Nanotoxicology最新文献

Introduction: Important cell-based models of intestinal inflammation have been advanced in hopes of predicting the impact of nanoparticles on disease. We sought to determine whether a high level and extended exposure of nanoplastic might result in the added intestinal inflammation caused by nanoplastic reported in a mouse model of irritable bowel disease. Methods: The cell models consist of a Transwell©-type insert with a filter membrane upon which lies a biculture monolayer of Caco-2 and HT29-MTX-E12 made up the barrier cells (apical compartment). This monolayer was exposed to digested 40 nm diameter polymethacrylate (PMA) with surface-functionalized COOH (PMA-) or NH₂ (PMA+) at a 'low level' (143 µg/cm² monolayer surface area) or 'high level' (571 µg/cm²) for 24 or 48 h. Beyond the apical compartment in the well of the tissue culture plate, was a monolayer of macrophages, previously differentiated from THP-1 cells (basolateral compartment). Thus, the immune competent tri-cultures were examined as two models: healthy and inflamed. The inflamed model, the barrier cell monolayer having been previously activated with IFN-γ and the macrophages having been previously activated with IFN-γ and LPS expressed a greater secretion of pro-inflammation cytokines. Results: Sedimentation, Diffusion and Dosimetry model (ISDD) simulated that 8%-12% of the PMA was deposited onto the barrier cell monolayer in 24-48-h. The structure of the barrier cells in the inflamed model was disorganized for both PMA, high level, 48-h experiments. While neither the amount of PMA nor the exposure duration influenced the lactate dehydrogenase (LDH) secretion in the healthy model, only the high levels of both PMA- and PMA+ in 48-h exposure experiments resulted in a significantly increased LDH secreted by the barrier cells in the inflamed model, compared to inflamed control. This study is the first to show an additive inflammation of nanoplastic in an inflamed intestinal model of the intestine.

In this study, we investigated the cytotoxic effect of highly soluble dextran-coated CeO₂ nanoparticles on human fetal lung fibroblasts MRC-5. We examined individual nanoparticle-treated cells by Raman spectroscopy and analyzed Raman spectra using non-negative principal component analysis and k-means clustering. In this way, we determined dose-dependent differences between treated cells, which were reflected through the intensity change of lipid, phospholipid and RNA-related Raman modes. Performing standard biological tests for cell growth, viability and induction of apoptosis in parallel, these changes were correlated with nanoparticle-induced apoptotic processes. The cells with specific spectral characteristics, referring to non-apoptotic, but possibly autophagic cell death modality, were also detected. Additionally, Raman imaging combined with principal component and vertex component analysis was used to map the spatial distribution of biological molecules in treated and untreated cells. This work provided the description of different resulting states of the treated cells depending on the dextran-coated CeO₂ nanoparticles dose, which can be later used in the design of the nanoparticles for industrial or medical applications. The wide content of information resulting from single-cell Raman spectroscopy has the potential to detect biochemical changes caused by nanoparticles that would otherwise require a series of expensive and time-consuming standard biological techniques.

Silver nanoparticles (AgNPs), recognized for their unique properties, are widely applied in fields such as agriculture, biotechnology, food security, and medicine. However, concerns persist regarding their interactions with living organisms and potential environmental impacts. This study investigates the effects of AgNPs on key soil microbial indicators that are essential for ecological functioning. A pot experiment was conducted with varying concentrations of AgNPs (0, 30, 60, 120, 240 mg kg^-1) and incubation periods (0, 15, 30, and 45 days). The results demonstrated a substantial reduction in microbial indicators, including bacterial and fungal colony-forming units (B.CFUs and F.CFUs), total microbial population (MPN), microbial basal respiration (BR), substrate-induced respiration (SIR), and microbial biomass carbon and nitrogen (MBC and MBN). These declines were more pronounced with increasing AgNP concentrations and prolonged incubation times, particularly within the first 15 days. Notably, even at lower concentrations, AgNPs exhibited significant toxicity to microbial indicators. The most severe impact was observed at 240 mg kg^-1 of AgNPs after 45 days, where B.CFUs, F.CFUs, MPN, MBC, and MBN showed substantial declines, with the greatest reduction at the highest concentration. Additionally, the microbial quotient (qmic) decreased by 66%, and variations in the respiratory quotient (qCO₂) were observed. Strong positive correlations were found among the microbial indicators, highlighting their interconnected responses to AgNP exposure. Overall, the study emphasizes the significant toxicity of AgNPs, raising concerns about their potential to disrupt soil ecosystems.

