicity, and direct impairment of cell components. Meanwhile, other factors such as disturbed distributions of trace elements, disrupted

• that the major mechanisms are oxidative stress (OS), inflammatory responses, apoptosis, genotoxicity, and direct impairment of cell components. However, it appears that TiO2 NPs-induced neurotoxicity results from multiple mechanisms. Furthermore, other minor mechanisms exist and include disturbed

• oxidative stress (OS), inflammatory responses, apoptosis, genotoxicity, and direct impairment of cell components. However, in most situations, neurotoxicity occurs through multiple mechanisms. Furthermore, other minor mechanisms include disturbed distributions of trace elements, disrupted signaling pathways

Application of biclustering of gene expression data and gene set enrichment analysis methods to identify potentially disease causing nanomaterials

• Andrew Williams and
• Sabina Halappanavar

Beilstein J. Nanotechnol. 2015, 6, 2438–2448, doi:10.3762/bjnano.6.252

• fibrosis. The pro-fibrogenic potential of CNTs is well established. Although CB has not been shown to induce fibrosis, it induces stronger inflammatory, oxidative stress and DNA damage responses than nano-TiO2 particles. Conclusion: The results of the analysis correctly identified all NMs to be

An ISA-TAB-Nano based data collection framework to support data-driven modelling of nanotoxicology

• Richard L. Marchese Robinson,
• Mark T. D. Cronin,
• Andrea-Nicole Richarz and
• Robert Rallo

Beilstein J. Nanotechnol. 2015, 6, 1978–1999, doi:10.3762/bjnano.6.202

• . For example, oxidative stress and inflammation might be detected via measuring the level of glutathione or various cytokine biomarkers respectively [97]. (These sub-lethal phenomena would not be considered “cytotoxicity” by all researchers [84].) The manner in which this template was designed to

Predicting cytotoxicity of PAMAM dendrimers using molecular descriptors

• David E. Jones,
• Hamidreza Ghandehari and
• Julio C. Facelli

Beilstein J. Nanotechnol. 2015, 6, 1886–1896, doi:10.3762/bjnano.6.192

• materials with expected low levels of toxicity. Cytotoxicity can be determined by a gamut of in vitro toxicity assays focusing on a number of cellular parameters including cell viability, oxidative stress, genotoxicity, and inflammatory response [9]. In this paper, we focus on the cell viability to

NanoE-Tox: New and in-depth database concerning ecotoxicity of nanomaterials

• Katre Juganson,
• Angela Ivask,
• Irina Blinova,
• Monika Mortimer and
• Anne Kahru

Beilstein J. Nanotechnol. 2015, 6, 1788–1804, doi:10.3762/bjnano.6.183

• reactive oxygen species and resulting induction of oxidative stress, and (iii) toxic effect of released ions from metal/metal oxide ENMs [13][25][28]. Analyses of the information in NanoE-Tox database (Table S2, Supporting Information File 1) revealed that the most often reported potential mechanism of

• ][183], oxidative stress [71][73][89][175][176][184][185], DNA damage/genotoxicity [102][186][187], and binding to sulfhydryl groups [100]. Similar effects were also demonstrated in case of ZnO NPs [84][85][86][188][189][190]. The mechanism of toxic action of insoluble ENMs like CeO2 [109][110], CNTs

• [116][133][191] and TiO2 [153][154][155][156][192] was usually reported as particle-driven mechanical membrane damage. NanoE-Tox database contains only one study suggesting the mechanism of toxicity of fullerenes (oxidative stress) [193] and there are no data about possible mechanism of action of FeOx

The eNanoMapper database for nanomaterial safety information

• Nina Jeliazkova,
• Charalampos Chomenidis,
• Philip Doganis,
• Bengt Fadeel,
• Roland Grafström,
• Barry Hardy,
• Janna Hastings,
• Markus Hegi,
• Vedrin Jeliazkov,
• Nikolay Kochev,
• Pekka Kohonen,
• Cristian R. Munteanu,
• Haralambos Sarimveis,
• Bart Smeets,
• Pantelis Sopasakis,
• Georgia Tsiliki,
• David Vorgrimmler and
• Egon Willighagen

