Bacterial Susceptibility to Ceria Nanoparticles: The Critical Role of Surrounding Molecules.

Investigating the ternary relationship among nanoparticles (NPs), their immediate molecular environment, and test organisms rather than the direct interaction between pristine NPs and test organisms has been thrust into the mainstream of nanotoxicological research. Diverging from previous work that predominantly centered on surrounding molecules affecting the toxicity of NPs by modulating their nanoproperties, this study has unveiled a novel dimension: surrounding molecules altering bacterial susceptibility to NPs, consequently impacting the outcomes of nanobio interaction. The study found that adding nitrate as the surrounding molecules could alter bacterial respiratory pathways, resulting in an enhanced reduction of ceria NPs (nanoceria) on the bacterial surfaces. This, in turn, increased the ion-specific toxicity originating from the release of Ce3+ ions at the nanobio interface. Further transcriptome analysis revealed more mechanistic details underlying the nitrate-induced changes in the bacterial energy metabolism and subsequent toxicity patterns. These findings offer a new perspective for the deconstruction of nanobio interactions and contribute to a more comprehensive understanding of NPs' environmental fate and ecotoxicity.

Evaluation of the teratogenic potency of bulk zinc oxide and its nanoparticles on embryos of the freshwater snail, Helisoma duryi.

Bulk zinc oxide (ZnO-BPs) and its nanoparticles (ZnO-NPs) are frequently used in various products for humans. Helisoma duryi embryos can serve as effective model organisms for studying the toxicity of NPs. This study aimed to compare the teratogenic potency of ZnO-BPs and ZnO NPs in the embryonic stages of H. duryi to evaluate the utility of this snail as a bioindicator for ZnO-NPs in the aquatic environment. The mechanisms of teratogenesis were evaluated by determination of the LC50, studying the effect of sub-lethal concentrations of both ZnO forms on the embryos, and studying their enzyme activity, oxidative stress, and biochemical analysis. The SDS-PAGE electrophoresis was undertaken to assess the effect of ZnO-BPs and ZnO NPs on protein synthesis. The results revealed that the veliger stage of H. duryi is the specific stage for bulk and nano ZnO. ZnO-NPs proved to be more toxic to snails' embryos than ZnO-BPs. Exposure to ZnO influences specific types of defects in development, which in the case of BPs are far less drastic than those caused by NPs. Thus, the toxicity of ZnO-NPs in embryonic development is due to their unique physicochemical properties. The observed malformations include mainly hydropic malformation, exogastrulation, monophthalmia, shell misshapen, and cell lyses. Almost all tested oxidative biomarkers significantly changed, revealing that ZnONPs display more oxidative stress than ZnO-BPs. Also, the low concentration of ZnO induces many disturbances in the organic substances of veliger larvae, such as a decrease in the total protein and total lipid levels and an increase in the glycogen level. The results indicated that ZnO-BPs increase the number of protein bands. Conversely, ZnO-NPs concealed one band from treated egg masses, which was found in the control group. Embryos of snail are an appropriate model to control freshwater snails. This study demonstrates that H. duryi embryos can serve as effective model organisms to study the toxicity of ZnO-NPs.

Synergy between nanoplastics and benzo[a]pyrene promotes senescence by aggravating ferroptosis and impairing mitochondria integrity in Caenorhabditis elegans.

Micro-nano plastics have been reported as important carriers of polycyclic aromatic hydrocarbons (PAHs) for long-distance migration in the environment. However, the combined toxicity from long-term chronic exposure beyond the vehicle-release mechanism remains elusive. In this study, we investigated the synergistic action of Benzo[a]pyrene (BaP) and Polystyrene nanoparticles (PS) in Caenorhabditis elegans (C. elegans) as a combined exposure model with environmental concentrations. We found that the combined exposure to BaP and PS, as opposed to single exposures at low concentrations, significantly shortened the lifespan of C. elegans, leading to the occurrence of multiple senescence phenotypes. Multi-omics data indicated that the combined exposure to BaP and PS is associated with the disruption of glutathione homeostasis. Consequently, the accumulated reactive oxygen species (ROS) cannot be effectively cleared, which is highly correlated with mitochondrial dysfunction. Moreover, the increase in ROS promoted lipid peroxidation in C. elegans and downregulated Ferritin-1 (Ftn-1), resulting in ferroptosis and ultimately accelerating the aging process of C. elegans. Collectively, our study provides a new perspective to explain the long-term compound toxicity caused by BaP and PS at real-world exposure concentrations.