Titanium dioxide nanoparticles (TiO₂NPs) as an emerging pollutant in aquatic environments can interact with metals reducing or enhancing their toxicity in these environments. This study examined and compared the toxic effects of mercury ions (Hg²⁺ ions) on immobilization percentage, fatty acid profile, and oxidative stress of Artemia salina nauplii, individually (Hg) and simultaneously in the presence of 0.10 mg.L^-1 (Hg-0.1TiO₂NPs) and 1.00 mg.L^-1 TiO₂NPs (Hg-1TiO₂NPs). The interaction between Hg²⁺ ions and TiO₂NPs was evaluated using DLS and AAS-VGA. Simultaneous exposures exhibited an unexpected dual effect on A. salina nauplii. A synergistic effect was observed in Hg-0.1TiO₂NPs, while increasing the TiO₂NPs concentration in Hg-1TiO₂NPs prevented the synergy of the mixture compounds offering an antagonistic effect on nauplii. This dual effect was assigned to a greater number of available active sites and agglomeration of TiO₂NPs at higher concentrations. Oxidative stress and lipid peroxidation induced by Hg were diminished in Hg-1TiO₂NPs in line with the immobilization results. In Hg, total amounts of saturated fatty acids (∑SFA) increased while total monounsaturated (∑MUFA) and total polyunsaturated (∑PUFA) ones decreased compared with the control. However, they showed no significant change considering the control in Hg-1TiO₂NPs, again confirming the antagonistic effect on nauplii. The unsaturated to saturated fatty acids ratio decreased in both Hg and Hg-1TiO₂NPs compared with the control, however, this reduction in Hg-1TiO₂NPs was lower than in Hg. The present results emphasized getting a more comprehensive understanding of how TiO₂NPs impact the bioavailability and toxicity of co-contaminants through their combined effects and interactions.

The rapid development of nanotechnology has resulted in the widespread use of nanoparticles (NPs) in various sectors due to their unique properties and diverse applications. However, the increased exposure of humans to NPs raises concerns about their potential negative impact on human health and the environment. The pathways through which NPs exert adverse effects, including inflammation and oxidative stress, are primarily influenced by their size, shape, surface charge, and chemistry, underscoring the critical need to comprehend and alleviate their potential detrimental impacts. In this context, the natural flavonoid quercetin is a promising candidate for counteracting the toxicity induced by NPs due to its anti-inflammatory and antioxidant properties. This review provides an overview of the existing literature on quercetin's protective effects against NPs-induced toxicity, highlighting its therapeutic benefits and mechanisms of action, focusing on its ability to alleviate oxidative stress, inflammation, and cellular damage caused by various types of NPs. Insights from both in vitro and in vivo studies demonstrate the effectiveness of quercetin in preserving cellular function, modulating apoptotic pathways, and maintaining tissue integrity in the presence of NPs. The potential of quercetin as a natural therapeutic agent against NPs-induced toxicity provides valuable insights for safer use of NPs in various daily applications.

Fullerenes (C₆₀, C₇₀) as carbon nanomaterials can enter the environment through natural processes and anthropogenic activities, while synthetic fullerenes are commonly used in medicine in targeted therapies in association with antibodies, or anticancer and antimicrobial drugs. As the nanoparticles, they can pass through cell membranes and organelles and accumulate in the entire cytoplasm. The red-fluorescent, water-soluble [70]fullerene derivative C₇₀-OMe-ser, which produces reactive oxygen species upon illumination with an appropriate wavelength, passed into the cytoplasm of the middle region in the Drosophila melanogaster digestive system. To determine whether [70]fullerene nanomaterials that produce fluorescence after entering the cell cytoplasm will hurt its homeostasis, it is necessary to investigate the activation of degenerative and possibly regenerative processes. In vivo, studies on the model species D. melanogaster may help to elucidate whether the water-soluble [70]fullerene derivative that produces fluorescence can still be considered among the most promising nanomaterials. The experiment involved feeding insects ad libitum with yeast paste supplemented with 40 µg of fullerenes/mL for 1 week and 1 month. Thus, adult females and males of D. melanogaster were divided into control (CWM, CWF, CMM, and CMF) and experimental groups (FWM, FWF, FMM, and FMF). The quantitative and qualitative analysis enabled the presentation of the effects of the water-soluble [70]fullerene derivatives on cell proliferation and degeneration. Our study presented that [70]fullerene derivative showed a cytoprotective effect and activated cell proliferation. Therefore, we could conclude that analyzed carbon nanomaterials seemed to be safe for the cells into which they have penetrated.

