Photoaged polystyrene microplastics result in neurotoxicity associated with neurotransmission and neurodevelopment in zebrafish larvae (Danio rerio).

Microplastics (MPs) are emerging pollutants widely distributed in the environment, inducing toxic effects in various organisms. However, the neurotoxicity and underlying mechanisms of simulated sunlight-aged MPs have rarely been investigated. In this study, zebrafish (Danio rerio) were exposed to environmentally relevant concentrations (0, 0.1, 1, 10, and 100 µg/L) of virgin polystyrene (V-PS) and aged polystyrene (A-PS) for 120 hpf to evaluate the neurotoxicity. The results demonstrated that simulated sunlight irradiation altered the physicochemical properties (morphology, functional groups, and chemical composition) of V-PS. Exposure to A-PS causes greater toxicity on locomotor ability in larval zebrafish than V-PS. Motor neuron development was disrupted by transgenic (hb9-GFP) zebrafish larvae exposed to A-PS, with significant alterations in neurotransmitter levels (ACh, DA, 5-HT, and GABA) and enzyme activity (AChE, ChAT, and ChE). Further investigation found that exposure to A-PS had a significantly impact on the expression of neurotransmission and neurodevelopment-related genes in zebrafish. These findings suggest that A-PS induces neurotoxicity by its effects on neurotransmission and neurodevelopment. This study highlights the neurotoxic effects and mechanisms of simulated sunlight irradiation of MPs, providing new insights for assessing the ecological risks of photoaged MPs in the environment.

Photoaged Polystyrene Nanoplastics Result in Transgenerational Reproductive Toxicity Associated with the Methylation of Histone H3K4 and H3K9 in Caenorhabditis elegans.

Polystyrene nanoplastics (PS-NPs) are emerging environmental contaminants that are ubiquitously detected in various environments and have toxic effects on various organisms. Nevertheless, the transgenerational reproductive toxicity and underlying mechanisms of PS-NPs remain largely unknown, especially for photoaged PS-NPs under ultraviolet irradiation. In this study, only the parental generation (P0) was exposed to virgin and aged PS-NPs at environmentally relevant concentrations (0.1-100 µg/L), and subsequent generations (F1-F4) were cultured under normal conditions. Ultraviolet irradiation induced the generation of environmentally persistent free radicals and reactive oxygen species, which altered the physical and chemical characteristics of PS-NPs. The results of toxicity testing suggested that exposure to aged PS-NPs caused a more severe decrease in brood size, egg ejection rate, number of fertilized eggs, and hatchability than did the virgin PS-NPs in the P0, F1, and F2 generations. Additionally, a single maternal exposure to aged PS-NPs resulted in transgenerational effects on fertility in the F1 and F2 generations. Increased levels of H3K4 and H3K9 methylation were observed in the F1 and F2 generations, which were concomitant with the transgenerational downregulation of the expression of associated genes, such as spr-5, set-17, and met-2. On the basis of correlation analyses, the levels of histone methylation and the expression of these genes were significantly correlated to transgenerational reproductive effects. Further research showed that transgenerational effects on fertility were not observed in spr-5(by134), met-2(n4256), and set-17(n5017) mutants. Overall, maternal exposure to aged PS-NPs induced transgenerational reproductive effects via H3K4 and H3K9 methylation, and the spr-5, met-2, and set-17 genes were involved in the regulation of transgenerational toxicity. This study provides new insights into the potential risks of photoaging PS-NPs in the environment.

Controllable Synthesis of Web-Footed PdCu Nanosheets and Their Electrocatalytic Applications.

Morphological control of noble-metal-based nanocrystals has attracted enormous attention because their catalytic behaviors can be optimized well by adjusting the size and shape. Herein, the controllable synthesis of web-footed PdCu nanosheets via a facile surfactant-free method is reported. It is discovered that the Cu(II) precursor in this synthetic system displays a critical role in growing branches along the lateral of nanosheets. This work demonstrates a Pd-based alloy nanoarchitecture for efficient and stable electrocatalysis of both ethanal and formic acid oxidation reactions.

[Study on In Vitro Degradation of Oxidized Regenerated Cellulose Absorbable Hemostatic Products].

