Nanotoxicology最新文献

The increasing release of nanomaterials into aquatic environments has raised global concern regarding their ecological impacts, particularly under ongoing climate change. Among these materials, metallic nanoparticles are of special interest due to their widespread use and environmental persistence. Silver nanoparticles (AgNPs) are extensively applied in industrial and medical products and are frequently detected in aquatic systems, where their toxicity may be strongly influenced by abiotic factors such as temperature. In ecotoxicological studies, silver nitrate (AgNO₃) is commonly used as a positive control to represent dissolved ionic silver and to enable comparison with nanoparticulate forms. However, the combined effects of AgNP exposure and thermal variation on crustacean physiology remain poorly understood. Here, we demonstrate that temperature markedly enhances the toxicity and physiological stress induced by AgNPs in the shrimp Palaemon pandaliformis, using AgNO₃ exclusively as an ionic silver control. Acute 96-hour toxicity assays showed consistently lower LC₅₀ values for AgNO₃ than for AgNPs across all temperatures, confirming its higher intrinsic toxicity, while both silver forms exhibited pronounced toxicity amplification at elevated temperature (25 °C). Sublethal responses revealed significantly increased oxygen consumption under combined thermal and silver stress, indicating elevated metabolic demand, whereas ammonia excretion declined with increasing concentration and temperature, suggesting impairment of branchial excretory function. Overall, our findings demonstrate that warming not only intensifies mortality but also exacerbates metabolic and excretory dysfunction associated with metallic nanoparticle exposure, highlighting the critical role of temperature in nanotoxicological risk assessment and supporting P. pandaliformis as a sensitive bioindicator under climate change scenarios.

Silicon dioxide nanoparticles (SiO₂ NPs) are widely utilized in industrial and biomedical applications owing to their unique physicochemical properties; however, their potential biological effects require comprehensive evaluation. In this study, the model organism Drosophila melanogaster was employed to investigate the impacts of dietary exposure to SiO₂ NPs of different sizes and concentrations on developmental and reproductive outcomes. The assessed parameters included egg-laying rate, pupation time, adult emergence time, pupation rate, adult emergence rate, larval weight, and sex ratio. The results revealed that at concentrations of 0.2% or lower, neither nanoparticle size produced significant effects on development or reproductive capacity. In contrast, exposure to 2% SiO₂ NPs (both 15 nm and 30 nm) led to reduced body weight in third instar larvae. Notably, 30 nm SiO₂ NPs exposure significantly decreased pupation and adult emergence rates and was associated with delayed pupation and emergence times. Although total egg production remained unchanged, flies exposed to 30 nm SiO₂ NPs exhibited an earlier oviposition peak. These findings suggest that exposure to SiO₂ NPs at the national standard concentration of 0.2% does not cause notable developmental effects in Drosophila, whereas a tenfold increase in concentration may induce developmental delays. Considering that the 0.2% standard is based on human exposure and accounting for interspecies extrapolation, the 2% concentration may still represent a relevant dose range. Overall, these results indicate that excessive intake of SiO₂ NPs could pose toxicological risks and provide a theoretical foundation for further studies on the mechanisms underlying SiO₂ NPs-induced toxicity.

Polyethylene glycol-Multiwalled carbon nanotubes (PEG-MWCNTs) hold significant potential for biomedical applications, including diagnostics and controlled drug delivery. However, their toxicity allied to the synthesis process remains a critical concern. Residual metal impurities from the synthesis process are suggested as potential contributors to the observed toxicity. This study evaluates the cellular, genomic, and morphological toxicity of PEG-MWCNTs in zebrafish embryos. MWCNTs were synthesized via chemical vapor deposition, purified with nitric acid, and functionalized with PEG-6000. They were further characterized by high-resolution transmission electron microscopy (TEM), zeta potential analysis, and FTIR spectroscopy. The different concentrations of PEG-MWCNT (0.01-10.24 mg/L) were used for acute toxicity testing in zebrafish embryos. The median lethal concentration (LC50) decreased over time, indicating increased toxicity with prolonged exposure. Toxic effects, including egg coagulation, yolk sac edema, pericardial edema, tail detachment, and delayed hatching, were observed at higher doses. Genotoxicity, assessed via the alkaline comet assay, revealed significant DNA damage at concentrations above 1.28 mg/L. Histological analysis further demonstrated cellular disruptions such as hyperemia, somite disorganization, and notochord deterioration. These findings can be utilized for further toxicity assessments, safe in vivo drug delivery, biomedical and environmental applications to ensure minimal ecological and health impacts.

