Metal and metal oxide nanoparticles-induced reactive oxygen species: Phytotoxicity and detoxification mechanisms in plant cell.

Nanotechnology is advancing rapidly in this century and the industrial use of nanoparticles for new applications in the modernization of different industries such as agriculture, electronic, food, energy, environment, healthcare and medicine is growing exponentially. Despite applications of several nanoparticles in different industries, they show harmful effects on biological systems, especially in plants. Various mechanisms for the toxic effects of nanoparticles have already been proposed; however, elevated levels of reactive oxygen species (ROS) molecules including radicals [(e.g., superoxide (O2•‒), peroxyl (HOO•), and hydroxyl (HO•) and non-radicals [(e.g., hydrogen peroxide (H2O2) and singlet oxygen (1O2) is more important. Excessive production/and accumulation of ROS in cells and subsequent induction of oxidative stress disrupts the normal functioning of physiological processes and cellular redox reactions. Some of the consequences of ROS overproduction include peroxidation of lipids, changes in protein structure, DNA strand breaks, mitochondrial damage, and cell death. Key enzymatic antioxidants with ROS scavenging ability comprised of superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX), peroxidase (POD), and glutathione reductase (GR), and non-enzymatic antioxidant systems including alpha-tocopherol, flavonoids, phenolic compounds, carotenoids, ascorbate, and glutathione play vital role in detoxification and maintaining plant health by balancing redox reactions and reducing the level of ROS. This review provides compelling evidence that phytotoxicity of nanoparticles, is mainly caused by overproduction of ROS after exposure. In addition, the present review also summarizes the intrinsic detoxification mechanisms in plants in response to nanoparticles accumulation within plant cells.

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.

Mixture toxicity study of two metal oxide nanoparticles and chlorpyrifos on Eisenia andrei earthworms.

Co-exposure soil studies of pollutants are necessary for an appropriate ecological risk assessment. Here, we examined the effects of two-component mixtures of metal oxide nanoparticles (ZnO NPs or goethite NPs) with the insecticide chlorpyrifos (CPF) under laboratory conditions in short-term artificial soil assays using Eisenia andrei earthworms. We characterized NPs and their mixtures by scanning electron microscopy, atomic force microscopy, dynamic light scattering and zeta potential, and evaluated effects on metal accumulation, oxidative stress enzymes, and neurotoxicity related biomarkers in single and combined toxicity assays. Exposure to ZnO NPs increased Zn levels compared to control in single and combined exposure (ZnO NPs + CPF) at 72 h and 7 days, respectively. In contrast, there was no indication of Fe increase in organisms exposed to goethite NPs. One of the most notable effects on oxidative stress biomarkers was produced by single exposure to goethite NPs, showing that the worms were more sensitive to goethite NPs than to ZnO NPs. Acetylcholinesterase and carboxylesterase activities indicated that ZnO NPs alone were not neurotoxic to earthworms, but similar degrees of inhibition were observed after single CPF and ZnO NPs + CPF exposure. Differences between single and combined exposure were found for catalase and superoxide dismutase (goethite NPs) and for glutathione S-transferase (ZnO NPs) activities, mostly at 72 h. These findings suggest a necessity to evaluate mixtures of NPs with co-existing contaminants in soil, and that the nature of metal oxide NPs and exposure time are relevant factors to be considered when assessing combined toxicity, as it may have an impact on ecotoxicological risk assessment.

Determining toxicity of europium oxide nanoparticles in immune cell components and hematopoiesis in dominant organs in mice: Role of lysosomal fluid interaction.