OBJECTIVE: To study the in vitro degradation of oxidized regenerated cellulose absorbable hemostatic products. METHODS: The morphology of the oxidized regenerated cellulose hemostatic products before and after degradation was observed by FTIR and SEM. The degradation products were determined by GPC and HILIC-ELSD. RESULTS: In the initial stage of degradation, there was a great change in morphology. GPC determined its degradation end point was 10 d; it was determined that its degradation products contained glucose (0.13%) and cellobiose (0.17%) and other components. CONCLUSIONS: A method was established for determining the end point of degradation of oxidized regenerated cellulose, which provided a new idea and reference for the study of the degradation end point.

[Research of Determining Complete Degradation Time in Vitro Based on Cellulose Absorbable Hemostatic Products].

To develop a method for determining complete degradation time of solublehemostatic products in vitro with accuracy, high speed and effectiveness, the current weight loss method originated from GB/T 16886 serial standards was optimized by using dialysis bag combined with assay of reducing sugar. The degradation was carried out with 3% hydrogen peroxide solution, at 37℃, 150 rpm. The dialysis bags were taken out in the 3rd, 6th, 8th, 10th and 14th day, vacuum drying folowed by percentage of weight loss testing. Cumulative content of reducing sugar in degradation solution out of dialysis bag was determined simultaneously. The correlation analysis was performed by SPSS 22.0 equipped with Pearson Correlation Coeffi cient. The correlation coeffi cient between percentage of weight loss and cumulative content of reducing sugar was 0.957, which ilustrated high correlation with each other. Hence dialysis bag combined with assay of reducing sugar is capable of evaluating the degradation endpoint of soluble hemostatic products in vitro. The method also provides a way for the evaluation of degradation of other degradable biomaterials in vitro.

Environmentally persistent free radicals on photoaging microplastics shortens longevity via inducing oxidative stress in Caenorhabditis elegans.

Microplastics (MPs) are ubiquitous environmental contaminants that exert multiple toxicological effects. Current studies have mainly focused on modeled or unaged MPs, which lack environmental relevance. The generation and toxicity of environmentally persistent free radicals (EPFRs) on photoaging polystyrene (PS) have not been well studied, and the role of EPFRs on the toxic effects of photoaged PS is easily ignored. Photoaging primarily produces EPFRs, followed by an increase in reactive oxygen species (ROS) content and oxidative potential, which alter the physicochemical properties of photoaged PS. The mean lifespan and lipofuscin content were significantly altered after acute exposure to photoaged PS for 45 d (PS-45) and 60 d (PS-60) in Caenorhabditis elegans. Intestinal ROS and gst-4::GFP expression were enhanced, concomitant with the upregulation of associated genes. Treatment with N-acetyl-l-cysteine by radical quenching test significantly decreased EPFRs levels on the aged PS and inhibited the acceleration of the aging and oxidative stress response in nematodes. Pearson's correlation analysis also indicated that the EPFRs levels were significantly associated with these factors. Thus, the EPFRs generated on photoaged PS contribute to the acceleration of aging by oxidative stress. This study provides new insights into the potential toxicity and highlights the need to consider the role of EPFRs in the toxicity assessment of photoaged PS.

Photoaging enhances combined toxicity of microplastics and tetrabromobisphenol A by inducing intestinal damage and oxidative stress in Caenorhabditis elegans.

Microplastics (MPs) are emerging environmental contaminants that often co-exist with tetrabromobisphenol A (TBBPA) in the environment. However, the joint effect of TBBPA and photoaged MPs at ambient concentrations remains unknown largely. In this study, the combined toxicity of ultraviolet-aged polystyrene (UV-PS) and TBBPA was investigated in Caenorhabditis elegans. UV irradiation could change the physical and chemical characteristics of polystyrene (PS), and UV-PS (90.218 µg/g) showed a stronger adsorption capacity than PS of 79.424 µg/g. Toxicity testing showed that 1 µg/L UV-PS enhanced the toxic effect of 1 µg/L TBBPA by reducing body length, locomotion behavior, and brood size in nematodes. Using ROS production, lipofuscin accumulation, and expression of gst-4::GFP as endpoints, the combined exposure of UV-PS and TBBPA induced stronger oxidative stress than TBBPA alone. Joint exposure to UV-PS and TBBPA significantly increased of Nile red and blue food dye in its intestinal tract compared to that in the TBBPA exposure group, indicating that co-exposure enhanced intestinal permeability. After co-exposure to UV-PS and TBBPA, the expression of the associated genes detected increased significantly. Therefore, UV-PS enhances the adverse effects of TBBPA through intestinal damage and oxidative stress in nematodes. These findings suggest that the co-presence of photoaged PS and TBBPA results in high environmental risks.

