The toxic effects of polystyrene microplastic/nanoplastic particles on retinal pigment epithelial cells and retinal tissue.

The increasing use of contact lenses, artificial tears, and anti-vascular endothelial growth factor (anti-VEGF) drug injections for age-related macular degeneration has heightened the likelihood of eye exposure to microplastic particles. Extensive research has established that microplastic particles can induce oxidative stress on the ocular surface, resulting in damage. However, the impact of these particles on the retina remains unclear. Therefore, this study investigated whether microplastics/nanoplastics (MPs/NPs) cause retinal damage. In vitro human retinal pigment epithelial (RPE) cells were exposed to polystyrene MPs and NPs for 48 h. Assessment of cell viability using WST-8; evaluation of TNF-α and IL-1ß expression; observation of cell morphology and particle invasion via TEM; measurement of ROS levels using the DCFDA reagent; and western blot analysis of SOD2, FIS1, Drp1, and LC3B expression were conducted. In vivo experiments involved intravitreal injection of MPs/NPs in rats, followed by retinal H&E staining 24 h later and evaluation of TNF-α and IL-1ß expression. Results indicated that exposure to MPs did not significantly alter RPE cell viability, whereas exposure to NPs led to a noticeable decrease. TEM images revealed NPs' penetration into cells, causing increased oxidative stress (SOD2), mitochondrial fission (FIS1, Drp1), and mitochondrial autophagy (LC3B). In vivo experiments demonstrated an increase in inflammatory cells in retinal tissues exposed to NPs, along with elevated levels of TNF-α and IL-1ß. Conclusively, both MPs and NPs impact the retina, with NPs displaying greater toxicity. NPs significantly elevate ROS levels in the retina and induce mitochondrial fission and mitophagy in RPE cells compared to MPs.

Integrin A5B1-mediated endocytosis of polystyrene nanoplastics: Implications for human lung disease and therapeutic targets.

The extensive use of plastic products has exacerbated micro/nanoplastic (MPs/NPs) pollution in the atmosphere, increasing the incidence of respiratory diseases and lung cancer. This study investigates the uptake and cytotoxicity mechanisms of polystyrene (PS) NPs in human lung epithelial cells. Transcriptional analysis revealed significant changes in cell adhesion pathways following PS-NPs exposure. Integrin α5ß1-mediated endocytosis was identified as a key promoter of PS-NPs entry into lung epithelial cells. Overexpression of integrin α5ß1 enhanced PS-NPs internalization, exacerbating mitochondrial Ca2+ dysfunction and depolarization, which induced reactive oxygen species (ROS) production. Mitochondrial dysfunction triggered by PS-NPs led to oxidative damage, inflammation, DNA damage, and necrosis, contributing to lung diseases. This study elucidates the molecular mechanism by which integrin α5ß1 facilitates PS-NPs internalization and enhances its cytotoxicity, offering new insights into potential therapeutic targets for microplastic-induced lung diseases.

Mitigated toxicity of polystyrene nanoplastics in combination exposure with copper ions by transformation into copper (I) oxide: Inhibits the oxidative potential of nanoplastics.

The combined impact of trace metals and polystyrene (PS) microplastics is extremely concerning for human health because PS microplastics can serve as a vehicle for other contaminants. Herein, we investigated the combined effect of copper ions (Cu2+) on the toxicity of PS nanoplastics in vivo and in vitro. The pristine PS (PPS) and ultraviolet irradiated oxidized PS (OPS) nanoplastics with 50 nm-size were conjugated with Cu2+ (13-27 mg/g) for 4 days to get four types of samples: PPS, OPS, PPS/Cu, and OPS/Cu. The comparative toxic potentials of test samples were evaluated using a mouse pharyngeal aspiration model and relevant human cell lines (A549 and differentiated THP-1 cells). The results showed an antagonistic effect in vivo and in vitro by the presence of Cu ions: PPS > PPS/Cu; OPS > OPS/Cu. Furthermore, the OPS produced significantly increased toxic potentials compared to the corresponding PPS: OPS > PPS; OPS/Cu > PPS/Cu. The antagonistic effect of Cu2+ on the toxicity of PS was due to the transformation of Cu2+ and balanced the surface charge of the nanoplastics, which inhibited the oxidative potential of corresponding nanoplastics. These antagonistic effects may provide a better understanding of the combined effects of metals on the intrinsic toxic potential of microplastics under natural conditions.

Treatment with quercetin mitigates polystyrene nanoparticle-induced reduction in neuron capacity by inhibiting dopaminergic neurodegeneration and facilitating dopamine metabolism in Caenorhabditis elegans.