Extensive application of rare earth element oxide nanoparticles (REE NPs) has raised a concern over the possible toxic health effects after human exposure. Once entering the body, REE NPs are primarily processed by phagocytes in particular macrophages and undergo biotic phosphate complexation in lysosomal compartment. Such biotransformation affects the target organs and in vivo fate of REE NPs after escaping the lysosomes. However, the immunomodulatory effects of intraphagolysosomal dissolved REE NPs remains insufficient. Here, europium oxide (Eu2O3) NPs were pre-incubated with phagolysosomal simulant fluid (PSF) to mimic the biotransformation of europium oxide (p-Eu2O3) NPs under acid phagolysosome conditions. We investigated the alteration in immune cell components and the hematopoiesis disturbance on adult mice after intravenous administration of Eu2O3 NPs and p-Eu2O3 NPs. Our results indicated that the liver and spleen were the main target organs for Eu2O3 NPs and p-Eu2O3 NPs. Eu2O3 NPs had a much higher accumulative potential in organs than p-Eu2O3 NPs. Eu2O3 NPs induced more alterations in immune cells in the spleen, while p-Eu2O3 NPs caused stronger response in the liver. Regarding hematopoietic disruption, Eu2O3 NPs reduced platelets (PLTs) in peripheral blood, which might be related to the inhibited erythrocyte differentiation in the spleen. By contrast, p-Eu2O3 NPs did not cause significant disturbance in peripheral PLTs. Our study demonstrated that the preincubation with PSF led to a distinct response in the immune system compared to the pristine REE NPs, suggesting that the potentially toxic effects induced by the release of NPs after phagocytosis should not be neglected, especially when evaluating the safety of NPs application in vivo.

Remediation of Metal Oxide Nanotoxicity with a Functional Amyloid.

Understanding the environmental health and safety of nanomaterials (NanoEHS) is essential for the sustained development of nanotechnology. Although extensive research over the past two decades has elucidated the phenomena, mechanisms, and implications of nanomaterials in cellular and organismal models, the active remediation of the adverse biological and environmental effects of nanomaterials remains largely unexplored. Inspired by recent developments in functional amyloids for biomedical and environmental engineering, this work shows their new utility as metallothionein mimics in the strategically important area of NanoEHS. Specifically, metal ions released from CuO and ZnO nanoparticles are sequestered through cysteine coordination and electrostatic interactions with beta-lactoglobulin (bLg) amyloid, as revealed by inductively coupled plasma mass spectrometry and molecular dynamics simulations. The toxicity of the metal oxide nanoparticles is subsequently mitigated by functional amyloids, as validated by cell viability and apoptosis assays in vitro and murine survival and biomarker assays in vivo. As bLg amyloid fibrils can be readily produced from whey in large quantities at a low cost, the study offers a crucial strategy for remediating the biological and environmental footprints of transition metal oxide nanomaterials.

The effect of three additives on properties of mineral trioxide aggregate cements: a systematic review and meta-analysis of in vitro studies.

BACKGROUND: Several efforts have been made to improve mechanical and biological properties of calcium silicate-based cements through changes in chemical composition of the materials. This study aimed to investigate the physical (including setting time and compressive strength) and chemical (including calcium ion release, pH level) properties as well as changes in cytotoxicity of mineral trioxide aggregate (MTA) after the addition of 3 substances including CaCl2, Na2HPO4, and propylene glycol (PG). METHODS: The systematic review was conducted in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). Electronic searches were performed on PubMed, Embase, and Scopus databases, spanning from 1993 to October 2023 in addition to manual searches. Relevant laboratory studies were included. The quality of the included studies was assessed using modified ARRIVE criteria. Meta-analyses were performed by RevMan statistical software. RESULTS: From the total of 267 studies, 24 articles were included in this review. The results of the meta-analysis indicated that addition of PG increased final setting time and Ca2+ ion release. Addition of Na2HPO4 did not change pH and cytotoxicity but reduced the final setting time. Incorporation of 5% CaCl2 reduced the setting time but did not alter the cytotoxicity of the cement. However, addition of 10% CaCl2 reduced cell viability, setting time, and compressive strength. CONCLUSION: Inclusion of 2.5% wt. Na2HPO4 and 5% CaCl2 in MTA can be advisable for enhancing the physical, chemical, and cytotoxic characteristics of the admixture. Conversely, caution is advised against incorporating elevated concentrations of PG due to its retarding effect. TRIAL REGISTRATION: PROSPERO registration number: CRD42021253707.

