Background
Some manufactured nanoparticles are metal-based and have a wide variety of applications in electronic, engineering and medicine. Until now, many studies have described the potential toxicity of NPs on pulmonary target, while little attention has been paid to kidney which is considered to be a secondary target organ. The objective of this study, on human renal culture cells, was to assess the toxicity profile of metallic nanoparticles (TiO2, ZnO and CdS) usable in industrial production. Comparative studies were conducted, to identify whether particle properties impact cytotoxicity by altering the intracellular oxidative status. 相似文献Background
Titanium dioxide (TiO2) nanoparticles and fullerene (C60) are two attractive manufactured nanoparticles with great promise in industrial and medical applications. However, little is known about the genotoxic response of TiO2 nanoparticles and C60 in mammalian cells. In the present study, we determined the mutation fractions induced by either TiO2 nanoparticles or C60 in gpt delta transgenic mouse primary embryo fibroblasts (MEF) and identified peroxynitrite anions (ONOO-) as an essential mediator involved in such process. 相似文献Background
Engineered nanoparticles are becoming increasingly ubiquitous and their toxicological effects on human health, as well as on the ecosystem, have become a concern. Since initial contact with nanoparticles occurs at the epithelium in the lungs (or skin, or eyes), in vitro cell studies with nanoparticles require dose-controlled systems for delivery of nanoparticles to epithelial cells cultured at the air-liquid interface. 相似文献Background
Increasing environmental and occupational exposures to nanoparticles (NPs) warrant deeper insight into the toxicological mechanisms induced by these materials. The present study was designed to characterize the cell death induced by carbon black (CB) and titanium dioxide (TiO2) NPs in bronchial epithelial cells (16HBE14o- cell line and primary cells) and to investigate the implicated molecular pathways.Results
Detailed time course studies revealed that both CB (13 nm) and TiO2(15 nm) NP exposed cells exhibit typical morphological (decreased cell size, membrane blebbing, peripheral chromatin condensation, apoptotic body formation) and biochemical (caspase activation and DNA fragmentation) features of apoptotic cell death. A decrease in mitochondrial membrane potential, activation of Bax and release of cytochrome c from mitochondria were only observed in case of CB NPs whereas lipid peroxidation, lysosomal membrane destabilization and cathepsin B release were observed during the apoptotic process induced by TiO2 NPs. Furthermore, ROS production was observed after exposure to CB and TiO2 but hydrogen peroxide (H2O2) production was only involved in apoptosis induction by CB NPs.Conclusions
Both CB and TiO2 NPs induce apoptotic cell death in bronchial epithelial cells. CB NPs induce apoptosis by a ROS dependent mitochondrial pathway whereas TiO2 NPs induce cell death through lysosomal membrane destabilization and lipid peroxidation. Although the final outcome is similar (apoptosis), the molecular pathways activated by NPs differ depending upon the chemical nature of the NPs. 相似文献Abstract
Au x Pd1−x (x = 0, 0.25, 0.5, 0.75, 1) nanoparticle (NP) catalysts (8–11 nm) were synthesized by a one-pot reaction strategy using colloidal chemistry. XPS depth profiles with variable X-ray energies and scanning transmission electron microscopy (STEM) analyses show that the as-synthesized Au x Pd1−x (x = 0.25 and 0.5) bimetallic NPs have gradient alloy structures with Au-rich cores and Pd-rich shells. The evolution of composition and structure in the surface region corresponding to a mean free path of 0.6–0.8 nm (i.e., 2–3 layers to the bulk from the particle surface) was studied with ambient pressure X-ray photoelectron spectroscopy (AP-XPS) under CO/O2 reaction in the Torr pressure regime. Under the reaction conditions of 80 mTorr CO and 200 mTorr O2 at 200 °C, the surface region of Au0.75Pd0.25 NP is Au-rich (~70% by Au). All Au x Pd1−x (x = 0.25, 0.5, 0.75) NP catalysts have higher turnover rates for the model CO/O2 reaction than pure Pd and pure Au NPs. The Pd-rich Au0.25Pd0.75 NPs show the highest turnover rates and the Pd-rich Au0.5Pd0.5 NPs the lowest turnover rates at 200 °C. Interestingly, the Au-rich Au0.75Pd0.25 NPs exhibit steady-state turnover rates which are intermediate to those of the Pd-rich bimetallic nanoparticles. 相似文献Abstract