The cellular components of the tumor microenvironment (TME) comprise cancer cells and nonmalignant cells including stromal and immune cells. Exosomes are extracellular vesicles secreted by various types of cells that play a crucial role in intercellular communications within TME. The main goal of this study was to elucidate how exosomes of macrophage cells treated with doxorubicin (DOX) and DOX-loaded cyclodextrin-based nanosponges (DOX-CDNSs), affect melanoma cancer cell proliferation. For this aim, the exosomes of the murine macrophage cell line (RAW 264.7) were isolated and characterized after treating the cells with DOX and DOX-CDNSs. The results demonstrated that DOX-CDNSs at a treatment concentration of 1 µg/mL, were nontoxic for macrophages and remarkably toxic against cancer cells. However, DOX was nontoxic for both cell types at the same treatment concentration. DOX and DOX-CDNSs remarkably declined the viability of both cell types at higher concentrations (25 and 50 µg/mL). Intriguingly, the exosomes of DOX-CD-NSs treated macrophages promoted the viability of cancer cells at the treatment concentrations of 1, 20, and 40 µg/mL. While the exosomes of DOX-treated macrophages increased cell viability of cancer cells only at the lowest concentration. In conclusion, this study suggests that utilization of CD-NSs may augment the toxicity of DOX against cancer cells, while it could direct macrophages toward secreting exosomes that favor the growth of cancer cells.

Toxicity associated with elevated levels of cobalt-chromium-molybdenum (CoCrMo) nanoparticles in total hip replacement (THR) patients has been a rising concern. Recent investigations demonstrated that these particles can induce polyneuropathy in THR patients. The current study aims to address a detailed molecular investigation of CoCrMo nanoparticle-mediated mitochondrial dynamics using induced pluripotent stem cell-derived neurons (iPSC neurons). Telencephalic neurons from iPSCs were used in this study. A statistically significant dose-dependent reduction in membrane potential and mitochondrial superoxide generation was observed after CoCrMo nanoparticle treatment. The gene expression analysis confirmed that the oxidative-specific genes were significantly upregulated in particle-treated cells compared to untreated cells. When iPSCs were exposed to CoCrMo nanoparticles, there was a significant reduction in the area, perimeter, and length of mitochondria. Live cell imaging (mitochondrial tracking) revealed a significant reduction in mitochondrial movements in the presence of CoCrMo nanoparticles. Further protein expression confirmed increased mitochondrial fission in CoCrMo particle-treated cells by significantly upregulating Drp-1 protein and downregulating Mfn-2. In conclusion, the results show that CoCrMo nanoparticles can significantly alter neuronal mitochondrial dynamics. The disturbance in balance restricts mitochondrial movement, reduces energy production, increases oxidative stress, and can cause subsequent neurodegeneration.

The present study rigorously examined the toxicological effects of nanoparticles (NPs), specifically nickel (Ni) and chromium oxide (Cr₃O₄) NPs, synthesized under controlled conditions and characterized. To evaluate their potential environmental impact exposed the freshwater fish Labeo rohita (L. rohita) to environmentally relevant concentrations of both NPs within a controlled laboratory conditions. Vital organs, including gills and liver were subjected to histopathological analysis, revealing profound alterations in tissue architecture that were distinctly correlated with pathological damage. The lesions exhibited moderate to severe changes that are further correlated with the semi-quantitative mean alteration value (MAV). Furthermore, conducted a quantitative assessment of tissue-specific morphological changes. Notably, there was a significant reduction in critical hematological changes, including red blood cell (RBC) and white blood cell (WBC) counts, hemoglobin concentrations and other parameters. All of which exhibited significant fluctuations in relation to increasing NPs concentrations. These findings underscore the critical necessity for continued investigation into the ecological risks associated with these nanoparticles.

Silver nanoparticles (AgNPs) have gained attention in medicine for their potent antibacterial, antiviral, and anti-inflammatory properties. The use of silver nanoparticles in ophthalmic solutions raises concerns regarding potential toxicity of nanoparticles to ocular tissues, such as the cornea, conjunctiva, and retina, which necessitates further toxicity assessments aiding in the development of safer ophthalmic solutions. This study investigates the impact of AgNPs on corneal tissue using ophthalmic investigations, Fourier transform infrared (FTIR) spectroscopy, and chemometric analyses. Three concentrations of AgNPs (0.48 µg/mL, 7.2 µg/mL, and 15.5 µg/mL) were topically applied twice daily for 10 days, synthesized biologically by reducing silver nitrate with almond kernels water extract. Corneas, obtained by cutting 2-3 mm below the ora serrata, were analyzed with FTIR spectroscopy and subjected to chemometric analyses. Results reveal AgNPs' influence on constituents with OH and NH groups, affecting corneal lipids and reducing the lipid saturation index. AgNPs alter both bulk and interfacial water, leading to changes in corneal hydration thus modifying corneal physico-chemical properties. The influence extends to the water environment around proteins and lipids, releasing bound water from phospholipids and disrupting hydrogen bonding networks around proteins. In conclusion, the applied AgNPs concentrations can be linked to dry eye onset.