Generation of environmentally persistent free radicals on photoaged tire wear particles and their neurotoxic effects on neurotransmission in Caenorhabditis elegans.

Tire wear particles (TWP) are a prevalent form of microplastics (MPs) extensively distributed in the environment, raising concerns about their environmental behaviors and risks. However, knowledge regarding the properties and toxicity of these particles at environmentally relevant concentrations, specifically regarding the role of environmentally persistent free radicals (EPFRs) generated during TWP photoaging, remains limited. In this study, the evolution of EPFRs on TWP under different photoaging times and their adverse effects on Caenorhabditis elegans were systematically investigated. The photoaging process primarily resulted in the formation of EPFRs and reactive oxygen species (O2•-, ⋅OH, and 1O2), altering the physicochemical properties of TWP. The exposure of nematodes to 100 µg/L of TWP-50 (TWP with a photoaging time of 50 d) led to a significant decrease in locomotory behaviors (e.g., head thrashes, body bends, and wavelength) and neurotransmitter contents (e.g., dopamine, glutamate, and serotonin). Similarly, the expression of neurotransmission-related genes was reduced in nematodes exposed to TWP-50. Furthermore, the addition of free-radical inhibitors significantly suppressed TWP-induced neurotoxicity. Notably, correlation analysis revealed a significantly negative correlation between EPFRs levels and the locomotory behaviors and neurotransmitter contents of nematodes. Thus, it was concluded that EPFRs on photoaged TWP induce neurotoxicity by affecting neurotransmission. These findings elucidate the toxicity effects and mechanisms of EPFRs, emphasizing the importance of considering their contributions when evaluating the environmental risks associated with TWP.

Photoaged microplastics induce neurotoxicity associated with damage to serotonergic, glutamatergic, dopaminergic, and GABAergic neuronal systems in Caenorhabditis elegans.

Microplastics (MPs) are ubiquitous environmental contaminants that cause neurotoxicity in various organisms. MPs are typically affected by light irradiation and undergo photoaging. However, the neurotoxic effects of photoaged polystyrene (P-PS) and its underlying mechanisms remain unclear. In this study, locomotion behaviors, neuronal development, neurotransmitter levels, and the expression of neurotransmission-related genes were investigated in Caenorhabditis elegans exposed to P-PS at environment-relevant concentrations (0.1-100 µg/L). The characterization results showed that photoaging accelerated the aging process and changed the physicochemical properties of the MPs. The toxicity results suggested that exposure to 1-100 µg/L P-PS caused more severe neurotoxicity than virgin polystyrene (V-PS) with endpoints of head thrashes, body bends, wavelength, and mean amplitude. Exposure to P-PS also altered the fluorescence intensity and neurodegeneration percentage of serotonergic, glutamatergic, dopaminergic, and aminobutyric acid (GABA) in transgenic nematodes. Similarly, significant reductions in the levels of these neurotransmitters were also observed. Based on Pearson's correlation, locomotion behaviors were negatively correlated with the neurotransmission of serotonin, glutamate, dopamine, and GABA. Further investigation suggested that the expression of neurotransmitter-related genes (e.g., tph-1, eat-4, and unc-46) was significantly altered in the nematodes. Collectively, the neurotoxic effects of P-PS were attributed to abnormal neurotransmission. This study highlights the potential toxicity of MPs photoaged under environmentally relevant conditions.

Carboxyl-modified polystyrene microplastics induces neurotoxicity by affecting dopamine, glutamate, serotonin, and GABA neurotransmission in Caenorhabditis elegans.