Au nanoparticles (NPs) were uniformly dispersed on ETS-10 titanosilicate using the cation exchange procedure and [Au(NH3)4](NO3)3 complex as the gold source. [Au(NH3)4]3+ cations were first introduced inside ETS-10 micropores, ligands were then released, Au3+ was reduced to Au+ forming electron-deficient Au clusters, and finally aggregation to Au NPs occurred. In comparison to the incipient-wetness and deposition–precipitation methods, the ion-exchange led to greater activity of the Au NPs in the oxidation of 1-phenylethanol by oxygen. 相似文献Background
The extensive biological applications of zinc oxide nanoparticles (ZnO NPs) in stomatology have created serious concerns about their biotoxicity. In our previous study, ZnO NPs were confirmed to transfer to the central nervous system (CNS) via the taste nerve pathway and cause neurodegeneration after 30 days of tongue instillation. However, the potential adverse effects on the brain caused by tongue-instilled ZnO NPs are not fully known.Methods
In this study, the biodistribution of Zn, cerebral histopathology and inflammatory responses were analysed after 30 days of ZnO NPs tongue instillation. Moreover, the molecular mechanisms underlying neuroinflammation in vivo were further elucidated by treating BV2 and PC12 cells with ZnO NPs in vitro.Results
This analysis indicated that ZnO NPs can transfer into the CNS, activate glial cells and cause neuroinflammation after tongue instillation. Furthermore, exposure to ZnO NPs led to a reduction in cell viability and induction of inflammatory response and calcium influx in BV2 and PC12 cells. The mechanism underlying how ZnO NPs induce neuroinflammation via the Ca2+-dependent NF-κB, ERK and p38 activation pathways was verified at the cytological level.Conclusion
This study provided a new way how NPs, such as ZnO NPs, induce neuroinflammation via the taste nerve translocation pathway, a new mechanism for ZnO NPs-induced neuroinflammation and a new direction for nanomaterial toxicity analysis.![点击此处可从《International Journal of Applied Ceramic Technology》网站下载免费的PDF全文](/ch/ext_images/free.gif)
Background
With the increased manufacture and use of carbon nanoparticles (CNP) there has been increasing concern about the potential toxicity of fugitive CNP in the workplace and ambient environment. To address this matter a number of investigators have conducted in vitro and in vivo toxicity assessments. However, a variety of different approaches for suspension of these particles (culture media, Tween 80, dimethyl sulfoxide, phosphate-buffered saline, fetal calf serum, and others), and different sources of materials have generated potentially conflicting outcomes. The quality of the dispersion of nanoparticles is very dependent on the medium used to suspend them, and this then will most likely affect the biological outcomes. 相似文献Background
A critical issue with nanomaterials is the clear understanding of their potential toxicity. We evaluated the toxic effect of 24 nanoparticles of similar equivalent spherical diameter and various elemental compositions on 2 human pulmonary cell lines: A549 and THP-1. A secondary aim was to elaborate a generic experimental set-up that would allow the rapid screening of cytotoxic effect of nanoparticles. We therefore compared 2 cytotoxicity assays (MTT and Neutral Red) and analyzed 2 time points (3 and 24 hours) for each cell type and nanoparticle. When possible, TC50 (Toxic Concentration 50 i.e. nanoparticle concentration inducing 50% cell mortality) was calculated. 相似文献Background
Genotoxicity is an important toxicological endpoint due to the link to diseases such as cancer. Therefore, an increased understanding regarding genotoxicity and underlying mechanisms is needed for assessing the risk with exposure to nanoparticles (NPs). The aim of this study was to perform an in-depth investigation regarding the genotoxicity of well-characterized Ni and NiO NPs in human bronchial epithelial BEAS-2B cells and to discern possible mechanisms. Comparisons were made with NiCl2 in order to elucidate effects of ionic Ni.Methods