In organisms, long-term nanopolystyrenes (PS-NPs) exposure can cause toxicity, including neurotoxicity. Quercetin, the flavonol with extensive distribution within plants, possesses diverse biological activities. Nevertheless, the possible effect of quercetin to suppress PS-NPs-induced neurotoxicity and its associated mechanism remains unknown. Thus, in the present work, Caenorhabditis elegans was utilized as the model animal to investigate quercetin's pharmacological effect on suppressing PS-NPs-induced neurotoxicity and the underlying mechanism. PS-NPs exposure at 1-100 µg/L remarkably reduced locomotion behavior, while only PS-NPs exposure at 100 µg/L significantly decrease sensory perception behavior. Meanwhile, the increase in the number of worms with dopaminergic neurodegeneration was detected in nematodes exposed to 100 µg/L PS-NPs and the decreased dopamine content was observed within nematodes exposed to 10-100 µg/L PS-NPs, demonstrating the function of dopaminergic neurodegeneration and disruption of dopamine metabolism in inducing PS-NPs toxicity on neuron capacity. After 100 µg/L PS-NPs exposure, the 25-100 µM quercetin treatment effectively increased the locomotion behavior and the sensory perception behavior. Developmentally, quercetin treatment (100 µM) remarkably enhanced fluorescence intensity while decreasing worm number with neurodegeneration within BZ555 transgenic strains exposed to 100 µg/L PS-NPs. Physiologically, quercetin treatment (100 µM) significantly enhanced dopamine content within nematodes exposed to 100 µg/L PS-NPs. Molecularly, quercetin treatment (100 µM) notably decreased the expressions of genes governing neurodegeneration (mec-4, deg-3, unc-68, itr-1, clp-1, and asp-3) while significantly increasing the expression of genes governing dopamine metabolism (cat-2, cat-1, dop-1, dop-2, dop-3). As revealed by molecular docking results, quercetin might bind to excitotoxic-like ion channels receptors (MEC-4 and DEG-3) and dopamine secreted protein (CAT-2). Consequently, findings in this work demonstrated that long-term PS-NPs exposure within the µg/L range (1-100 µg/L) was toxic to neuron capacity, which was associated with the enhancement in dopaminergic neurodegeneration and disruption of dopamine metabolism. Notably, PS-NPs-mediated neurotoxicity to nematodes is probably suppressed through subsequent quercetin treatment.

Unraveling the toxicity mechanisms of nanoplastics with various surface modifications on Skeletonema costatum: Cellular and molecular perspectives.

Nanoplastics are ubiquitous in marine environments, exhibiting high bioavailability and potential toxicity to marine organisms. However, the impacts of nanoplastics with various surface modifications on marine microalgae remain largely unexplored. This study explored the toxicity mechanisms of two nanoplastic types-polystyrene (PS) and polymethyl methacrylate (PMMA)-with distinct surface modifications on Skeletonema costatum at cellular and molecular levels. Results showed that nanoplastics significantly impaired the growth of microalgae, particularly PS-NH2, which caused the most pronounced growth inhibition, reaching 56.99 % after a 96-h exposure at 50 mg/L. Transcriptomic profiling revealed that nanoplastics disrupted the expression of genes predominantly involved in ribosome biogenesis, aminoacyl-tRNA biosynthesis, amino acid metabolism, and carbohydrate metabolism pathways. The integrated biochemical and transcriptomic evidence highlighted that PS-NH2 nanoplastics had the most adverse impact on microalgae, affecting fundamental pathways such as ribosome biogenesis, energy metabolism, photosynthesis, and oxidative stress. Our findings underscore the influence of surface-modified nanoplastics on algal growth and contribute new understanding to the toxicity mechanisms of these nanoplastics in marine microalgae, offering critical information for assessing the risks of emerging pollutants.

Long-Term Exposure to Polystyrene Microspheres and High-Fat Diet-Induced Obesity in Mice: Evaluating a Role for Microbiota Dysbiosis.