Evaluation of the genotoxicity, cytotoxicity, and bioactivity of calcium silicate-based cements.

BACKGROUND: As calcium silicate-based cements (CSCs) have found success in various vital pulp therapy applications, several new CSC products have emerged. This study aimed to assess the genotoxicity, cytotoxicity, and bioactivity of four CSCs by comparing the newly introduced materials Bio MTA+ and MTA Cem with previously studied materials, Biodentine and NeoMTA. METHODS: Genotoxicity was evaluated using the micronucleus (MN) assay in human peripheral blood lymphocyte cells, measuring MN frequency and nuclear division index (NDI). Cytotoxicity was assessed in human dental pulp stem cells through the Water-Soluble Tetrazolium Salt-1 (WST-1) colorimetric assay. Bioactivity was determined by ELISA, measuring the levels of angiogenic and odontogenic markers (BMP-2, FGF-2, VEGF, and ALP). Statistical analyses included ANOVA, Dunnet and Sidak tests, and Wald chi-square test. (p < .05). RESULTS: The MN frequency in the groups was significantly lower than that in the positive control group (tetraconazole) (p < .05). NDI values decreased with increasing concentration (p < .05). Bio MTA+ and NeoMTA showed decreased cell viability at all concentrations in 7-day cultures (p < .01). All materials increased BMP-2, FGF-2, and VEGF levels, with Biodentine and NeoMTA showing the highest levels of BMP-2 and FGF-2 on day 7. Biodentine displayed the highest VEGF levels on day 7. Biodentine and NeoMTA groups exhibited significantly higher ALP activity than the Bio MTA+ and MTA Cem groups by day 7. CONCLUSION: Bio MTA+ and MTA Cem demonstrated no genotoxic or cytotoxic effects. Moreover, this study revealed bioactive potentials of Bio MTA+ and MTA Cem by enhancing the expression of angiogenic and osteogenic growth factors.

Cytotoxicity prediction of nano metal oxides on different lung cells via Nano-QSAR.

In recent years, nanomaterials have found extensive applications across diverse domains owing to their distinctive physical and chemical characteristics. It is of great importance in theoretical and practical terms to carry out the relationship between structural characteristics of nanomaterials and different cytotoxicity and to achieve practical assessment and prediction of cytotoxicity. This study investigated the intrinsic quantitative constitutive relationships between the cytotoxicity of nano-metal oxides on human normal lung epithelial cells and human lung adenocarcinoma cells. We first employed quasi-SMILES-based nanostructural descriptors by selecting the five physicochemical properties that are most closely related to the cytotoxicity of nanometal oxides, then established SMILES-based descriptors that can effectively describe and characterize the molecular structure of nanometal oxides, and then built the corresponding Nano-Quantitative Structure-Activity Relationship (Nano-QSAR) prediction models, finally, combined with the theory of reactive oxygen species (ROS) biotoxicity, to reveal the mechanism of toxicity and differences between the two cell types. The established model can efficiently and accurately predict the properties of targets, reveal the corresponding toxicity mechanisms, and guide the safe design, synthesis, and application of nanometal oxides.

Dynamic interplay of metal and metal oxide nanoparticles with plants: Influencing factors, action mechanisms, and assessment of stimulatory and inhibitory effects.

Nanoparticles (NPs) of metals and metal oxides have received increasing attention regarding their characteristic behavior in plant systems. The fate and transport of metal NPs and metal oxide NPs in plants is of emerging concern for researchers because they ultimately become part of the food chain. The widespread use of metal-based NPs (MBNPs) in plants has revealed their beneficial and harmful effects. This review addresses the main factors affecting the uptake, translocation, absorption, bioavailability, toxicity, and accumulation of MBNPs in different plant species. It appraises the mechanism of nanoparticle-plant interaction in detail and provides understanding of the estimation strategies for the associated pros and cons with this interplay. Critical parameters of NPs include, but are not limited to, particle size and shape, surface chemistry, surface charge, concentration, solubility, and exposure route. On exposure to MBNPs, the molecular, physiological, and biochemical reactions of plants have been assessed. We have filled knowledge gaps and answered research questions regarding the positive and negative effects of metal and metal oxide NPs on seed germination, callus induction, growth and yield of plant, nutritional content, antioxidants, and enzymes. Besides, the phytotoxicity, cytotoxicity, genotoxicity, and detoxification studies of MBNPs in plants have been outlined. Furthermore, the recent developments and future perspectives of the two-way traffic of interplay of MBNPs and plants have been provided in this comprehensive review.