Microplastics (MPs) are ubiquitous in various environmental media and have potential toxicity. However, the neurotoxicity of carboxyl-modified polystyrene microplastics (PS-COOH) and their mechanisms remain unclear. In this study, Caenorhabditis elegans was used as a model to examine the neurotoxicity of polystyrene microplastic (PS) and PS-COOH concentrations ranging from 0.1 to 100 µg/L. Locomotion behavior, neuron development, neurotransmitter level, and neurotransmitter-related gene expression were selected as assessment endpoints. Exposure to low concentrations (1 µg/L) of PS-COOH caused more severe neurotoxicity than exposure to pristine PS. In transgenic nematodes, exposure to PS-COOH at 10-100 µg/L significantly increased the fluorescence intensity of dopaminergic, glutamatergic, serotonergic, and aminobutyric acid (GABA)ergic neurons compared to that of the control. Further studies showed that exposure to 100 µg/L PS-COOH can significantly affect the levels of glutamate, serotonin, dopamine, and GABA in nematodes. Likewise, in the present study, the expression of genes involved in neurotransmission was altered in worms. These results suggest that PS-COOH exerts neurotoxicity by affecting neurotransmission of dopamine, glutamate, serotonin, and GABA. This study provides new insights into the underlying mechanisms and potential risks associated with PS-COOH.

UV-aged microplastics induces neurotoxicity by affecting the neurotransmission in larval zebrafish.

Microplastics (MPs) are nearly ubiquitous in aquatic ecosystems and may affect aquatic organisms. In this study, virgin and aged polystyrene MPs (PS-MPs) of size 1 µm were selected to analyze their adverse effects on larvae zebrafish. Exposure to PS-MPs significantly reduced the average swimming speed of zebrafish, and the behavioral effects caused by aged PS-MPs on zebrafish were more pronounced. Fluorescence microscopy revealed that 10-100 µg/L of PS-MPs accumulated in tissues of zebrafish. As an endpoint of neurotransmitter concentration, exposure to aged PS-MPs at doses ranging from 0.1 to 100 µg/L significantly increased the dopamine (DA), 5-hydroxytryptamine (5-HT), γ-aminobutyric acid (GABA), and acetylcholine (ACh) levels in zebrafish. Similarly, exposure to aged PS-MPs significantly altered the expression of genes related to these neurotransmitters (e.g., dat, 5ht1aa, and gabral genes). According to Pearson correlation analyses, neurotransmissions was significantly correlated with neurotoxic effects of aged PS-MPs. Thus, aged PS-MPs cause neurotoxicity in zebrafish through their effects on DA, 5-HT, GABA, and ACh neurotransmissions. The results highlight the importance of the neurotoxicity of aged PS-MPs in zebrafish, which has important implications for the risk assessment of aged MPs and the conservation of aquatic ecosystems.

The generation of environmentally persistent free radicals on photoaged microbeads from cosmetics enhances the toxicity via oxidative stress.

Microbeads used in personal care products have been one of the important sources of microplastics (MPs), and little has been reported on their environmental behaviors and health risks. The characteristics of environmentally persistent free radicals (EPFRs) and the toxicity assessment of MPs (environmentally relevant concentrations) from cosmetics during photoaging remains largely unknown. In this study, the formation of EPFRs on polyethylene (PE) microbeads from facial scrubs under light irradiation and their toxicity were investigated using C. elegans as a model organism. The results suggested that light irradiation induced the generation of EPFRs, which accelerates the aging process and alters the physicochemical properties of PE microbeads. Acute exposure to PE (1 mg/L) at photoaged times of 45-60 d significantly decreased the physiological indicators (e.g., head thrashes, body bends, and brood size). The oxidative stress response and stress-related gene expression were also enhanced in nematodes. The addition of N-acetyl-l-cysteine induced significant inhibition of toxicity and oxidative stress in nematodes exposed to 45-60 d of photoaged PE. The Pearson correlation results showed that the concentration of EPFRs was significantly correlated with physiological indicators, oxidative stress, and related-genes expression in nematodes. The data confirmed that the generation of EPFRs combined with heavy metals and organics contributed to toxicity induced by photoaged PE, and oxidative stress might be involved in regulating adverse effects in C. elegans. The study provides new insight into the potential risks of microbeads released into the environment during photoaging. The findings also highlight the necessity for considering the role of EPFRs formation in evaluating the impacts of microbeads.