BACKGROUND: Microplastics (MPs) have become a global environmental problem, emerging as contaminants with potentially alarming consequences. However, long-term exposure to polystyrene microspheres (PS-MS) and its effects on diet-induced obesity are not yet fully understood. OBJECTIVES: We aimed to investigate the effect of PS-MS exposure on high-fat diet (HFD)-induced obesity and underlying mechanisms. METHODS: In the present study, C57BL/6J mice were fed a normal diet (ND) or a HFD in the absence or presence of PS-MS via oral administration for 8 wk. Antibiotic depletion of the microbiota and fecal microbiota transplantation (FMT) were performed to assess the influence of PS-MS on intestinal microbial ecology. We performed 16S rRNA sequencing to dissect microbial discrepancies and investigated the dysbiosis-associated intestinal integrity and inflammation in serum. RESULTS: Compared with HFD mice, mice fed the HFD with PS-MS exhibited higher body weight, liver weight, metabolic dysfunction-associated steatotic liver disease (MASLD) activity scores, and mass of white adipose tissue, as well as higher blood glucose and serum lipid concentrations. Furthermore, 16S rRNA sequencing of the fecal microbiota revealed that mice fed the HFD with PS-MS had greater α-diversity and greater relative abundances of Lachnospiraceae, Oscillospiraceae, Bacteroidaceae, Akkermansiaceae, Marinifilaceae, Deferribacteres, and Desulfovibrio, but lower relative abundances of Atopobiaceae, Bifidobacterium, and Parabacteroides. Mice fed the HFD with PS-MS exhibited lower expression of MUC2 mucin and higher levels of lipopolysaccharide and inflammatory cytokines [tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), IL-1ß, and IL-17A] in serum. Correlation analyses revealed that differences in the microbial flora of mice exposed to PS-MS were associated with obesity. Interestingly, microbiota-depleted mice did not show the same PS-MS-associated differences in Muc2 and Tjp1 expression in the distal colon, expression of inflammatory cytokines in serum, or obesity outcomes between HFD and HFD + PS-MS. Importantly, transplantation of feces from HFD + PS-MS mice to microbiota-depleted HFD-fed mice resulted in a lower expression of mucus proteins, higher expression of inflammatory cytokines, and obesity outcomes, similar to the findings in HFD + PS-MS mice. CONCLUSIONS: Our findings provide a new gut microbiota-driven mechanism for PS-MS-induced obesity in HFD-fed mice, suggesting the need to reevaluate the adverse health effects of MPs commonly found in daily life, particularly in susceptible populations. https://doi.org/10.1289/EHP13913.

A study on the effect of fluorescently stained micro(nano)plastics on the full life history of Skeletonema costatum.

As a new type of environmental pollutant, micro(nano)plastics have become a research hotspot in recent years, and their effects on the full life history of marine microalgae have not been studied. To investigate the effects of micro(nano)plastics on the growth, photosynthesis, physiological morphology and interaction of microalgae during the full life cycle, we selected fluorescently stained polystyrene (PS) plastic microbeads as the target pollutant. By sampling and testing the growth rate, photosynthesis and physiological morphology parameters of algal species, the influence of different concentrations of PS (10, 50 and 100 mg/L) and different particle sizes (0.1, 0.5 and 1 µm) on the full life history of Skeletonema costatum (S. costatum) was investigated. The results showed that after adding PS (particle sizes of 0.5 and 1 µm), the response of S. costatum showed a dual character, while adding the same kind of microplastics (MPs) with a particle size of 0.1 µm inhibited S. costatum throughout the full life cycle. Compared with previous studies, short-term experimental data may overestimate the true ecological risks of MPs. In addition, 0.1 µm fluorescent-stained MPs obviously accumulated around the microalgae, indicating that MPs mainly adhered to the surface of algal cells and may enter the food chain by direct or indirect ways, which can cause negative effects on the aquatic ecosystem. This study supports a more accurate assessment of the true risk of MPs to marine aquatic ecosystems.

Photoaging of polystyrene-based microplastics amplifies inflammatory response in macrophages.

The continuous release of municipal and industrial products into the environment poses a growing concern for public health. Among environmental pollutants, polystyrene (PS) stands out as a primary constituent of environmental plastic waste, given its widespread use and high production rates owing to its durability and user-friendly properties. The detection of polystyrene microparticles (PS-MPs) in various living organisms has been well-documented, posing a serious threat due to their potential passage into the human ecosystem. In this manuscript, we aimed to study the toxicological effects of low concentrations of pristine and photoaged PS-MPs in a murine macrophage cell line. To this purpose, PS-MPs were photoaged by indoor exposure to visible light to simulate environmental weathering due to solar irradiation (PS-MPs3h). Physical characterization revealed that the irradiation treatment results in particle degradation and the possible release of nanoparticles. Monocultures of the RAW264.7 cell line were then exposed to PS-MPs and PS-MPs3h at concentrations comparable to experimental measurements from biological samples, to assess cytotoxicity, intracellular oxidative stress, primary genotoxicity, and inflammatory effects. Significant toxicity-related outcomes were observed in cells treated with both pristine PS-MPs and PS-MPs3h even at low concentrations (0,10 µg/ml and 1 µg/ml). PS-MPs3h exhibited greater adverse effects compared to PS-MPs, including reduced cell viability, increased ROS production, elevated DNA damage, and upregulation of IL-6 and NOS2 gene expression. Therefore, we can conclude that changes induced by environmental aging in the physicochemical composition of PS microplastics play a crucial role in the adverse health outcomes associated with microplastic exposure.