This study proposes a novel multimodal framework for assessing the time-dependent toxicity of iron oxide nanoparticles (SPIONs), aiming to improve in vitro to in vivo extrapolation (IVIVE). The framework integrates experimental data from Caco-2 cells and C. elegans with sequential mathematical modeling and neural network analysis. By accounting for complex, time-dependent processes such as cellular uptake, intracellular transport, and SPION degradation, this approach addresses the unique toxicological profile of nanoparticles. In vitro experiments evaluated cytotoxicity, reactive oxygen species (ROS) production, and antioxidant enzyme expression over 96 hours, revealing strong correlations between nanoparticle uptake, iron levels, oxidative stress, and cell viability. Mathematical models, validated against experimental data, enable the calculation of IC50 values and facilitate interspecies extrapolation. This integrated methodology, achieving an R² > 0.85 for predictive correlations, holds significant promise for reducing reliance on animal testing in future nanotoxicity evaluations.

The objective of the paper was to conduct a thorough statistical meta-analysis of a publicly available database by examining cell membrane damage (CMD), mitochondrial membrane potential (MMP), nuclear size (NS), nuclear intensity (NI), and cell viability (CVV) responses toward nanoparticles. The set of individual 880 and the subset of 630 measurements contained exposure dose, particle diameter, nanoparticle identity (TiO₂, Ag, SiO₂, CeO₂, ZnO, Cu), and cell type (A549, HCT116, HepaRG, HEPG2, RAW264.7) correlated to toxicity markers. The exposure dose was revealed as the most consistent predictor of toxicity across all endpoints, with higher doses significantly influencing toxicity. The compound-specific response was another important factor, where Ag, ZnO, and Cu, were consistently more cytotoxic, while ZnO and Cu correlated to loss of CVV and MMP. Contrary, TiO₂, CeO₂ and SiO₂ displayed partial protective effects, depending on cell context. The effect of particle size was compound- and endpoint-specific, e.g. smaller particles of CeO₂ displayed greater disruption to nuclear architecture (NS, NI) and MMP, while size had minimal effect on CVV for other compounds. HepaRG cells were the most sensitive, specifically from Cu and ZnO, while epithelial lines (e.g. HCT116, HEPG2) showed more complex patterns. Generally, the dose was confirmed as the most impactful predictor, due to consistent and statistically significant effects. Compounds and cell lines were determined as factors of next-highest importance, displaying mixed but significant effects, and the particle size showed lowest effects. These findings highlight the importance of multi-endpoint, multi-cell-type frameworks in nanotoxicology for compound- and cell-specific risk assessments.

Background and aims: Air pollution represents the second most significant global health burden, and existing epidemiological studies have reported that air pollution is harmful to the liver. To comprehensively understand the relationship between air pollution and liver health, this study quantitatively assessed the effects of air pollutants on liver diseases based on published population studies.

