Nanotoxicology最新文献

Titanium dioxide nanoparticles (TiO₂-NPs) are one of the most commercially manufactured and widely applied NPs. However, often TiO₂-NPs leak into the environment and make aquatic animals exposure inevitable. Consequently, a deeper comprehension of TiO₂-NPs toxicity is utmost important. The 96-hour lethal concentration of TiO₂-NP in rohu (Labeo rohita) was 77.49 mg/L. An in-vivo toxicity assessment of TiO₂-NP was conducted at sub lethal concentration of 1 mg/L (2%), 2.5 mg/L (5%), and 5 mg/L (10%) at 24 hours post exposure (hpe), 4 days post exposure (dpe), and 14 dpe in an aquatic lower vertebrate, rohu. Quantitative bioaccumulation analysis showed highest TiO₂-NPs bioaccumulation in intestine followed by liver, gill, kidney, spleen, and negligible in muscle. TiO₂-NP at 5 mg/L concentration induced the immunotoxic response by destabilization of serum lysozyme and antiprotease activity which was further potentiated by increased production of myeloperoxidase, respiratory burst activity leading to higher production of reactive oxygen species that contribute to oxidative stress, inflammation and cellular damage. Molecular study demonstrated that TiO₂-NP is recognized and processed by signaling PRR, TLR22 leading to initiation of the downstream immune-signaling cascade and pro-inflammatory cytokines production. The TiO₂-NP induced the oxidative stress gene (SOD, CAT, and GPx) expression significantly at 1, 2.5 and 5 mg/L. Nevertheless, apoptotic biomarker (caspase3, BAX and p53) were induced significantly on 14th dpe at 5 mg/L dose exposure. Our study infer that TiO₂-NP induced immunotoxic response at higher concentration of 5 mg/L, nevertheless it acts as immunostimulator at lower concentration of 1 mg/L in L. rohita.

The mouth cavity is the second most complex microbial community in the human body. It is composed of bacteria, viruses, fungi, and protozoa. An imbalance in the oral microbiota may lead to various conditions, including caries, soft tissue infections, periodontitis, root canal infections, peri-implantitis (PI), pulpitis, candidiasis, and denture stomatitis. Additionally, several locally administered antimicrobials have been suggested for dentistry in surgical and non-surgical applications. The main drawbacks are increased antimicrobial resistance, the risk of upsetting the natural microbiota, and hypersensitivity responses. Because of their unique physiochemical characteristics, nanoparticles (NPs) can circumvent antibiotic-resistance mechanisms and exert antimicrobial action via a variety of new bactericidal routes. Because of their anti-microbial properties, carbon-based NPs are becoming more and more effective antibacterial agents. Periodontitis, mouth infections, PI, dentin and root infections, and other dental diseases are among the conditions that may be treated using carbon NPs (CNPs) like graphene oxide and carbon dots. An outline of the scientific development of multifunctional CNPs concerning oral disorders will be given before talking about the significant influence of CNPs on dental health. Some of these illnesses include Periodontitis, oral infections, dental caries, dental pulp disorders, dentin and dental root infections, and PI. We also review the remaining research and application barriers for carbon-based NPs and possible future problems.

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.

The widespread utilization of titanium oxide nanoparticles (TiONPs) in various industrial applications has raised concerns about their potential ecological risks in marine environment. Assessing the toxicity of TiONPs on primary producers is essential to understand their impact on marine ecosystem. This study investigates the acute toxicity effect of TiONPs on Isochrysis galbana COR-A3 cells, focusing on structural and physiological changes that can compromise algal viability and ecological function. Cells were exposed to TiONPs concentration of 10-50 mg/L and assessments were conducted over 96 h to evaluate cell viability, biochemical composition, photo-physiology, oxidative stress and morphological deformations. At 50 mg/L concentration, cell viability was significantly reduced by 73.42 ± 3.46% and subsequent decrease of 42.8%, 29.2%, 44.2% in carbohydrate, protein and lipid content were observed. TiONPs exposure elevates the reactive oxygen species production and thereby impairing the photosystem II efficiency and disrupting the cellular metabolism. Morphological analysis revealed significant cell membrane disruption and plasmolysis. These cascading effects reveal TiONPs ability to interfere with algal physiological process, potentially affecting the primary productivity in marine ecosystem. Our findings highlight the ecological risk associated with the TiONPs, emphasizing the need for regulatory measures to mitigate the nanoparticle pollution in aquatic environment. This study provides more insights on the TiONPs induced toxicity in marine microalgae by altering the photosynthetic performance and biochemical integrity.

The intestinal epithelium plays a pivotal role as a vital barrier between the external environment and the human body, regulating nutrient absorption and preventing the entry of harmful substances. The human oral exposure to silver nanoparticles (AgNP) raises concerns about their potential toxicity, especially at the intestinal level. The objective of this work was to investigate the potential pro-inflammatory effects of polyvinylpyrrolidone (PVP)-AgNP of two different sizes, 5 and 50 nm, at the intestinal level, while also assessing the protective ability of quercetin against these effects. To address this, an intestinal co-culture model comprising C2BBe1 cells and THP-1 derived macrophages was established, and the effects of 5 or 50 nm PVP-AgNP were studied, alone or in combination with quercetin, over two-time points, 4 and 24 hours. PVP-AgNP, of both sizes, disrupted the barrier integrity within 4 hours of exposure. However, a notable intensification in pro-inflammatory effects was evident only after 24 hours of exposure, especially with smaller PVP-AgNP (5 nm). This resulted in heightened cellular death, increased levels of reactive species, activation of nuclear factor kappa B (NF-кB), and production of interleukin (IL)-8. Quercetin demonstrates the ability to maintain barrier integrity and mitigate oxidative stress, thereby offering protection against the detrimental effects induced by AgNP at the intestinal level.

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.

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.

Urotropine, an antibacterial agent to treat urinary tract bacterial infections, can be also considered as a repurposed drug with formaldehyde-mediated anticancer activity. Recently, we have synthesized urotropine surface modified iron oxide nanoparticles (URO@Fe₃O₄ NPs) with improved colloidal stability and limited cytotoxicity against human fibroblasts. In the present study, we have investigated URO@Fe₃O₄ NP-mediated responses in a panel of forty phenotypically different breast cancer cell lines along with three non-cancerous corresponding cell lines. URO@Fe₃O₄ NPs promoted oxidative stress and FOXO3a-based antioxidant response in breast cancer cells. Elevated levels of GPX4 and decreased levels of ACSL4 in URO@Fe₃O₄ NP-treated breast cancer cells protected against ferroptotic cell death. On the contrary, URO@Fe₃O₄ NPs impaired the activity of PERK, a part of unfolded protein response (UPR), especially when the glucose supply was limited, that was accompanied by genetic instability, and apoptotic and/or necrotic cell death in breast cancer cells. In conclusion, this is the first comprehensive analysis of anticancer effects of URO@Fe₃O₄ NPs against a panel of forty breast cancer cell lines with different receptor status and in glucose replete and deplete conditions. We suggest that presented results might be helpful for designing new nano-based anti-breast cancer strategies.

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.

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.