Polystyrene nanoparticles with different particle sizes cause autophagy by ROS/ERS/FOXO1 axis in the Cyprinus carpio kidney affecting immunological function.

Microplastic pollution poses challenges for ecosystems worldwide, and nanoplastics (NPs, 1-1000 nm) have been identified as persistent pollutants. However, although some studies have described the hazards of NPs to aquatic organisms, the toxicological processes of NPs in the common carp kidney and the biotoxicity of differently sized NPs remain unclear. In this study, we used juvenile common carp as an in vivo model that were constantly exposed to freshwater at 1000 µg/L polystyrene nanoparticle (PSNP) concentrations (50, 100, and 400 nm) for 28 days. Simultaneously, we constructed an in vitro model utilizing grass fish kidney cells (CIK) to study the toxicological effects of PSNPs of various sizes. We performed RT-PCR and Western blot assays on the genes involved in FOXO1, HMGB1, HIF-1α, endoplasmic reticulum stress, autophagy, and immunoreaction. According to these results, exposure to PSNPs increased reactive oxygen species (ROS) levels, and the carp kidneys experienced endoplasmic reticulum stress. Additionally, PSNPs promoted renal autophagy by activating the ROS/ERS/FOXO1 (ERS: endoplasmic reticulum stress) pathway, and it affected immunological function by stimulating the ROS/HMGB1/HIF-1α signaling pathway. This study provides new insights into the contamination hazards of NPs in freshwater environments, as well as the harm they pose to the human living environments. The relationship between particle size and the degree of damage caused by PSNPs to organisms is a potential future research direction.

Nanoplastic at environmentally relevant concentrations induces toxicity across multiple generations associated with inhibition in germline G protein-coupled receptor CED-1 in Caenorhabditis elegans.

Nanoplastics at environmentally relevant concentrations (ERCs) could cause transgenerational toxicity on organisms. Caenorhabditis elegans is an important model for the study of transgenerational toxicology of pollutants. Nevertheless, the underlying mechanisms for the control of transgenerational nanoplastic toxicity by germline signals remain largely unclear. In C. elegans, exposure to 1-100 µg/L polystyrene nanoparticle (PS-NP) decreased expression of germline ced-1 encoding a G protein-coupled receptor at parental generation (P0-G). After PS-NP exposure at P0-G, transgenerational decrease in germline ced-1 expression could be detected. Meanwhile, the susceptibility to transgenerational PS-NP toxicity was observed in ced-1(RNAi) animals. After PS-NP exposure at P0-G, germline RNAi of ced-1 increased expressions of met-2 and set-6 encoding histone methylation transferases. The susceptibility of ced-1(RNAi) to transgenerational PS-NP toxicity could be inhibited by RNAi of met-2 and set-6. Moreover, in PS-NP exposed met-2(RNAi) and set-6(RNAi) nematodes, expressions of ins-39, wrt-3, and/or efn-3 encoding secreted ligands were decreased. Therefore, our results demonstrated that inhibition in germline CED-1 mediated the toxicity induction of nanoplastics at ERCs across multiple generations in nematodes.

Microplastic-induced hepatic adverse effects evaluated in advanced quadruple cell human primary models following three weeks of repeated exposure.

Nano and microplastics are defined as particles smaller than 100 nm and 5 mm respectively. The widespread production and use of plastics in everyday life has resulted in significant accumulation of plastic debris in the environment. Over the last two decades there are increased concerns regarding the potential entry and accumulation of plastics in the human body with ingestion being one of the most important routes of exposure. However, the magnitude and nature of potential toxic effects of plastic exposure to human health is not yet fully understood. The liver is the body's principal detoxification organ and critically to this study recognized as the main accumulation site for particulates. In this study as the first of its kind the health impacts of long term low repeated polystyrene microplastics (1 and 5 µm) exposure was investigated in a functionally active 3D liver microtissue model, composed of primary human hepatocytes, Kupffer cells, sinusoidal endothelial cells and hepatic stellate cells. The highlight from the data includes microplastic-induced dose (3.125-25 µg/ml) and time dependent (up to 504 h) increase in cell death and inflammation manifested by enhanced release of IL6, IL8 and TNF-α. The exposure to repeated dosing of the plastics also resulted in notable pathology manifested as aberrant tissue architecture, such as dilated bile canaliculi and large lipid droplets inside the hepatic cells. This toxicity matched extremely well to the accumulation of the materials with the cells of microtissue predominately in the organ macrophages. This study highlights the real issue and danger of microplastic exposure with potential for long-term accumulation and adverse effects of non-biodegradable plastics within the liver.