Microbial colonization of microplastics in wastewater accelerates the aging process associated with oxidative stress and the insulin/IGF1 signaling pathway.

Although polystyrene (PS)-induced toxicity in organisms has been documented, adverse effects on lifespan and molecular mechanisms underlying microbial colonization of PS remain elusive. Herein, physicochemical properties of biofilm-developed PS (B-PS) incubated in wastewater were altered compared with virgin PS (V-PS). Bacterial community adherence to the B-PS surface were also impacted. Acute exposure to V-PS (100 µg/L) and B-PS (10 µg/L) significantly altered the mean lifespan and lipofuscin accumulation of Caenorhabditis elegans, suggesting that B-PS exposure at environmentally relevant concentrations could more severely accelerate the aging process than V-PS. Generation of ROS, gst-4::GFP expression, and oxidative stress-related gene expression were significantly altered following B-PS exposure. Moreover, B-PS exposure increased the nucleus-cytoplasm translocation of DAF-16 and altered the expression of genes encoding the insulin/IGF1 signaling (IIS) pathway. Compared with wild-type nematodes, the daf-16 mutation markedly enhanced lipofuscin accumulation and reduced mean lifespan, whereas daf-2, age-1, pdk-1, and akt-1 mutants could recover lipofuscin accumulation and mean lifespan. Accordingly, B-PS exposure accelerated the aging process associated with oxidative stress and the IIS pathway, and the DAF-2-AGE-1-PDK-1-AKT-1-DAF-16 signaling cascade may play a critical role in regulating the lifespan of C. elegans. This study provides new insights into the potential risks associated with microbial colonization of microplastics.

Photoaged microplastics induce neurotoxicity via oxidative stress and abnormal neurotransmission in zebrafish larvae (Danio rerio).

Microplastics (MPs) are ubiquitous environmental contaminants and cause neurotoxicity in various organisms. However, previous studies that analyzed the effects of MPs mainly focused on virgin polystyrene (V-PS) as representative models of MPs, and the mechanism underlying the neurotoxicity of photoaged polystyrene (P-PS) remains largely unknown. In this study, zebrafish (Danio rerio) were exposed to environmentally relevant concentrations (0.1-100 µg/L) of V-PS and P-PS(10 µm). The results indicated that UV radiation accelerated the aging process and changed physical and chemical properties of PS. Whereas exposure to both V-PS and P-PS at low concentrations (100 µg/L) significantly reduced the locomotor behavior of zebrafish larvae, P-PS caused more severe neurotoxicity compared to V-PS. The activity of antioxidant enzymes (SOD, CAT, and GST) and MDA content were significantly altered in zebrafish exposed to 10-100 µg/L of P-PS. Similarly, exposure to P-PS significantly increased neurotransmitter (5-HT, GABA, DA, and ACh) levels and activity of AChE, ChAT, and ChE. Star plots based on integrated biomarker response (IBR) values showed more incline toward neurotransmitter biomarkers in response to increasing P-PS concentration, and the behavioral parameters negatively correlated with the neurotransmitter biomarkers. Further investigations revealed that the expression of neurotransmission- (e.g., ache, drd3, 5th2c, and gat1) and oxidative stress- (e.g., cat1, sod1, gpx1a, and gstrl) related genes was significantly affected by PS in larval zebrafish. Thus, this study provides new insights on the potential risks of MPs into the environment.

Membrane-Specific Binding of 4 nm Lipid Nanoparticles Mediated by an Entropy-Driven Interaction Mechanism.