Beilstein J. Nanotechnol. 2015, 6, 1609–1634, doi:10.3762/bjnano.6.165

• proposed to extend the list of endpoints for hazard identification to include cell uptake, cell viability, oxidative stress, inflammation, fibrosis, immunotoxicity, cardiovascular toxicity, ventilation rate, gill pathologies, mucus secretion and brain pathology. The EU guidance document lists the main

• average, though this is not always specified), a minimum and maximum value, or a single value and a standard deviation. Biological measurements are linked to assays (such as cytotoxicity, cell growth, cell viability, genotoxicity, and oxidative stress), endpoints measured on that assay (e.g., ROS

Influence of gold, silver and gold–silver alloy nanoparticles on germ cell function and embryo development

• Ulrike Taylor,
• Daniela Tiedemann,
• Christoph Rehbock,
• Wilfried A. Kues,
• Stephan Barcikowski and
• Detlef Rath

Beilstein J. Nanotechnol. 2015, 6, 651–664, doi:10.3762/bjnano.6.66

• toxic potential of gold as well as silver nanoparticles showing a decrease in toxicity with increasing agglomeration, i.e., particle size [95][96]. Internalisation of nanoparticles into the embryos in a concentration dependent manner was also a consistent finding [83][90]. Oxidative stress was confirmed

Novel ZnO:Ag nanocomposites induce significant oxidative stress in human fibroblast malignant melanoma (Ht144) cells

• Syeda Arooj,
• Samina Nazir,
• Akhtar Nadhman,
• Nafees Ahmad,
• Bakhtiar Muhammad,
• Ishaq Ahmad,
• Kehkashan Mazhar and
• Rashda Abbasi

Beilstein J. Nanotechnol. 2015, 6, 570–582, doi:10.3762/bjnano.6.59

• . These results indicate that ZnO NPs induce the production of 1O2 and this production is significantly improved in ZnO:Ag nanocomposites in aqueous solution. Induction of oxidative stress: lipid peroxidation (LPO) To investigate the induction of oxidative stress by the nanocomposites, cells were cultured

• , respectively. For nanoparticles treated samples no significant increase in MDA levels was observed either under light or dark condition. ROS species in ZnO:Ag nanocomposites induced oxidative stress in HT144 cells ROS are a family of oxygen-centered species including 1O2, HO• and H2O2. To characterize the

• , reduction in size of the NPs and increase in the photocatalytic activity [26][34]. It is, however, not well-understood how these NPs exactly work in the exposed cells. ZnO NPs were reported to cause toxicity by generating ROS [35], causing DNA damage, oxidative stress [36], an increase in caspase-3 activity

Hematopoietic and mesenchymal stem cells: polymeric nanoparticle uptake and lineage differentiation

• Ivonne Brüstle,
• Thomas Simmet,
• Gerd Ulrich Nienhaus,
• Katharina Landfester and
• Volker Mailänder

Beilstein J. Nanotechnol. 2015, 6, 383–395, doi:10.3762/bjnano.6.38

• nanoparticles, the secretion of IL-8 was dramatically increased in the presence of the PLLA–Fe particles in hMSCs. This is likely because of the release of iron ions from the particles. Free iron ions within the cell can lead to an increase in oxidative stress [30][31][32], and a higher level of reactive oxygen

The effect of surface charge on nonspecific uptake and cytotoxicity of CdSe/ZnS core/shell quantum dots

• Vladimir V. Breus,
• Anna Pietuch,
• Marco Tarantola,
• Thomas Basché and
• Andreas Janshoff

Beilstein J. Nanotechnol. 2015, 6, 281–292, doi:10.3762/bjnano.6.26

• resulting from CdSe and CdTe QD exposure to cultured cells was attributed to the presence of Cd2+ ions during the initial stages of synthesis or during in situ release, resulting in mitochondrial damage and oxidative stress [8][9]. The isolation of toxic core contents by coating the CdSe nanocrystals with a

Functionalization of α-synuclein fibrils

• Simona Povilonienė,
• Vida Časaitė,
• Virginijus Bukauskas,
• Arūnas Šetkus,
• Juozas Staniulis and
• Rolandas Meškys

Beilstein J. Nanotechnol. 2015, 6, 124–133, doi:10.3762/bjnano.6.12

• distinct features (e.g., size, shape, secondary structure) of in vitro-assembled α-Syn fibrils can be modulated by varying experimental conditions such as pH, ionic strength, temperature, etc. [14][15][16]. Also, several factors, including oxidative stress, post-translational modifications, proteolysis