Zinc oxide nanoparticles induces cell death and consequently leading to incomplete neural tube closure through oxidative stress during embryogenesis.

The implementation of Zinc oxide nanoparticles (ZnO NPs) raises concerns regarding their potential toxic effects on human health. Although more and more researches have confirmed the toxic effects of ZnO NPs, limited attention has been given to their impact on the early embryonic nervous system. This study aimed to explore the impact of exposure to ZnO NPs on early neurogenesis and explore its underlying mechanisms. We conducted experiments here to confirm the hypothesis that exposure to ZnO NPs causes neural tube defects in early embryonic development. We first used mouse and chicken embryos to confirm that ZnO NPs and the Zn2+ they release are able to penetrate the placental barrier, influence fetal growth and result in incomplete neural tube closure. Using SH-SY5Y cells, we determined that ZnO NPs-induced incomplete neural tube closure was caused by activation of various cell death modes, including ferroptosis, apoptosis and autophagy. Moreover, dissolved Zn2+ played a role in triggering widespread cell death. ZnO NPs were accumulated within mitochondria after entering cells, damaging mitochondrial function and resulting in the over production of reactive oxygen species, ultimately inducing cellular oxidative stress. The N-acetylcysteine (NAC) exhibits significant efficacy in mitigating cellular oxidative stress, thereby alleviating the cytotoxicity and neurotoxicity brought about by ZnO NPs. These findings indicated that the exposure of ZnO NPs in early embryonic development can induce cell death through oxidative stress, resulting in a reduced number of cells involved in early neural tube closure and ultimately resulting in incomplete neural tube closure during embryo development. The findings of this study could raise public awareness regarding the potential risks associated with the exposure and use of ZnO NPs in early pregnancy.

Electrophysiological and biochemical effect of zinc oxide nanoparticles on heart functions of male Wistar rats.

Zinc oxide nanoparticles (ZnO NPs) are one of the most abundantly used nanomaterials in cosmetics and topical products, and nowadays, they are explored in drug delivery and tissue engineering. Some recent data evidenced that they are responsible for cardiotoxic effects and systemic toxicity. The present study aimed to investigate the toxic effect of ZnO NPs (39 nm) on the heart of Wistar rats and to perform a dose-response relationship using three different dose levels (25, 50, 100 mg/kg bw) of ZnO NPs on the electrocardiogram (ECG) readings, the levels of biochemical function parameters of heart, and the oxidative stress and antioxidant biomarkers. Furthermore, zinc concentration level and histopathological examination of heart tissues were determined. ZnO NPs showed a dose-dependent effect, as the 100 mg/kg bw ZnO NPs treated group showed the most significant changes in ECGs parameters: R-R distance, P-R interval, R and T amplitudes, and increased levels of heart enzymes Creatine Kinase- MB (CK-MB) and Lactate dehydrogenase (LDH). On the other hand, elevated zinc concentration levels, oxidative stress biomarkers MDA and NO, and decreased GSH levels were found also in a dose-dependent manner, the results were supported by impairment in the histopathological structure of heart tissues. While the dose of 100 mg/kg bw of ZnO bulk group showed no significant effects on heart function. The present study concluded that ZnO NPs could induce cardiac dysfunctions and pathological lesions mainly in the high dose.

Nano titanium dioxide alleviates the toxic effects of tris (2-chloropropyl) phosphate on the digestive gland and hemolymph of thick-shell mussel Mytilus coruscus.

