Physiological effects of magnetite (Fe3O4) nanoparticles on perennial ryegrass (Lolium perenne L.) and pumpkin (Cucurbita mixta) plants

Abstract

To date, knowledge gaps and associated uncertainties remain unaddressed on the effects of nanoparticles (NPs) on plants. This study was focused on revealing some of the physiological effects of magnetite (Fe₃O₄) NPs on perennial ryegrass (Lolium perenne L.) and pumpkin (Cucurbita mixta cv. white cushaw) plants under hydroponic conditions. This study for the first time reports that Fe₃O₄ NPs often induced more oxidative stress than Fe₃O₄ bulk particles in the ryegrass and pumpkin roots and shoots as indicated by significantly increased: (i) superoxide dismutase and catalase enzyme activities, and (ii) lipid peroxidation. However, tested Fe₃O₄ NPs appear unable to be translocated in the ryegrass and pumpkin plants. This was supported by the following data: (i) No magnetization was detected in the shoots of either plant treated with 30, 100 and 500 mg l^?1 Fe₃O₄ NPs; (ii) Fe K-edge X-ray absorption spectroscopic study confirmed that the coordination environment of Fe in these plant shoots was similar to that of Fe-citrate complexes, but not to that of Fe₃O₄ NPs; and (iii) total Fe content in the ryegrass and pumpkin shoots treated with Fe₃O₄ NPs was not significantly increased compared to that in the control shoots.     

Titanium dioxide nanoparticles induced intracellular calcium homeostasis modification in primary human keratinocytes. Towards an in vitro explanation of titanium dioxide nanoparticles toxicity

Abstract

Deciphering the molecular basis of toxicology mechanism induced by nanoparticles (NPs) remains an essential challenge. Ion Beam Analysis (IBA) was applied in combination with Transmission Electron Microscopy and Confocal Microscopy to analyze human keratinocytes exposed to TiO₂-NPs. Investigating chemical elemental distributions using IBA gives rise to a fine quantification of the TiO₂-NPs uptake within a cell and to the determination of the intracellular chemical modifications after TiO₂-NPs internalization. In addition, fluorescent dye-modified TiO₂-NPs have been synthesized to allow their detection, precise quantification and tracking in vitro. The internalization of these TiO₂-NPs altered the calcium homeostasis and induced a decrease in cell proliferation associated with an early keratinocyte differentiation, without any indication of cell death. Additionally, the relation between the surface chemistry of the TiO₂-NPs and their in vitro toxicity is clearly established and emphasizes the importance of the calcium homeostasis alteration in response to the presence of TiO₂-NPs.     

Effect of nanomaterials on the compound action potential of the shore crab,Carcinus maenas

Abstract

Little is known about the effects of manufactured nanomaterials on the function of nerves. The experiment aimed to test the effects of three different nanomaterials (1 mg l^-1 of TiO₂ NPs, Ag NPs or SWCNT) on the compound action potential of the shore crab (Carcinus maenas) compared with an appropriate bulk powder or metal salt control (bulk TiO₂ powder, AgNO₃ and carbon black respectively). In single action potential recordings, there were no effects of any of the nanomaterials on the peak amplitude, duration, rate of rise (depolarisation), or rate of decrease (repolarisation) of the compound action potential in crab saline, despite settling of each nanomaterial directly onto the nerve preparation. The ability of the crab nerve to be stimulated to tetanus was also unaffected by exposure to the nanomaterials compared with the appropriate bulk powder or metal salt control. Solvent controls with sodium dodecyl sulfate (SDS) also had no effect on action potentials. Overall, the study concludes that there were no effects of the materials at the concentrations tested on the compound action potential of the shore crab in physiological saline.     

A murine model of the effects of inhaled CuO nanoparticles on cells of innate and adaptive immunity – a kinetic study of a continuous three-month exposure

Abstract

The inhalation or application of nanoparticles (NPs) has serious impacts on immunological reactivity. However, the effects of NPs on the immune system are influenced by numerous factors, which cause a high variability in the results. Here, mice were exposed to a three month continuous inhalation of copper oxide (CuO) NPs, and at different time intervals (3, 14, 42 and 93?days), the composition of cell populations of innate and adaptive immunity was evaluated in the spleen by flow cytometry. The ability of spleen cells from exposed and control mice to respond to stimulation with T- or B-cell mitogens by proliferation and by production of cytokines IL-2, IL-6, IL-10, IL-17 and IFN-γ was characterized. The results showed that the inhalation of CuO NPs predominantly affects the cells of innate immunity (changes in the proportion of eosinophils, neutrophils, macrophages and antigen-presenting cells) with a minimal effect on the percentage of T and B lymphocytes. However, the proliferative and secretory activity of T cells was already significantly enhanced after 3?days from the start of inhalation, decreased on day 14 and normalized at the later time intervals. There was no correlation between the impacts of NPs on the cells of innate and adaptive immunity. The results have shown that the inhalation of CuO NPs significantly alters the composition of cell populations of innate immunity and modulates the proliferation and production of cytokines by cells of the adaptive immune system. However, the immunomodulatory effects of inhaled NPs strongly depend on the time of inhalation.     

