Nanotoxicology最新文献

The early development of nanotechnology has spurred major interest on the toxicity of nanoparticles (NPs) due to their ability to penetrate the biological barriers such as the BBB. This review aims at addressing how silver (AgNPs), titanium dioxide (TiO₂NPs), zinc oxide (ZnONPs), iron oxide (Fe₃O₄NPs), carbon NPs, Copper (Cu-NPs), silicon oxide (SiO₂ NPs) nanoparticles and quantum dots cause neurotoxicity. Some of the major signaling that occur are the signaling related to oxidative stress, neuroinflammation, mitochondrial dysfunction and cell equilibrium, hence results in neuronal damage and neurodegeneration. It is critical to describe that there are multiple ways by how NPs may be toxic based on their size and surface, dosage, and the recipient's age and health condition. A review on in vitro and in vivo analysis provides information about the toxic potentials of NPs and preventive measures including modification of NP surface and antioxidant treatment. The results underline the necessity of comprehensive safety assessments to allow the further utilization of nanoparticles across the economy.

The understanding of nanomaterial toxicity is aided by biokinetic information pointing to potential target organs. Silver (Ag), copper oxide (CuO), and zinc oxide (ZnO) are often referred to as soluble materials in the literature. In addition, data suggest gold (Au) nanoparticles to be soluble in the mammalian body. We identified inhalation studies on these materials and extracted data on physicochemical properties, organ distribution, and excretion. Silver and gold were retained in the lung for an extended period (>2,000 and >672 hours, respectively); copper initially increased in lung and then returned to baseline at ∼500 hours. Zinc increased in the lungs after short-term exposure to zinc oxide, but not after prolonged exposure. In blood, silver initially increased after inhalation but then gradually declined over ∼200 hours. Gold was elevated in the blood after exposure to 4, 7, 11, and 13 nm particles (but not particles of 20, 34, and 105 nm) and remained elevated for at least 672 hours after exposure to the 4 and 11 nm particles. Silver increased in the liver and spleen and was still present 2,000 hours post exposure. Gold was elevated in several organs, including the spleen and kidney, for more than 600 hours post exposure, indicating persistence in some organs. Both silver and gold were increased in the brain and olfactory bulb. Overall, we found no large differences in the biodistribution of the four nanomaterials but note that silver and gold were still increased in several organs at the last investigated post-exposure time points.

Vehicle engine exhausts contain complex mixtures of gaseous and particulate pollutants, which are known to affect lung functions adversely. Many in vitro studies have shown that exposure to engine exhaust can induce oxidative stress in lung cells, leading to cellular inflammation and cytotoxicity. However, it remains challenging to identify key harmful components and their specific adverse effects via traditional toxicological assessments. Machine learning (ML) methods offer new ways of analyzing such complex datasets and have gained attention in predicting toxicity outcomes and identifying key pollutants in mixtures responsible for adverse effects in a non-biased way. This study aims to understand the contribution of exhaust components to lung cell toxicity using ML techniques. Data were reanalyzed from previous studies (2015-2018), where a 3D human epithelial airway tissue model was exposed to gasoline and diesel engine exhausts under air-liquid interface (ALI) conditions with different fuels and exhaust after-treatment systems. This dataset included exhaust characteristics (particle number (PN), carbon monoxide (CO), total gaseous hydrocarbons (THC), and nitrogen oxides (NOx) levels) and corresponding biological responses (cytotoxicity, oxidative stress, and inflammatory responses). The relationships between pollutants and biological responses were explored using ML techniques, including hierarchical and nonhierarchical clustering and principal component analysis. The findings reveal both gaseous (CO, THC, and NOx) and particulate pollutants contribute to oxidative stress, inflammation, and cytotoxicity in lung cells, highlighting the significant role of each gaseous component. In addition, unmeasured factors beyond CO, THC, NOx, and PN likely contribute to biological effects, indicating the need for a more detailed characterization of exhaust parameters in ML analysis. By successfully integrating ML techniques, this study shows the potential of ML in identifying pollutant-specific contributions to cell toxicity. These insights can guide the analysis of complex exposure scenarios and inform regulatory measures and technical developments in emission control.

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.