In the marine environment, nanoparticles play a role in adsorbing and catalytically degrading organic pollutants, thereby mitigating their toxic effects on aquatic organisms. This study aimed to investigate the impact of nano titanium dioxide (nTiO2) and tris (2-chloropropyl) phosphate (TCPP) on the hemolymph and digestive function of the thick-shell mussel Mytilus coruscus. Mussels were divided into a control group, a group exposed to TCPP alone, a group exposed to a combination of TCPP and 0.5 mg/L nTiO2, and a group exposed to a combination of TCPP and 1 mg/L nTiO2. After 14 days of exposure, oxidative stress responses, including superoxide dismutase (SOD) activity and malondialdehyde (MDA) content, immune defense responses, including acid phosphatase (ACP) and alkaline phosphatase (AKP) activities, and gene expression, including HSP70 expression, were measured in the hemolymph and digestive glands of the mussels. Compared to the control group, mussels solely exposed to 100 µg/L TCPP exhibited a significant reduction in SOD activity in the hemolymph. When TCPP was co-exposed with 0.5 mg/L nTiO2, there were significant increases in MDA content and AKP activity in both the digestive gland and hemolymph compared to the control group. Upon co-exposure of TCPP with 1 mg/L nTiO2, MDA content and AKP activity in the digestive gland significantly decreased, while SOD, ACP, and AKP activity in the hemolymph significantly increased and MDA content significantly decreased, returning to the control group levels. Furthermore, in the combined exposure, HSP70 gene expression significantly decreased as the nTiO2 concentration increased from 0.5 mg/L to 1 mg/L. In summary, TCPP impacted the hemolymph and digestive function of mussels, whereas a concentration of 1 mg/L nTiO2 effectively alleviated the toxic effects of TCPP. This study is crucial for assessing the ecological risks of nanoparticles and emerging organic pollutants in marine environments, and provides new insights into the interaction between nTiO2 and TCPP, as well as the influence of nTiO2 concentration on mitigating TCPP toxicity.

Transcriptomic analysis reveals nanoplastics-induced apoptosis, autophagy and immune response in Litopenaeus vannamei.

Increasing attention is being paid to the toxic physiological effects of nanoplastics (NPs) on aquatic organisms. However, few studies have systematically evaluated the regulatory mechanisms of NPs on immune response in crustaceans. In this study, a 28-day chronic exposure experiment was conducted in which shrimps were exposed to various 80-nm polystyrene NPs concentrations (0, 0.1, 1, 5 and 10 mg/L). Transcriptomic analysis was used to investigate the regulatory mechanisms of NPs in immune response of Litopenaeus vannamei. With increasing NPs concentration, the total hemocyte count (THC) content decreased, while phagocytosis rate (PR) and respiratory burst (RB) showed trends of first rising and then falling. High concentration (10 mg/L) of NPs caused the destruction of hepatopancreas tissue structure, the shedding of microvilli, the increase number of hepatocyte apoptosis and autophagy structure. With increasing NPs concentration, the lysozyme (Lys), superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities first increased and then decrease, while contents of lipid peroxidation and malondialdehyde increased; the expression levels of Toll, MyD88, GPx, SOD, proPO, Lys, and ALF generally increased at first and then decreased. Transcriptional sequencing analysis showed that the pathway of differentially expressed genes in KEGG enrichment mainly included lysosome (ko04142), apoptosis (ko04210) pathways, indicating that the NPs mainly affected the immune regulatory mechanism. Further analysis by Gene Set Enrichment Analysis (GSEA) showed that the up-regulation pathways of NPs activation mainly included immune response-related pathways such as mitochondrial autophagy, DNA repair, autophagosomes signaling pathway. Our results indicated that NPs exposure induced oxidative stress, apoptosis and autophagy in shrimps. This study provides a basis for further understanding of the mechanisms of antioxidant immune regulation by NPs in shrimp and may serve as a reference for healthy ecological culture of shrimp.

Nanoplastics trigger the aging and inflammation of porcine kidney cells.