Interaction of dermatologically relevant nanoparticles with skin cells and skin

• Annika Vogt,
• Fiorenza Rancan,
• Sebastian Ahlberg,
• Berouz Nazemi,
• Chun Sik Choe,
• Maxim E. Darvin,
• Sabrina Hadam,
• Ulrike Blume-Peytavi,
• Kateryna Loza,
• Jörg Diendorf,
• Matthias Epple,
• Christina Graf,
• Eckart Rühl,
• Martina C. Meinke and
• Jürgen Lademann

Beilstein J. Nanotechnol. 2014, 5, 2363–2373, doi:10.3762/bjnano.5.245

• antioxidant levels as indicators of oxidative stress [16], it is now increasingly being used to study particle–skin interactions [17][18]. Yet, not all particle types are equally suited for such investigations. In the following, we report our results on confocal Raman microscopy for analyzing the skin

• alterations were correlated with those findings (unpublished data). TEM studies confirmed intracellular uptake of AgNP accumulation in vesicles, most likely endosomes (Figure 2b). Toxicity of metal particles is widely attributed to the production of reactive oxygen species (ROS) [38] and oxidative stress

• . Reported studies on nanoparticle-induced oxidative stress use different read-outs for radical production including fluorochromic assays [39], depletion of antioxidants [40], enzyme activity (e.g., catalase [41], superoxide dismutase), or oxidative DNA damage. For example, reactive oxygen species-mediated

Nanobioarchitectures based on chlorophyll photopigment, artificial lipid bilayers and carbon nanotubes

• Marcela Elisabeta Barbinta-Patrascu,
• Stefan Marian Iordache,
• Ana Maria Iordache,
• Nicoleta Badea and
• Camelia Ungureanu

Beilstein J. Nanotechnol. 2014, 5, 2316–2325, doi:10.3762/bjnano.5.240

• oxidative stress. Luminol was introduced as light amplifier in this system in order to increase the detection sensitivity of activated oxygen species. The antioxidant activity (AA, %) was calculated as a percentage of free radical scavenging of each sample using: where I0 is the maximum CL intensity for a

Effect of silver nanoparticles on human mesenchymal stem cell differentiation

• Christina Sengstock,
• Jörg Diendorf,
• Matthias Epple,
• Thomas A. Schildhauer and
• Manfred Köller

Beilstein J. Nanotechnol. 2014, 5, 2058–2069, doi:10.3762/bjnano.5.214

• ]. Silver-mediated oxidative stress can lead to the nuclear translocation of NF-κB, which regulates pro- and anti-inflammatory genes [53][54][55]. For example, we previously demonstrated that Ag-NP-induced an activation of hMSCs and monocytes that was characterized by differential cytokine release (e.g

PVP-coated, negatively charged silver nanoparticles: A multi-center study of their physicochemical characteristics, cell culture and in vivo experiments

• Sebastian Ahlberg,
• Alexandra Antonopulos,
• Jörg Diendorf,
• Ralf Dringen,
• Matthias Epple,
• Rebekka Flöck,
• Wolfgang Goedecke,
• Christina Graf,
• Nadine Haberl,
• Jens Helmlinger,
• Fabian Herzog,
• Frederike Heuer,
• Stephanie Hirn,
• Christian Johannes,
• Stefanie Kittler,
• Manfred Köller,
• Katrin Korn,
• Wolfgang G. Kreyling,
• Fritz Krombach,
• Jürgen Lademann,
• Kateryna Loza,
• Eva M. Luther,
• Marcelina Malissek,
• Martina C. Meinke,
• Daniel Nordmeyer,
• Anne Pailliart,
• Jörg Raabe,
• Fiorenza Rancan,
• Barbara Rothen-Rutishauser,
• Eckart Rühl,
• Carsten Schleh,
• Andreas Seibel,
• Christina Sengstock,
• Lennart Treuel,
• Annika Vogt,
• Katrin Weber and
• Reinhard Zellner

Beilstein J. Nanotechnol. 2014, 5, 1944–1965, doi:10.3762/bjnano.5.205

• types (alveolar epithelial cells, macrophages, and dendritic cells), adverse effects were also only found at high silver concentrations. The silver ions that are released from silver nanoparticles may be harmful to skin with disrupted barrier (e.g., wounds) and induce oxidative stress in skin cells