Lipid nanoparticles (LNPs) are a leading biomimetic drug delivery platform due to their distinctive advantages and highly tunable formulations. A mechanistic understanding of the interaction between LNPs and cell membranes is essential for developing the cell-targeted carriers for precision medicine. Here the interactions between sub 10 nm cationic LNPs (cLNPs; e.g., 4 nm in size) and varying model cell membranes are systematically investigated using molecular dynamics simulations. We find that the membrane-binding behavior of cLNPs is governed by a two-step mechanism that is initiated by direct contact followed by a more crucial lipid exchange (dissociation of cLNP's coating lipids and subsequent flip and intercalation into the membrane). Importantly, our simulations demonstrate that the membrane binding of cLNPs is an entropy-driven process, which thus enables cLNPs to differentiate between membranes having different lipid compositions (e.g., the outer and inner membranes of bacteria vs the red blood cell membranes). Accordingly, the possible strategies to drive the membrane-targeting behaviors of cLNPs, which mainly depend on the entropy change in the complicated entropy-enthalpy competition of the cLNP-membrane interaction process, are investigated. Our work unveils the molecular mechanism underlying the membrane selectivity of cLNPs and provides useful hints to develop cLNPs as membrane-targeting agents for precision medicine.

Reproductive toxicity of UV-photodegraded polystyrene microplastics induced by DNA damage-dependent cell apoptosis in Caenorhabditis elegans.

Although many studies have investigated the toxic effects of polystyrene microplastics (PS-MPs), toxicity of natural aged of PS-MPs to soil organisms remains unclear. The photodegradation of virgin PS-MPs under UV irradiation was investigated, and reproductive toxicity of pristine and UV-photodegraded PS-MPs at environmental concentrations (0.1-100 µg/L) was examined to Caenorhabditis elegans. Using brood size and egg ejection rate as endpoints, acute exposure to aged PS-MPs resulted in more severe reproductive toxicity than pristine PS-MPs. Exposure to 100 µg/L aged PS-MPs significantly increased the number of HUS-1::GFP foci and the expression of genes required for DNA damage, such as clk-2, cep-1, and egl-1, suggesting induction of DNA damage. Additionally, the number of cell corpses and apoptosis-related gene expression (e.g., ced-3, ced-4, and ced-9) were significantly altered, indicating induction of apoptosis. Germline apoptosis induced by aged PS-MPs was altered in egl-1, hus-1, cep-1, ced-3, ced-4, and ced-9 mutants. Thus, the reproductive toxicity of aged PS-MPs may be due to DNA damage-induced cell apoptosis, and the HUS-1-CEP-1-EGL-1-CED-9-CED-4-CED-3 signalling pathway is involved in regulating cell apoptosis in nematodes.

Impact of vehicle type, tyre feature and driving behaviour on tyre wear under real-world driving conditions.

Tyre wear generates not only large pieces of microplastics but also airborne particle emissions, which have attracted considerable attention due to their adverse impacts on the environment, human health, and the water system. However, the study on tyre wear is scarce in real-world driving conditions. In the present study, the left-front and left-rear tyre wear in terms of volume lost in mm3 of 76 taxi cars was measured about every three months. This study covered 22 months from September 2019 to June 2021 and included more than 500 measurements in total. Some of the data was used to evaluate the effects of vehicle type and tyre type on tyre wear. In addition, a machine learning method (i.e., Extreme gradient boosting (XGBoost)) was used to probe the effect of driving behaviour on tyre wear by monitoring real-time driving behaviour. The current statistical results showed that, on average, the tyre wear was 72 mg veh-1 km-1 for a hybrid car and 53 mg veh-1 km-1 for a conventional internal combustion engine car. The average tyre wear measured for a taxi vehicle configuration featuring winter tyres was 160 mg veh-1 km-1, which was 1.4 and 3.0 times as much as those with all-season tyres and summer tyres, respectively. The wear rate of left-front tyres was 1.7 times higher than that of left-rear tyres. The XGBoost results indicated that compared to driving behaviour, tyre type and tyre position had more important effects on tyre wear. Among driving behaviours, braking and accelerating events presented the most considerable impact on tyre wear, followed by cornering manoeuvres and driving speed. Thus, it seems that limiting harsh braking and acceleration has the potential to reduce tyre wear significantly.

Transgenerational neurotoxicity of polystyrene microplastics induced by oxidative stress in Caenorhabditis elegans.