Nanoplastics have now become a pervasive contaminant, being detected in various environmental media. However, our understanding of the specific toxicological effects of nanoplastics (NPs) on the kidneys remains unclear, which is a scientific problem that needs to be solved. To address this question, we employed two kidney cell lines as in vitro models to study the toxicological effects of NPs on porcine kidney cells. Firstly, we observed that NPs can be internalized into the cytoplasm in a time- and dose-dependent manner by using a laser confocal microscope. We further discovered that NPs can trigger inflammatory responses and lead to porcine kidney cell senescence by detection of senescence marker molecules. Furthermore, the potential molecular mechanism(s) by which NPs induce porcine kidney cell senescence were explored, we found that NPs induce oxidative stress in the porcine kidney cells, leading to the accumulation of reactive oxygen species (ROS) within mitochondria, ultimately triggering inflammatory responses and senescence in the kidney cells. In summary, our experimental results not only provide new evidence for the toxicity of NPs but also offer new ideas and directions for future research. This discovery will aid in our deeper understanding of the potential health impacts of NPs on domestic pigs.

Silica nanoparticles-induced cytotoxicity and genotoxicity in A549 cell lines.

Among the myriad of nanoparticles, silica nanoparticles (SiO2NPs) have gained significant attention since they are extensively produced and used across several kinds of industries. Because of its widespread usage, there has been increasing concern about the potential health effects. This study aims to evaluate the effects of SiO2NPs on Interleukin-6 (IL-6) gene expression in human lung epithelial cell lines (A549). In this study, A549 cells were exposed to SiO2NPs at concentrations of 0, 1, 10, 50, 100, and 200 µg/mL for 24 and 48 h. The IL-6 gene expression was assessed using Real-Time RT-PCR. Additionally, the impact of SiO2NPs on the viability of A549 cells was determined by MTT assay. Statistical analysis was performed using GraphPad Prism software 8.0. MTT assay results indicated a concentration-dependent impact on cell survival. After 24 h, survival decreased from 80 to 68% (1-100 µg/mL), rising to 77% at higher concentrations. After 48 h, survival dropped from 97 to 80%, decreasing to 90% at higher concentrations. RT-PCR showed a dose-response relationship in cellular toxicity up to 10 µg/mL. At higher concentrations, there was increased IL-6 gene expression, mitigating SiO2NP-induced cytotoxic effects. The study shows that the viability and proliferation of A549 cells are impacted by different SiO2NPs concentrations. There may be a potential correlation between IL-6 gene expression reduction and a mechanism linked to cellular toxicity. However, at higher concentrations, an unknown mechanism increases IL-6 gene expression, reducing SiO2NPs' cytotoxic effects. These effects are concentration-dependent and not influenced by exposure times. Further investigation is recommended to determine this mechanism's nature and implications, particularly in cancer research.

Micro and nanoplastics pollution: Sources, distribution, uptake in plants, toxicological effects, and innovative remediation strategies for environmental sustainability.

Microplastics and nanoplastics (MNPs), are minute particles resulting from plastic fragmentation, have raised concerns due to their widespread presence in the environment. This study investigates sources and distribution of MNPs and their impact on plants, elucidating the intricate mechanisms of toxicity. Through a comprehensive analysis, it reveals that these tiny plastic particles infiltrate plant tissues, disrupting vital physiological processes. Micro and nanoplastics impair root development, hinder water and nutrient uptake, photosynthesis, and induce oxidative stress and cyto-genotoxicity leading to stunted growth and diminished crop yields. Moreover, they interfere with plant-microbe interactions essential for nutrient cycling and soil health. The research also explores the translocation of these particles within plants, raising concerns about their potential entry into the food chain and subsequent human health risks. The study underscores the urgency of understanding MNPs toxicity on plants, emphasizing the need for innovative remediation strategies such as bioremediation by algae, fungi, bacteria, and plants and eco-friendly plastic alternatives. Addressing this issue is pivotal not only for environmental conservation but also for ensuring sustainable agriculture and global food security in the face of escalating plastic pollution.