• nanoparticles neither caused toxicity nor oxidative stress, while an incubation for 4 h with 100 µM (10.8 µg mL−1) silver in the form of silver nitrate strongly damaged cultured astrocytes and deprived these cells almost completely of the important antioxidant glutathione [108]. The high resistance of cultured

• , i.e., oxidative stress and different pro-inflammatory cytokines/chemokines, were observed. Compared to a representative lung deposition attributable to occupational exposure of 5–100 nm silver nanoparticles calculated after 24 h, as described by Gangwal et al. [131], an expected deposited dose in

Carbon-based smart nanomaterials in biomedicine and neuroengineering

• Antonina M. Monaco and
• Michele Giugliano

Beilstein J. Nanotechnol. 2014, 5, 1849–1863, doi:10.3762/bjnano.5.196

• expression of genes responding to oxidative stress were observed [73]. However, Xing et al. [74] observed that embryonic stem cells responded to incubation with NDs with an increased expression of MOGG-1 and P53, which are proteins related to DNA repair processes. This genotoxicity was increased when cells

Biocompatibility of cerium dioxide and silicon dioxide nanoparticles with endothelial cells

• Claudia Strobel,
• Martin Förster and
• Ingrid Hilger

Beilstein J. Nanotechnol. 2014, 5, 1795–1807, doi:10.3762/bjnano.5.190

• increase in oxidative stress after CeO2 nanoparticles exposure was shown [25][26][27]. Under certain circumstances nanoparticles can pass specific biological barriers (e.g., skin via wounds or lesions) and ultimately enter the blood vessel system. In consequence, interactions between endothelial cells and

• nanoparticles. Several studies reported either anti-oxidative properties or an increase of oxidative stress. In particular 8 nm-sized CeO2 nanoparticles suppressed ROS production [45], while 30 nm-sized nanoparticles induced oxidative stress in human bronchial epithelial cells (Beas-2B) [25]. Therefore, general

• cytokine/cell). Determination of reactive oxygen species (ROS) after nanoparticle exposure To assess the oxidative stress after nanoparticle exposure, the activity of reactive oxygen species (ROS) was measured using the OxiSelect™ Intracellular ROS Assay Kit (Green Fluorescence, Cell Biolabs, Inc., USA

Precise quantification of silica and ceria nanoparticle uptake revealed by 3D fluorescence microscopy

• Adriano A. Torrano and
• Christoph Bräuchle

Beilstein J. Nanotechnol. 2014, 5, 1616–1624, doi:10.3762/bjnano.5.173

• properties have been described as beneficial applications in nanomedicine [17][18][19]. On the other hand, oxidative stress and impaired cell viability were shown to be a function of the particle dose and the exposure time [1][20]. However, most of the studies concerning the interaction of silica and ceria

Silica nanoparticles are less toxic to human lung cells when deposited at the air–liquid interface compared to conventional submerged exposure

• Alicja Panas,
• Andreas Comouth,
• Harald Saathoff,
• Thomas Leisner,
• Marco Al-Rawi,
• Michael Simon,
• Gunnar Seemann,
• Olaf Dössel,
• Sonja Mülhopt,
• Hanns-Rudolf Paur,
• Susanne Fritsch-Decker,
• Carsten Weiss and
• Silvia Diabaté

Beilstein J. Nanotechnol. 2014, 5, 1590–1602, doi:10.3762/bjnano.5.171

• induced IL-8 already at much lower diesel exhaust particle concentrations deposited at the ALI in comparison to submerged exposure [40]. ALI and submerged exposure have also recently been compared for their response to a chemical inducer of oxidative stress. In line with our findings, a tetra-culture of

Current state of laser synthesis of metal and alloy nanoparticles as ligand-free reference materials for nano-toxicological assays

• Christoph Rehbock,
• Jurij Jakobi,
• Lisa Gamrad,
• Selina van der Meer,
• Daniela Tiedemann,
• Ulrike Taylor,
• Wilfried Kues,
• Detlef Rath and
• Stephan Barcikowski

Beilstein J. Nanotechnol. 2014, 5, 1523–1541, doi:10.3762/bjnano.5.165

• inducing toxic effects due to oxidative stress. These effects are reviewed elsewhere in more detail [82][83], while this paragraph further focuses on noble metals such as gold for which ion release is negligible. Biocompatible Au-SMS were synthesized in a cylindrical batch where laser-generated gold

• relevant in AuAg nanoparticles, composed of two metals with deviating redox potentials. Additionally, it should be noted that ion release and oxidative stress are not necessarily independent. For example, in the case of ZnO nanoparticles the formation of ROS due to released Zn2+ ions was reported to be the

In vitro interaction of colloidal nanoparticles with mammalian cells: What have we learned thus far?