Microplastics (MPs), emerging environmental contaminants, exhibit multiple toxicities in organisms. However, the transgenerational neurotoxicity of MPs has received little attention. Caenorhabditis elegans has been used as a model organism for studying transgenerational toxicity. In this study, the transgenerational neurotoxicity and oxidative stress of MPs were investigated over five generations (F0-F4) of C. elegans. The parental generation (F0) was exposed to polystyrene microplastics (PS-MPs) at concentrations of 0.1-100 µg/L, and subsequent generations (F1-F4) were cultured under toxicant-free conditions. The results indicated that exposure to PS-MPs at concentrations of 10-100 µg/L significantly decreased head thrash and body bends in nematodes, and this reduction was also observed in subsequent generations (F1-F2). This suggested that neurotoxicity induced by PS-MPs can be transferred from the parent to subsequent generations. Maternal exposure to 100 µg/L PS-MPs significantly enhanced ROS production and lipofuscin accumulation in subsequent generations (F1-F2), indicating that the induction of oxidative stress plays an important role in the transgenerational neurotoxicity in C. elegans. Moreover, maternal exposure to PS-MPs resulted in the transgenerational upregulation of genes related to oxidative stress (clk-1, ctl-1, sod-3, sod-4, and sod-5) in the F1-F3 generations, which indicated that these genes may be involved in regulating transgenerational neurotoxicity in C. elegans.

Chronic exposure to UV-aged microplastics induces neurotoxicity by affecting dopamine, glutamate, and serotonin neurotransmission in Caenorhabditis elegans.

Microplastics are ubiquitous in all environments and exert toxic effects in various organisms. However, the neurotoxicity and underlying mechanisms of long-term exposure to MPs aged under UV radiation remain largely unclear. In this study, Caenorhabditis elegans was treated with 0.1-100 µg/L virgin and aged polystyrene microplastics (PS-MPs) for 10 d, with locomotion behavior, neuronal development, neurotransmitter content, and neurotransmission-related to gene expression as endpoints. Using locomotion behavior as an endpoint, chronic exposure to aged PS-MPs at low concentrations (1 µg/L) caused more severe neurotoxicity than that to virgin PS-MPs. In transgenic nematodes, exposure to 10-100 µg/L aged PS-MPs significantly influenced the fluorescence intensity and percentage of worms with neurodegeneration of dopaminergic, glutamatergic, and serotonergic neurons compared with control. Further investigations showed that the content of glutamate, serotonin, and dopamine was significantly influenced in nematodes chronically exposed to 100 µg/L of aged PS-MPs. Similarly, neurotransmission-related gene (e.g., eat-4, dat-1, and tph-1) expression was also altered in nematodes. These results indicate that aged PS-MPs exert neurotoxicity owing to their effects on dopamine, glutamate, and serotonin neurotransmission. This study provides insights into the underlying mechanisms and potential risks of PS-MPs after UV radiation.

Polystyrene microplastics (PS-MPs) toxicity induced oxidative stress and intestinal injury in nematode Caenorhabditis elegans.

To understand the toxicity and mechanism of polystyrene microplastics (PS-MPs) exposure, Caenorhabditis elegans (C. elegans) was exposed to various concentrations (0, 0.1, 1, 10, and 100 µg/L) of PS-MPs, and the levels physiological, biochemical, and molecular parameters were measured as endpoints. Subacute exposure to 1-100 µg/L of PS-MPs resulted in adverse physiological effects in C. elegans, and PS-MPs were ingested and accumulated in the intestine of C. elegans. Exposure to 100 µg/L of PS-MPs significantly increased reactive oxygen species (ROS) production, lipofuscin accumulation, and the expression oxidative stress-related genes, which suggests that PS-MPs exposure induced oxidative stress by ROS. In addition, exposure to 100 µg/L of PS-MPs caused a hyperpermeable state of the intestinal barrier and altered the expression of genes related to intestinal development, which indicates intestinal damage in C. elegans. According to Pearson correlation analyses, oxidative stress and intestinal damage were significantly correlated with adverse effects of PS-MPs in C. elegans. Therefore, it was speculated that the toxicity induced by PS-MPs resulted from the combination of oxidative stress and intestinal injury.