Oral exposure to polystyrene nanoplastics altered the hypothalamic-pituitary-testicular axis role in hormonal regulation, inducing reproductive toxicity in albino rats.

BACKGROUND: Nanoplastics can be considered a novel contaminant for the environment because of their extensive applications in modern society, which represents a possible threat to humans. Nevertheless, the negative effect of polystyrene nanoplastics (PS-NPs) on male reproduction, fertility, and progeny outcomes is not well known. Thus, the aim of the present work was to calculate the median lethal dose (LD50) and investigate the consequences of exposure to PS-NPs (25 nm) on male reproductive toxicity. METHODS: This investigation first determined the LD50 of PS-NPs in male Wistar rats, and then in a formal study, 24 rats were distributed into three groups (n = 8): the control group; the low-dose group (3 mg/kg bw); and the high-dose group (10 mg/kg bw) of PS-NPs administered orally for 60 days. On the 50th day of administration, the fertility test was conducted. RESULTS: The LD50 was determined to be 2500 mg/kg. PS-NP administration induced significant alternations, mainly indicating mortality in the high-dose group, a significant elevation in body weight gain, declined sperm quality parameters, altered reproductive hormonal levels, thyroid endocrine disruption, an alternation of the normal histo-architecture and the histo-morphometric analysis of the testes, and impaired male fertility. CONCLUSION: Altogether, the current findings provide novel perspectives on PS-NP general toxicity with specific reference to male reproductive toxicity.

Preclinical Safety Assessment of Lepidium sativum L. Seed Extract and its Nanoparticles via Acute and Subacute Oral Administration.

BACKGROUND: Lepidium sativum (LS) seed extract has various pharmacological properties, such as antioxidant, hepatoprotective, and anticancer activities. However, the translation of L. sativum seed extract to the clinical phase is still tedious due to its bioavailability and stability issues. This problem can be solved by encapsulating it in a nanodelivery system to improve its therapeutic potency. METHODS: In this study, we have determined and compared the in vivo toxicity of ethanolic extracts of L. sativum seeds (EELS) and solid lipid nanoparticles (SLNs). To conduct toxicity (acute and subacute toxicity) assessments, EELS and SLNs were orally administered to Swiss albino mice. Animal survival, body weight, the weight of vital organs in relation to body weight, haematological profile, biochemistry profile, and histopathological alterations were examined. RESULTS: Animals administered with 2000 mg/kg and 5000 mg/kg in an acute toxicity study exhibited no toxicological symptoms regarding behaviour, gross pathology, and body weight. As per a study on acute toxicity, the LD50 (lethal dose) for SLNs and EELS was over 400 mg/kg and over 5000 mg/kg, respectively. When animals were given SLNs (50 and 100 mg/kg, orally) and EELS (250, 500, and 1000 mg/kg, orally) for 28 days, subacute toxicity study did not exhibit any clinical changes. There were no differences in weight gain, haematological parameters, or biochemical parameters compared to the control groups (p > 0.05). The organs of the treated animals showed no abnormalities in the histological analysis (liver, heart, kidney, and spleen). CONCLUSION: The result confirms ethanolic extracts of L. sativum seeds and their SLNs to not have harmful effects following acute and subacute administration to mice. For further studies, patents available on Lepidium may be referred for its preclinical and clinical applications.

Lead-rivet strategy of growing perovskite nanocrystals for excellent toxicity inhibition and spinning application.