• Moritz Nazarenus,
• Qian Zhang,
• Mahmoud G. Soliman,
• Pablo del Pino,
• Beatriz Pelaz,
• Susana Carregal-Romero,
• Joanna Rejman,
• Barbara Rothen-Rutishauser,
• Martin J. D. Clift,
• Reinhard Zellner,
• G. Ulrich Nienhaus,
• James B. Delehanty,
• Igor L. Medintz and
• Wolfgang J. Parak

Beilstein J. Nanotechnol. 2014, 5, 1477–1490, doi:10.3762/bjnano.5.161

• clearly can trigger toxic effects in cells such as cytotoxicity, oxidative stress, (pro-)inflammation, and genotoxicity [150][151][152]. While again the detailed mechanisms are very complex and by far not understood in a comprehensive way, yet again there are certain characteristic features [153]. Toxic

Mimicking exposures to acute and lifetime concentrations of inhaled silver nanoparticles by two different in vitro approaches

• Fabian Herzog,
• Kateryna Loza,
• Sandor Balog,
• Martin J. D. Clift,
• Matthias Epple,
• Peter Gehr,
• Alke Petri-Fink and
• Barbara Rothen-Rutishauser

Beilstein J. Nanotechnol. 2014, 5, 1357–1370, doi:10.3762/bjnano.5.149

• (diameter 100 nm; coated with polyvinylpyrrolidone: PVP). Ag NPs were found to be highly aggregated within ALI exposed cells with no impairment of cell morphology. Furthermore, a significant increase in release of cytotoxic (LDH), oxidative stress (SOD-1, HMOX-1) or pro-inflammatory markers (TNF-α, IL-8

• , increased levels of oxidative stress and reactive oxygen species (ROS) were detected over a time period of 48 h [22][25][26]. Environmental stressors trigger the production of intracellular ROS, which can overwhelm the cellular antioxidant defence system. ROS can cause DNA damage, which results in the

• could be observed when simultaneously exposed with Ag NPs. Ag NPs were not found to interfere with the ELISA assay (data not shown). Gene expression of pro-inflammatory and oxidative stress markers As described in [44], the total RNA content of the triple cell co-cultures was collected 4 and 24 h after

Antimicrobial properties of CuO nanorods and multi-armed nanoparticles against B. anthracis vegetative cells and endospores

• Pratibha Pandey,
• Merwyn S. Packiyaraj,
• Himangini Nigam,
• Gauri S. Agarwal,
• Beer Singh and
• Manoj K. Patra

Beilstein J. Nanotechnol. 2014, 5, 789–800, doi:10.3762/bjnano.5.91

• Appelrot et al. have found the antibacterial activity of CuO nanoparticles to be due to the generation of ROS by the NPs attached to the bacterial cells, which in turn enhanced the intracellular oxidative stress [25]. By using electron microscopy they also detected the presence of small nanoparticles of

Manipulation of isolated brain nerve terminals by an external magnetic field using D-mannose-coated γ-Fe₂O₃ nano-sized particles and assessment of their effects on glutamate transport

• Tatiana Borisova,
• Natalia Krisanova,
• Arsenii Borуsov,
• Roman Sivko,
• Ludmila Ostapchenko,
• Michal Babic and
• Daniel Horak

Beilstein J. Nanotechnol. 2014, 5, 778–788, doi:10.3762/bjnano.5.90

• higher Ti contents in the hippocampus region. This lead to oxidative stress in the brain of exposed mice, an increase in the activity of catalase, and the excessive release of glutamic acid and nitric oxide [29]. In this study, neurotoxic effects of D-mannose-coated γ-Fe2O3 nanoparticles have been