Methods and results: 46 papers from PubMed, Cochrane Library, and Web of Science were included in this study. The study we included covered Asia, Europe, and the Americas, mainly from China (23/46), the United States (7/46), and the United Kingdom (3/46). This study has been registered on PROSPERO (CRD42024515689). A WHO-approved risk of bias (ROB) assessment tool specialized for air quality research was applied to evaluate the bias in the included studies. Statistical analyses were performed in R 4.3.2 with fixed/random-effects models (threshold: I²>50%). Effect values (odds ratio [ORs]/weighted mean differences [WMDs]) were standardized per 10 μg/m³ increment, with sensitivity analysis (leave-one-out), and publication bias tests (Begg/Egger) at P < 0.05. The results indicated that each 10 μg/m³ increment in particulate matter 2.5 mum (PM_2.5) was associated with increased levels of aspartate aminotransferase (AST) (3.25%, 95% CI: 0.87-5.68), alanine aminotransferase (ALT) (1.82%, 95% CI: 0.60-3.04), and gamma-glutamyl transferase (GGT) (1.86%, 95% CI: 0.70-3.01); as well as increased risk of metabolic dysfunction-associated fatty liver disease (MAFLD) (OR = 1.32, 95% CI: 1.21-1.44), liver cancer incidence (OR = 1.22, 95% CI: 1.11-1.35), and liver cancer mortality (OR = 1.47, 95% CI: 1.14-1.90). Particulate matter 10 mum (PM₁₀) and nitrogen dioxide (NO₂) exposure also correlated with elevated liver enzymes. The present study has demonstrated that long-term exposure to air pollutants was associated with a higher risk of developing liver diseases in comparison to short-term exposure. The cohort study yielded more statistically significant findings than the cross-sectional study.

Conclusion: The evidence presented in this study suggested that air pollution was associated with an increased risk of liver enzyme abnormality, incidence of MAFLD, as well as incidence and mortality of liver cancer, reminding the public, environmental and clinical experts, to pay attention to the liver health associated with air pollution.

Colloidal silver is marketed as a dietary supplement, despite lacking essential mineral properties, scientific health benefits and potential toxicity. Therefore, we aimed to evaluate the effects of two commercially available colloidal silver formulations, Almacura (AL) and Prata Vida (PV), on the human hepatoma cell line Huh-7. We determined the IC₅₀ values for the AL formulation as 0.69 µg/mL (cell viability by MTT assay), 0.79 µg/mL (cell count via PI/Hoechst nuclear staining), and 0.93 µg/mL (membrane integrity by PI uptake assay). Similarly, the IC50 values for the PV formulation were 0.62 µg/mL (cell viability by MTT assay), 0.86 µg/mL (cell count via PI/Hoechst nuclear staining), and 1.02 µg/mL (membrane integrity by PI uptake assay). We also examined the contributions of the supernatant, enriched in Ag⁺ ions, and the pellet, mainly composed of AgNPs, to cytotoxicity. Using the MTT assay, we found IC50 values of 0.80 µg/mL for AL and 0.85 µg/mL for PV, indicating that the supernatant is the primary driver of the observed cytotoxicity. High-content imaging (HCI) was performed using the Live Cell Painting assay to evaluate dose-response effects, revealing that both formulations showed cellular changes at lower concentrations compared to MTT assays. In conclusion, this study raises important concerns regarding the safety of commercial colloidal silver, highlighting the need for regulatory standards that consider nanoparticle characteristics and their biological interactions.