Lead halide perovskite has demonstrated remarkable potential in the wearable field due to its exceptional photoelectric conversion capability. However, its lead toxicity issue has consistently been subject to criticism, significantly impeding its practical application. To address this challenge, an innovative approach called lead-rivet was proposed for the in-situ growth of perovskite crystalline structures. Through the formation of S-Pb bonds, each Pb2+ ion was firmly immobilized on the surface of the silica matrix, enabling in situ growth of perovskite nanocrystals via ion coordination between Cs+ and halide species. The robust S-Pb bonding effectively restricted the mobility of lead ions and stabilized the perovskite structure without relying on surface ligands, thereby not only preventing toxicity leakage but also providing a favorable interface for depositing protective shells. The obtained perovskites exhibit intense and narrow-band fluorescence with full-width at half-maximum less than 23 nm and show excellent stability to high temperature (above 202 °C) and high humidity (water immersion over 27 days), thus making it possible to be used in varies textile technologies including melt spinning and wet spinning. The lead leakage rate of particles is only 4.15 % demonstrating excellent toxicity inhibition performance. The prepared fibers maintained good extensibility and flexibility which could be used for 3D-printing and textiles weaving. Most importantly, the detected Pb2+ leaching was negligible as low as to 0.732 ppb which meet the standard of World Health Organization (WHO) for drinking water (<10 ppb), and the cell survival rate remained 99.196 % for PLA fluorescent filament after 24 h cultivation which showing excellent safety to human body and environment. This study establishes a controllable and highly adaptable synthesis method, thereby providing a promising avenue for the safe utilization of perovskite materials.

Photoaged nanoplastics with multienzyme-like activities significantly shape the horizontal transfer of antibiotic resistance genes.

Nanoplastics (NPs), identified as emerging pollutants, pose a great risk to environment and global public health, exerting profound influences on the prevalence and dissemination of antibiotic resistance genes (ARGs). Despite evidence suggesting that nano-sized plastic particles can facilitate the horizontal gene transfer (HGT) of ARGs, it is imperative to explore strategies for inhibiting the transfer of ARGs. Currently, limited information exists regarding the characteristics of environmentally aged NPs and their impact on ARGs propagation. Herein, we investigated the impact of photo-aged NPs on the transfer of ARG-carrying plasmids into Escherichia coli (E. coli) cells. Following simulated sunlight irradiation, photo-aged nano-sized polystyrene plastics (PS NPs) exhibited multiple enzyme-like activities, including peroxidase (POD) and oxidase (OXD), leading to a burst of reactive oxygen species (ROS). At relatively low concentrations (0.1, 1 µg/mL), both pristine and aged PS NPs facilitated the transfer of pUC19 and pHSG396 plasmids within E. coli due to moderate ROS production and enhanced cell membrane permeability. Intriguingly, at relatively high concentrations (5, 10 µg/mL), aged PS NPs significantly suppressed plasmids transformation. The non-unidirectional impact of aged PS NPs involved the overproduction of ROS (•OH and •O2-) via nanozyme activity, directly degrading ARGs and damaging plasmid structure. Additionally, oxidative damage to bacteria resulted from the presence of much toxic free radicals, causing physical damage to cell membranes, reduction of the SOS response and restriction of adenosine-triphosphate (ATP) supply, ultimately leading to inactivation of recipient cells. This study unveils the intrinsic multienzyme-like activity of environmentally aged NPs, highlighting their potential to impede the transfer and dissemination of ARGs.

Polylactic acid nanoplastics (PLA-NPLs) induce adverse effects on an in vitro model of the human lung epithelium: The Calu-3 air-liquid interface (ALI) barrier.

The expected increments in the production/use of bioplastics, as an alternative to petroleum-based plastics, require a deep understanding of their potential environmental and health hazards, mainly as nanoplastics (NPLs). Since one important exposure route to NPLs is through inhalation, this study aims to determine the fate and effects of true-to-life polylactic acid nanoplastics (PLA-NPLs), using the in vitro Calu-3 model of bronchial epithelium, under air-liquid interphase exposure conditions. To determine the harmful effects of PLA-NPLs in a more realistic scenario, both acute (24 h) and long-term (1 and 2 weeks) exposures were used. Flow cytometry results indicated that PLA-NPLs internalized easily in the barrier (∼10 % at 24 h and ∼40 % after 2 weeks), which affected the expression of tight-junctions formation (∼50 % less vs control) and the mucus secretion (∼50 % more vs control), both measured by immunostaining. Interestingly, significant genotoxic effects (DNA breaks) were detected by using the comet assay, with long-term effects being more marked than acute ones (7.01 vs 4.54 % of DNA damage). When an array of cellular proteins including cytokines, chemokines, and growth factors were used, a significant over-expression was mainly found in long-term exposures (∼20 proteins vs 5 proteins after acute exposure). Overall, these results described the potential hazards posed by PLA-NPLs, under relevant long-term exposure scenarios, highlighting the advantages of the model used to study bronchial epithelium tissue damage, and signaling endpoints related to inflammation.