Toxicokinetics of rare earth element oxides administered intravenously to rats.

Rare earth elements (REEs) are increasingly used in a wide range of applications. However, their toxicokinetic behaviors in animals and humans are not yet fully documented, hindering health risk assessments. We used a rat experimental model to provide novel data on the toxicokinetics of the insoluble oxide forms of praseodymium (Pr), neodymium (Nd), cerium (Ce) and yttrium (Y) administered intravenously. Detailed blood, urinary and fecal time courses were documented through serial sampling over 21 days in male Sprague-Dawley rats exposed to a mixture of these REE oxides administered at two different doses (0.3 or 1 mg kg-1 bw of each REE oxide commercially sold as bulk µm-sized particles). Tissue REE levels at the time of sacrifice were also measured. Significant effects of the dose on REE time courses in blood and on cumulative urinary and fecal excretion rates were observed for all four REE oxides assessed, as lower cumulative excretion rates were noted at the higher REE dose. In the liver, the main accumulation organ, the fraction of the administered REE dose remaining in the tissue at necropsy was similar at both doses. Toxicokinetic data for the REE oxides were compared to similar data for their chloride salts (also administered intravenously in a mixture, at 0.3 and 1 mg kg-1 bw of each REE chloride) obtained from a previous study. Compared to their chloride counterparts, faster elimination of REE oxides from the blood was observed in the first hours post-dosing. Furthermore, higher mean residence time (MRT) values as well as slower cumulative urinary and fecal excretion were determined for the REE oxides. Also, while liver REE retention was similar for both REE forms, the fractions of the administered REEs recovered in the spleen and lungs were noticeably higher for the REE oxides, at both dose levels. This study highlights the importance of both the dose and form of the administered REEs on their toxicokinetic profiles. Results indicate that chronic exposure and increased doses of REEs may favor bioaccumulation in the body, in particular for insoluble oxide forms of REEs, which are eliminated more slowly from the body.

Biotoxicity of Halide Perovskites in Mice.

Halide perovskites are crystalline semiconductors with exceptional optoelectronic properties, rapidly developing toward large-scale applications. Lead (II) (Pb2+ ) is the core element used to prepare halide perovskites. Pb2+ can displace key 2+ elements, including calcium, zinc and iron, that regulate vital physiological functions. Sn2+ can replace Pb2+ within the perovskite structure and, if accidentally dispersed in the environment, it readily oxidizes to Sn4+ , which is compatible with physiological functions and thus potentially safe. The 3+ salt bismuth (III) (Bi3+ ) is also potentially safe for the same reason and useful to prepare double perovskites. Here, this work studies the biotoxicity of Pb, Sn, and Bi perovskites in mice for the first time. This work analyses histopathology and growth of mice directly exposed to perovskites and investigate the development of their offspring generation. This study provides the screening of organs and key physiological functions targeted by perovskite exposure to design specific studies in mammalians.

MnO2 nanoparticles trigger hepatic lipotoxicity and mitophagy via mtROS-dependent Hsf1Ser326 phosphorylation.