Angiopoietin-1 accelerates restoration of endothelial cell barrier integrity from nanoparticle-induced leakiness

Abstract

Nanoparticles (NPs) have been widely used in biomedical field for therapeutic treatments, drug carriers, and bio-imaging agent. Recent studies have highlighted the possibility of utilizing inorganic NPs in inducing endothelial leakiness through endothelial remodeling to promote drug transport across the barrier. However, an uncontrolled and persistent leakiness could lead to promiscuous transport of molecules and cells across the barrier, highlighting the pressing need to control the timely recovery from endothelial cell leakiness. Herein, we show that angiopoietin-1 (Ang1) could promote recovery of human microvascular endothelial cells (HMVECs) from titanium dioxide nanoparticle (TiO₂ NPs)-induced endothelial leakiness. Ang1 is known as an anti-permeability growth factor which forms complexes with its receptor Tie2 at the cell-to-cell junctions. We find that the introduction of Ang1 not only accelerates the recovery of NP-induced endothelial leakiness (NanoEL) but also promotes cell rigidity by increasing tubulin acetylation, thereby remodels the endothelial cells to further mitigate the effects of NP exposure through the activation of the Akt pathway. Using in vitro metastasis model, we further show that HMVECs treated with TiO₂ NPs followed by Ang1 could reduce migration of human skin cancer A431 cells across the endothelial barrier. In summary, Ang1 plays important roles in promoting the recovery of endothelial cell leakiness and endothelial stability through a mechano-transduction pathway and shows great potential as key modulator that allows material scientist to regulate endothelial leakiness induced by NPs.     

In vitro intestinal toxicity of copper oxide nanoparticles in rat and human cell models

Abstract

Human oral exposure to copper oxide nanoparticles (NPs) may occur following ingestion, hand-to-mouth activity, or mucociliary transport following inhalation. This study assessed the cytotoxicity of Cupric (II) oxide (CuO) and Cu₂O-polyvinylpyrrolidone (PVP) coated NPs and copper ions in rat (intestine epithelial cells; IEC-6) and human intestinal cells, two- and three-dimensional models, respectively. The effect of pretreatment of CuO NPs with simulated gastrointestinal (GI) fluids on IEC-6 cell cytotoxicity was also investigated. Both dose- and time-dependent decreases in viability of rat and human cells with CuO and Cu₂O-PVP NPs and Cu²⁺ ions was observed. In the rat cells, CuO NPs had greater cytotoxicity. The rat cells were also more sensitive to CuO NPs than the human cells. Concentrations of H₂O₂ and glutathione increased and decreased, respectively, in IEC-6 cells after a 4-h exposure to CuO NPs, suggesting the formation of reactive oxygen species (ROS). These ROS may have damaged the mitochondrial membrane of the IEC-6 cells causing a depolarization, as a dose-related loss of a fluorescent mitochondrial marker was observed following a 4-h exposure to CuO NPs. Dissolution studies showed that Cu₂O-PVP NPs formed soluble Cu whereas CuO NPs essentially remained intact. For GI fluid-treated CuO NPs, there was a slight increase in cytotoxicity at low doses relative to non-treated NPs. In summary, copper oxide NPs were cytotoxic to rat and human intestinal cells in a dose- and time-dependent manner. The data suggests Cu₂O-PVP NPs are toxic due to their dissolution to Cu ions, whereas CuO NPs have inherent cytotoxicity, without dissolving to form Cu ions.     

SILAC-based quantitative proteomics identifies size-dependent molecular mechanisms involved in silver nanoparticles-induced toxicity

Abstract

Silver nanoparticles are currently one of the most widely used metallic nanoparticles. Due to their antibacterial properties, they are applied in textiles, house-holds items, and medical devices, among many other products. Understanding the potential toxicity associated with silver nanoparticles and the differential effect that nanoparticles of different size might induce is crucial, due to the increasing human and environmental exposure to this type of nanoparticles. In this work, we explored the different biomolecular mechanisms underlying the toxicity of silver nanoparticles in a size-dependent manner. Quantitative proteomic analysis of hepatic cells exposed to 10 and 60?nm silver nanoparticles demonstrated the alteration of a different set of proteins depending on the particle size. We demonstrated that while 10?nm silver nanoparticles induce nucleolar stress and ribosome biogenesis halt, both types of nanoparticles induce DNA damage and oxidative stress but through different pathways. In addition, both types of nanoparticles also affected cell proliferation, disrupted the cell cycle and ultimately, induced apoptosis. The alteration of different cellular mechanisms in a size-dependent manner, have relevant implications not only from a toxicity point of view, but also for the potential applications of silver nanoparticles.