Integrated multilevel investigation of photosynthesis revealed the algal response distinction to differentially charged nanoplastics.

Nanoplastics (NPs), especially those with different charges, as one of emerging contaminants pose a threat to aquatic ecosystems. Although differentially charged NPs could induce distinct biological effects, mechanistic understanding of the critical physiological processes of aquatic organisms from an integrated multilevel perspective on aquatic organisms is still uncertain. Herein, multi-effects of differentially charged nanosized polystyrene (nPS) including neutral nPS, nPS-COOH, and nPS-NH2 on the photosynthesis-related physiological processes of algae were explored at the population, individual, subcellular, protein, and transcriptional levels. Results demonstrated that both nPS and nPS-COOH exhibited hormesis to algal photosynthesis but nPS-NH2 triggered severe inhibition. As for nPS-NH2, the integrity of algal subcellular structure, chlorophyll biosynthesis, and expression of photosynthesis-related proteins and genes were interfered. Intracellular NPs' content in nPS treatment was 25.64 % higher than in nPS-COOH treatment, and the content of chloroplasts in PS and nPS-COOH treatment were 3.09 % and 4.56 % higher than control, respectively. Furthermore, at the molecular levels, more photosynthesis-related proteins and genes were regulated under nPS-COOH exposure than those exposed to nPS. Light-harvesting complex II could be recognized as an underlying explanation for different effects between nPS and nPS-COOH. This study first provides a novel approach to assess the ecological risks of NPs at an integrated multilevel.

Neurotoxicity and Developmental Neurotoxicity of Copper Sulfide Nanoparticles on a Human Neuronal In-Vitro Test System.

Nanoparticles (NPs) are becoming increasingly important novel materials for many purposes, including basic research, medicine, agriculture, and engineering. Increasing human and environmental exposure to these promising compounds requires assessment of their potential health risks. While the general direct cytotoxicity of NPs is often routinely measured, more indirect possible long-term effects, such as reproductive or developmental neurotoxicity (DNT), have been studied only occasionally and, if so, mostly on non-human animal models, such as zebrafish embryos. In this present study, we employed a well-characterized human neuronal precursor cell line to test the concentration-dependent DNT of green-manufactured copper sulfide (CuS) nanoparticles on crucial early events in human brain development. CuS NPs turned out to be generally cytotoxic in the low ppm range. Using an established prediction model, we found a clear DNT potential of CuS NPs on neuronal precursor cell migration and neurite outgrowth, with IC50 values 10 times and 5 times, respectively, lower for the specific DNT endpoint than for general cytotoxicity. We conclude that, in addition to the opportunities of NPs, their risks to human health should be carefully considered.

Micro/nano-plastics impacts in cardiovascular systems across species.

The widespread presence of microplastics and nanoplastics (MPs/NPs) in the environment has become a critical public health issue due to their potential to infiltrate and affect various biological systems. Our review is crucial as it consolidates current data and provides a comprehensive analysis of the cardiovascular impacts of MPs/NPs across species, highlighting significant implications for human health. By synthesizing findings from studies on aquatic and terrestrial organisms, including humans, this review offers insights into the ubiquity of MPs/NPs and their pathophysiological roles in cardiovascular systems. We demonstrated that exposure to MPs/NPs is linked to various cardiovascular ailments such as thrombogenesis, vascular damage, and cardiac impairments in model organisms, which likely extrapolate to humans. Our review critically evaluated methods for detecting MPs/NPs in biological tissues, assessing their toxicity, and understanding their behaviour within the vasculature. These findings emphasise the urgent need for targeted public health strategies and enhanced regulatory measures to mitigate the impacts of MP/NP pollution. Furthermore, the review underlined the necessity of advancing research methodologies to explore long-term effects and potential intergenerational consequences of MP/NP exposure. By mapping out the intricate links between environmental exposure and cardiovascular risks, our work served as a pivotal reference for future research and policymaking aimed at curbing the burgeoning threat of plastic pollution.