Manganese (Mn) is an essential element for maintaining normal metabolism in vertebrates. Mn dioxide nanoparticles (MnO2 NPs), a novel Mn source, have shown great potentials in biological and biomedical applications due to their distinct physical and chemical properties. However, little is known about potential adverse effects on animal or cellular metabolism. Here, we investigated whether and how dietary MnO2 NPs affect hepatic lipid metabolism in vertebrates. We found that, excessive MnO2 NPs intake increased hepatic and mitochondrial Mn content, promoted hepatic lipotoxic disease and lipogenesis, and inhibited hepatic lipolysis and fatty acid ß-oxidation. Moreover, excessive MnO2 NPs intake induced hepatic mitochondrial oxidative stress, damaged mitochondrial function, disrupted mitochondrial dynamics and activated mitophagy. Importantly, we uncovered that mtROS-activated phosphorylation of heat shock factor 1 (Hsf1) at Ser326 residue mediated MnO2 NPs-induced hepatic lipotoxic disease and mitophagy. Mechanistically, MnO2 NPs-induced lipotoxicity and mitophagy were via mtROS-induced phosphorylation and nucleus translocation of Hsf1 and its DNA binding capacity to plin2/dgat1 and bnip3 promoters, respectively. Overall, our findings uncover novel mechanisms by which mtROS-mediated mitochondrial dysfunction and phosphorylation of Hsf1S326 contribute to MnO2 NPs-induced hepatic lipotoxicity and mitophagy, which provide new insights into the effects of metal oxides nanoparticles on hepatotoxicity in vertebrates.

The protective impact of curcumin, vitamin D and E along with manganese oxide and Iron (III) oxide nanoparticles in rats with scrotal hyperthermia: Role of apoptotic genes, miRNA and circRNA.

BACKGROUND: Infertility is one of the major factors affecting most people around the world. Short-term exposure to high temperatures can cause hyperthermia, which is one of the causes of male infertility. The aim of this study was to investigate the protective effect of curcumin, vitamins D and E along with Iron (III) oxide nanoparticles (Fe2O3-NPs) and manganese oxide nanoparticles (MnO2-NPs) on semen parameters and its effect on miRNA21 and circRNA0001518 expression. MATERIAL AND METHODS: In this study, the lower part of the rat was exposed to 43 °C for 5 weeks every other day for 5 weeks. Then the animals were killed. Tissue samples were collected for sperm parameters analysis, and tissue samples were taken for evaluation of apoptosis levels in germ cells, and RNA extraction in order to examine the expression of Bax, Bcl-2, miRNA, and CircRNA genes. RESULTS: The results of this study showed that administration of curcumin, vitamin D, and vitamin E with Fe2O3-NPs and MnO2-NPs can improve the parameters of semen, Bax gene expression, Bcl-2 as well as miRNA and CircRNA in rats with testicular hyperthermia. In addition, curcumin by reducing the toxicity of Fe2O3 nanoparticles was able to reduce its negative effects and also reduce apoptosis in germ cells. This decrease in apoptosis was attributed to decreased Bcl-2 gene expression and increased expression of Bax, miRNA-21, and circRNA0001518. CONCLUSION: All the results of this study confirmed that Fe2O3-NPs and Mno2-NPs containing antioxidants or vitamins are useful in improving fertility in rats due to scrotal hyperthermia. Although Fe2O3-NPs and Mno2-NPs containing both antioxidants and vitamins had a greater effect on improving fertility and reducing the toxic effects of nanoparticles.

Vitamin C enhances the sensitivity of osteosarcoma to arsenic trioxide via inhibiting aerobic glycolysis.