The effect of non-functionalized polystyrene nanoparticles (PS-NPs) with diameters of 29, 44, and 72 nm on plasmid DNA integrity and the expression of genes involved in the architecture of chromatin was investigated in human peripheral blood mononuclear cells (PBMCs). The cells were incubated with PS-NPs at concentrations ranging from 0.001 to 100 µg/mL for 24 hours. Gene expression profiling was carried out using quantitative real-time PCR for the following genes: those involved in DNA methylation (DNMT1, DNMT3A), DNA demethylation (TET2, TET3), and chromatin remodeling, including histone methylation (EHMT1, EHMT2) and histone deacetylation (HDAC3, HDAC5). Furthermore, the expression of selected epigenetic markers related to histone acetylation and methylation (H3ac, H3K4me3, H3K9me3) at the protein level was examined using Western blotting. To assess the potential direct interaction of PS-NPs with DNA, a plasmid relaxation assay was performed in an extracellular system. The results demonstrated that PS-NPs do not cleave plasmid DNA directly. The gene expression analysis indicated that PS-NPs did not alter the expression of DNMT1, TET2, TET3, EHMT1, EHMT2, HDAC3, or HDAC5 in PBMCs. However, statistically significant changes in the expression of the DNMT3A gene were observed after exposure to 29 nm nanoparticles (p = 0.016, Kruskal-Wallis test), although post hoc comparisons did not reveal significant differences between individual treatment groups, and no clear dose-dependent trend was evident. PS-NPs induced a statistically significant decrease in post-translational histone modifications, specifically H3ac and H3K4me3. These findings suggest that PS-NPs may influence the epigenetic mechanisms involved in the regulation of chromatin architecture.

Multi-walled carbon nanotubes (MWCNTs) are used to reinforce plastics, but recent studies have demonstrated that exposure to MWCNTs via inhalation or intratracheal instillation induced lung cancer in rats. The present study was designed to determine the role of nuclear factor erythroid 2-related factor (Nrf2) in MWCNT-induced inflammatory response in the lung of mice. Anesthetized male Nrf2 null mice and age-matched wild-type mice were exposed once to MWCNTs at either 0, 10, or 20 µg/mouse by pharyngeal aspiration. Bronchoalveolar lavage fluid (BALF) and lung tissues were collected after 7 days to evaluate pulmonary inflammation. Exposure to MWCNTs significantly increased BALF total cell counts and total protein level in wild-type mice, but not in Nrf2 null mice. MWCNT-exposed wild-type mice showed the significant increases in interleukin (IL)-1β, IL-6, and keratinocyte-derived chemokines (KC) levels in BALF, but these were not seen in BALF of Nrf2 null mice. Exposure to MWCNTs at 10 and 20 μg/mouse for 7 days did not significantly increase oxidative stress in both genotypes, but exposure to MWCNTs increased the levels of IL-1β and caspase-1 only in the lungs of wild-type mice. Our results demonstrate that Nrf2 promotes MWCNT-induced pulmonary inflammation, probably through inflammasome activation.

The deformation and leaching of substances from micro/nanoplastics under biotic and abiotic conditions is an important yet often overlooked issues for the environment and human health. Furthermore, their interaction with biomolecules can result in corona formation and the surface deformation of micro/nanoplastics. However, the interaction between micro/nanoplastics and biomolecules, e.g. pancreatin, and the resulting deformation/leaching mechanisms, as well as their biological impact, remains insufficiently understood. Therefore, this study aims to examine the deformation/leaching processes of micro/nanoplastics due to the action of the pancreatin. The interaction mechanism between micro/nanoplastics and pancreatin was investigated using multi-spectroscopic and molecular docking approaches. The deformation of micro/nanoplastics was tested based on their functional groups and structure, and their leaching into the pancreatin solution was assessed by measuring aromaticity and oxidative inputs. In addition, deformation and leaching effects of micro/nanoplastics on pancreatin were investigated using its structural characteristics (e.g. aromatic side chains, activity, and agglomeration), as well as bacterial toxicity using Escherichia coli (e.g. viability, biofilm, and oxidative stress). The Fluorescence and UV-VIS spectroscopic results, as well as molecular docking simulations, revealed interactions between micro/nanoplastics and pancreatin. Deformation of the micro/nanoplastics was confirmed using higher carbonyl and hydroxyl indices by ATR-FTIR, and removal and introduction signals by ¹H-NMR. The higher aromaticity and oxidative potential of the pancreatin indicated the leaching of chemicals from the micro/nanoplastics. Furthermore, the metabolic and oxidative responses of E. coli exposed to leachates were influenced by the deformation and leaching of micro/nanoplastics, as well as by the structural characteristics of the pancreatin.