Toxicity of different-sized cobalt ferrite (CoFe2O4) nanoparticles to Oncorhynchus mykiss at early development stages.

As innovative and versatile agents with potential applications in a wide range of fields including medicine, electronics, wastewater treatment, cosmetics, and energy storage devices, magnetic nanoparticles (NPs) are significant attention. However, our knowledge of the harmful effects of different-sized NPs, particularly of their effects on aquatic animals, is limited. In this study, we evaluated the impact of different-sized (sub-2, 5, and 15 nm) cobalt ferrite (CoFe2O4) NPs on the biological parameters of rainbow trout (Oncorhynchus mykiss) embryos and larvae. The NPs were characterized using techniques such as high-resolution transmission electron microscopy (HRTEM) for imaging, X-ray diffraction (XRD) for crystallographic analysis, and energy-dispersive X-ray spectroscopy (EDX) for elemental analysis, and were tested for impact through a series of toxicity, genotoxicity, and biochemical assays at a concentration of 100 mg/L. The obtained results showed that toxicity of CoFe2O4 NPs depended on the size of NPs and the developmental stage of the fish. Our results, which revealed significant changes in biological parameters of O. mykiss under exposure to CoFe2O4 NPs, imply that these NPs may be not environmentally safe. The hierarchical cluster analysis showed that embryos of the control group were clearly separated from those exposed to NPs of various sizes. However, in the exposed larvae, the effects of control and the smallest-sized NPs (sub-2 nm) differed from those induced by larger NPs (5 nm and 15 nm). Additional research is necessary to comprehend the mechanisms underlying the observed variations, which would be advantageous for both managing the risk of NPs to humans and advancing the field of aquatic nanotoxicology.

TiO2 nanoparticle photoactivation and oxidation reactions in freshwater and marine systems: The role of radical scavengers.

Titanium dioxide nanoparticles (TiO2-NP) present in wastewater effluent are discharged into freshwater and saltwater (i.e., marine) systems. TiO2-NP can be solar-driven photoactivated by ultraviolet (UV)-light producing reactive oxygen species including hydroxyl radicals (·OH). ·OH are non-selective and react with a broad range of species in water. In other studies, photoactivation of TiO2-NP has been correlated with oxidative stress and ecotoxicological impacts on plant and animal biota. This study examined the photoactivation of TiO2-NP in freshwater and saltwater systems, and contrasted the oxidation potential in both systems using methylene blue (MB) as a reaction probe. Maximum MB loss (51.9%, n = 4; 95% confidence interval 49.4-54.5) was measured in salt-free, deionized water where ·OH scavenging was negligible; minimum MB loss (1%) was measured in saltwater due to significant ·OH scavenging, indicating the inverse correlation between MB loss and radical scavenging. A kinetic analysis of scavenging by seawater constituents indicated Cl- had the greatest impact due to high concentration and high reaction rate constant. Significant loss of MB occurred in the presence of Br- relative to other less aggressive scavengers present in seawater (i.e., HCO3-, HSO4-). This result is consistent with the formation of Bromate, a strong oxidant that subsequently reacts with MB. In freshwater samples collected from different water bodies in Oklahoma (n = 12), the average MB loss was 13.4%. Greater MB loss in freshwater systems relative to marine systems was due to lower ·OH scavenging by various water quality parameters. Overall, TiO2-NP photoactivation in freshwater systems has the potential to cause greater oxidative stress and ecotoxicological impacts than in marine systems where ·OH scavenging is a dominant reaction.