Osteosarcoma (OS) is a common malignant tumor disease in the department of orthopedics, which is prone to the age of adolescents and children under 20 years old. Arsenic trioxide (ATO), an ancient poison, has been reported to play a critical role in a variety of tumor treatments, including OS. However, due to certain poisonous side effects such as cardiotoxicity and hepatotoxicity, clinical application of ATO has been greatly limited. Here we report that low doses of ATO (1 µM) observably reduced the half-effective inhibitory concentration (IC50) of vitamin C on OS cells. Compared with the treatment alone, the synthetic application of vitamin C (VitC, 800 µM) and ATO (1 µM) significantly further inhibited the proliferation, migration, and invasion of OS cells and promoted cell apoptosis in vitro. Meanwhile, we observed that the combined application of VitC and ATO directly suppresses the aerobic glycolysis of OS cells with the decreased production of pyruvate, lactate, and ATP via inhibiting the expression of the critical glycolytic genes (PGK1, PGM1, and LDHA). Moreover, the combination of VitC (200 mg/kg) and ATO (1 mg/kg) with tail vein injection significantly delayed OS growth and migration of nude mice by inhibiting aerobic glycolysis of OS. Thus, our results demonstrate that VitC effectively increases the sensitivity of OS to low concentrations of ATO via inhibiting aerobic glycolysis to alleviate the toxic side effects of high doses of arsenic trioxide, suggesting that synthetic application of VitC and ATO is a promising approach for the clinical treatment of human OS.

On the Mechanisms of the Cardiotoxic Effect of Lead Oxide Nanoparticles.

Lead compounds are one of the most common pollutants of the workplace air and the environment. In the occupational setting, the sources of their emission, including in nanoscale form, are various technological processes associated with lead smelting and handling of non-ferrous metals and their alloys, the production of copper and batteries. Both lead poisoning and lead exposure without obvious signs of poisoning have a detrimental effect on the cardiovascular system. The purpose of this research was to investigate the mechanisms of the cardiotoxic effect of lead oxide nanoparticles (PbO NPs). The toxicological experiment involved male albino rats subchronically exposed to PbO NPs (49.6 ± 16.0 nm in size) instilled intraperitoneally in a suspension. We then assessed post-exposure hematological and biochemical parameters of blood and urine, histological and ultrastructural changes in cardiomyocytes, and non-invasively recorded electrocardiograms and blood pressure parameters in the rodents. Myocardial contractility was studied on isolated preparations of cardiac muscles. We established that PbO NPs induced oxidative stress and damage to the ultrastructure of cardiomyocytes, and decreased efficiency of the contractile function of the myocardium and blood pressure parameters. We also revealed such specific changes in the organism of the exposed rats as anemia, hypoxia, and hypocalcemia.

Impact of physico-chemical properties on the toxicological potential of reduced graphene oxide in human bronchial epithelial cells.

The increasing use of graphene-based materials (GBM) requires their safety evaluation, especially in occupational settings. The same physico-chemical (PC) properties that confer GBM extraordinary functionalities may affect the potential toxic response. Most toxicity assessments mainly focus on graphene oxide and rarely investigate GBMs varying only by one property. As a novelty, the present study assessed the in vitro cytotoxicity and genotoxicity of six reduced graphene oxides (rGOs) with different PC properties in the human bronchial epithelial 16HBE14o - cell line. Of the six materials, rGO1-rGO4 only differed in the carbon-to-oxygen (C/O) content, whereas rGO5 and rGO6 were characterized by different lateral size and number of layers, respectively, but similar C/O content compared with rGO1. The materials were characterized by transmission electron microscopy, X-ray photoelectron spectroscopy, laser diffraction and dynamic light scattering, and Brunauer-Emmett-Teller analysis. Cytotoxicity (Luminescent Cell Viability and WST-8 assays), the induction of reactive oxygen species (ROS; 2',7'-dichlorofluorescin diacetate-based assay), the production of cytokines (enzyme-linked immunosorbent assays) and genotoxicity (comet and micronucleus assays) were evaluated. Furthermore, the internalization of the materials in the cells was confirmed by laser confocal microscopy. No relationships were found between the C/O ratio or the lateral size and any of the rGO-induced biological effects. However, rGO of higher oxygen content showed higher cytotoxic and early ROS-inducing potential, whereas genotoxic effects were observed with the rGO of the lowest density of oxygen groups. On the other hand, a higher number of layers seems to be associated with a decreased potential for inducing cytotoxicity and ROS production.

Bisphenol A degradation by chlorine dioxide (ClO2) and S(IV)/ClO2 process: Mechanism, degradation pathways and toxicity assessment.