BEAS-2B cells were exposed to Ni and NiO NPs, as well as NiCl2, and uptake and cellular dose were investigated by transmission electron microscopy (TEM) and inductively coupled plasma mass spectrometry (ICP-MS). The NPs were characterized in terms of surface composition (X-ray photoelectron spectroscopy), agglomeration (photon cross correlation spectroscopy) and nickel release in cell medium (ICP-MS). Cell death (necrosis/apoptosis) was investigated by Annexin V-FITC/PI staining and genotoxicity by cytokinesis-block micronucleus (cytome) assay (OECD 487), chromosomal aberration (OECD 473) and comet assay. The involvement of intracellular reactive oxygen species (ROS) and calcium was explored using the fluorescent probes, DCFH-DA and Fluo-4.Results
NPs were efficiently taken up by the BEAS-2B cells. In contrast, no or minor uptake was observed for ionic Ni from NiCl2. Despite differences in uptake, all exposures (NiO, Ni NPs and NiCl2) caused chromosomal damage. Furthermore, NiO NPs were most potent in causing DNA strand breaks and generating intracellular ROS. An increase in intracellular calcium was observed and modulation of intracellular calcium by using inhibitors and chelators clearly prevented the chromosomal damage. Chelation of iron also protected against induced damage, particularly for NiO and NiCl2.Conclusions
This study has revealed chromosomal damage by Ni and NiO NPs as well as Ni ionic species and provides novel evidence for a calcium-dependent mechanism of cyto- and genotoxicity.Background
The biological effects of nanoparticles depend on several characteristics such as size and shape that must be taken into account in any type of assessment. The increased use of titanium dioxide nanoparticles (TiO2NPs) for industrial applications, and specifically as a food additive, demands a deep assessment of their potential risk for humans, including their abilities to cross biological barriers.Methods
We have investigated the interaction of three differently shaped TiO2NPs (nanospheres, nanorods and nanowires) in an in vitro model of the intestinal barrier, where the coculture of Caco-2/HT29 cells confers inherent intestinal epithelium characteristics to the model (i.e. mucus secretion, brush border, tight junctions, etc.).Results
Adverse effects in the intestinal epithelium were detected by studying the barrier’s integrity (TEER), permeability (LY) and changes in the gene expression of selected specific markers. Using Laser Scanning Confocal Microscopy, we detected a different behaviour in the bio-adhesion and biodistribution of each of the TiO2NPs. Moreover, we were able to specifically localize each type of TiO2NPs inside the cells. Interestingly, general DNA damage, but not oxidative DNA damage effects, were detected by using the FPG version of the comet assay.Conclusions
Results indicate different interactions and cellular responses related to differently shaped TiO2NPs, nanowires showing the most harmful effects.The aim of this study was to synthesize green cerium oxide nanoparticles (CeO2–NPs) and coat them with chitosan polymers to increase bioavailability and their effectiveness in anti-cancer studies. For the synthesis of CeO2–NPs, aqueous rosemary leaf extract (RLE) was used as a reducing and stabilizing agent, and after characterizing the nanoparticles (DLS and XRD), a coating of chitosan around the nanoparticles (CeCh–NPs) was created by ionic gelation method. After characterizing (DLS, Zeta potential, FTIR and FESEM) and confirming the presence of nanoparticles, its toxicity effects were evaluated by MTT method and its pro-apoptotic effects were evaluated by qPCR (Caspase 3 and 9) and flow cytometric analysis. CeO2–NPs were formed with uniform dispersion (PDI: 0.25) in nanometer dimensions (184.84 nm) and after coating, their size increase to 202.35 nm was confirmed by DLS method. The CeCh–NPs were spherical, stable (ζ potential:?+?35.4 mV) and uniformly dispersed (PDI: 0.27). The median concentrations of nanoparticles against AGS, A459, PC3 and HFF cells were reported to be about 156.02, 169.1, 155.8 and 307.5 μg/ml. Increased expression of caspase 3 and 9 genes as well as increased percentage of SubG1 phase cells in flow cytometry confirmed the occurrence of apoptosis in treated cells. The results of this study confirmed the anticancer properties of CeCh–NPs by relying on the apoptosis process.
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