Recently, it has been reported that chlorine dioxide (ClO2) and (bi)sulfite/ClO2 showed excellent performance in micropollutant removal from water; however, the degradation mechanisms and application boundaries of the two system have not been identified. In this study, bisphenol A (BPA) was chosen as the target contaminant to give multiple comparisons of ClO2 and S(IV)/ClO2 process regarding the degradation performance of contaminant, generation of reactive species, transformation of products and toxicity variation. Both ClO2 and S(IV)/ClO2 can degrade BPA within 3 min. The BPA degradation mechanism was mainly based on direct oxidation in ClO2 process while it was attributed to radicals (especially SO4·-) generation in S(IV)/ClO2 process. Meanwhile, the effect of pH and coexisting substances (Cl-, Br-, HCO3- and HA) were evaluated. It was found that ClO2 preferred the neutral and alkaline condition and S(IV)/ClO2 preferred the acidic condition for BPA degradation. An unexpected speed-up of BPA degradation was observed in ClO2 process in the presence of Br-, HCO3- and HA. In addition, the intermediate products in BPA degradation were identified. Three exclusive products were found in ClO2 process, in which p-benzoquinone was considered to be the reason of the acute toxicity increase in ClO2 process.

Study on myocardial toxicity induced by lead halide perovskites nanoparticles.

Lead halide perovskites (LHPs) are outstanding candidates for next-generation optoelectronic materials, with considerable prospects of use and commercial value. However, knowledge about their toxicity is scarce, which may limit their commercialization. Here, for the first time, we studied the cardiotoxicity and molecular mechanisms of representative CsPbBr3 nanoparticles in LHPs. After their intranasal administration to Institute of Cancer Research (ICR) mice, using advanced synchrotron radiation, mass spectrometry, and ultrasound imaging, we revealed that CsPbBr3 nanoparticles can severely affect cardiac systolic function by accumulating in the myocardial tissue. RNA sequencing and Western blotting demonstrated that CsPbBr3 nanoparticles induced excessive oxidative stress in cardiomyocytes, thereby provoking endoplasmic reticulum stress, disturbing calcium homeostasis, and ultimately leading to apoptosis. Our findings highlight the cardiotoxic effects of LHPs and provide crucial toxicological data for the product.

MnO2 nanoparticles and MnSO4 differentially affected hepatic lipid metabolism through miR-92a/acsl3-dependent de novo lipogenesis in yellow catfish Pelteobagrusfulvidraco.

With the increasing production and use of MnO2 NPs and MnSO4 in various fields, their discharge into the aquatic environment is inevitable, which poses potential threats to aquatic organisms and humans. However, to date, few studies have been conducted to investigate the potential mechanism of the toxicity of MnO2 NPs, and a comprehensive understanding of the differences between this mechanism and the toxicity mechanism of inorganic Mn (MnSO4) is still lacking. Since lipid metabolism-relevant parameters have been widely recognized as novel biomarkers for risk assessment of environmental contaminants, the present study investigated the differential mechanisms of how MnO2 NPs and MnSO4 affect hepatic lipid metabolism in a freshwater fish yellow catfish. Compared to MnSO4, dietary MnO2 NPs caused liver injury, increased hepatic lipid accumulation and induced lipotoxicity, and up-regulated mRNA expression of de novo lipogenic genes. Moreover, MnO2 NPs downregulated the expression of miR-92a and miR-92b-3p, microRNAs involved in regulation of lipid metabolism, in the liver. Mechanistically, we found that acls3, an acetyl-coenzyme A synthetase, is target gene of miR-92a, and miR-92a-acsl3-dependent de novo lipogenesis contributes to lipid accumulation and lipotoxicity induced by MnO2 NPs. Collectively, these findings provided novel insights into mechanism whereby miRNAs mediate nanoparticles- and inorganic Mn-induced hepatic lipotoxicity and changes of lipid metabolism in vertebrates. Our findings also shed new perspective for ecotoxicity and ecological risk of MnO2 NPs and MnSO4 in aquatic environment.