Polystyrene nanoplastics alter intestinal toxicity of 2,4-DTBP in a sex-dependent manner in zebrafish (Danio rerio).

Nanoplastics (NPs) and 2,4-di-tert-butylphenol (2,4-DTBP) are ubiquitous emerging environmental contaminants detected in aquatic environment. While the intestinal toxicity of 2,4-DTBP alone has been studied, its combined effects with NPs remain unclear. Herein, adult zebrafish were exposed to 80 nm polystyrene nanoplastics (PS-NPs) or/ and 2,4-DTBP for 28 days. With co-exposure of PS-NPs, impact of 2,4-DTBP on feeding capacity and intestinal histopathology was enhanced in males while attenuated in females. Addition of PS-NPs significantly decreased the uptake of 2,4-DTBP in females, while the intestinal concentrations of 2,4-DTBP were not different between the sexes in co-exposure groups. Furthermore, lower intestinal pH and higher contents of digestive enzymes were detected in male fish, while bile acid was significantly increased in co-exposed females. In addition, co-exposure of PS-NPs stimulated female fish to remodel microbial composition to potentially enhance xenobiotics degradation, while negative Aeromonas aggravated inflammation in males. These results indicated that in the presence of PS-NPs, the gut microenvironment in females can facilitate the detoxification of 2,4-DTBP, while exaggerating toxiciy in males. Overall, this study demonstrates that toxicological outcomes of NPs-chemical mixtures may be modified by sex-specific physiology and microbiota composition, furthering understanding for environmental risk assessment and management of aquatic environments.

Hydrogen bonding-mediated interaction underlies the enhanced membrane toxicity of chemically transformed polystyrene microplastics by cadmium.

The global attention on microplastic pollution and its implications for human health has grown in recent years. Additionally, the co-existence of heavy metals may significantly alter microplastics' physicochemical characteristics, potentially amplifying their overall toxicity-a facet that remains less understood. In this study, we focused the membrane toxicity of modified polystyrene microplastics (PS-MPs) following cadmium (Cd) pretreatment. Our findings revealed that Cd-pretreated PS-MPs exacerbated their toxic effects, including diminished membrane integrity and altered phase fluidity in simulated lipid membrane giant unilamellar vesicles (GUVs), as well as heightened membrane permeability, protein damage, and lipid peroxidation in red blood cells and macrophages. Mechanistically, these augmented membrane toxicities can be partially ascribed to modifications in the surface roughness and hydrophilicity of Cd-pretreated PS-MPs, as well as to interactions between PS-MPs and lipid bilayers. Notably, hydrogen bonds emerged as a crucial mechanism underlying the enhanced interaction of PS-MPs with lipid bilayers.

Polystyrene nanoplastics significantly facilitate largemouth bass ranavirus infection of host cells.

Novel pollutants nanoplastics (NPs) are widely distributed in aquatic environments and may pose a health threat to aquatic organisms. Notably, the contribution of NPs to the occurrence of viral diseases in aquatic animals remains largely uncertain. In this study, the effects of polystyrene nanoplastics (PS-NPs) on Largemouth bass ranavirus (LMBV)-infected MsF cells were investigated. MsF cells took up PS-NPs in a time- and dose-dependent manner and significantly affect cell viability at an exposure concentration of 500 µg/mL. Western blot and qPCR assays indicated that exposure to PS-NPs accelerated LMBV replication in MsF cells. PS-NPs act synergistically with LMBV to disrupt the cellular antioxidant system, as evidenced by increased ROS production and decreased mRNA levels of antioxidant-associated genes. Furthermore, PS-NPs was found to exacerbate LMBV-induced inflammatory responses, as demonstrated by disturbed expression of inflammation-related factors. In addition, our results suggest that PS-NPs reduce IFN production by inhibiting the expression of molecules related to the cGAS-STING signaling pathway, thereby promoting viral replication. Collectively, our findings suggest the potential threat of NPs to infectious diseases caused by freshwater fish viruses and provide new insights for fish disease prevention and control.

Polystyrene microplastics aggravate radiation-induced intestinal injury in mice.

Radiotherapy is a common treatment for abdominal and pelvic tumors, while the radiation-induced intestinal injury (RIII) is one of the major side-effects of radiotherapy, which reduces the life quality and impedes the treatment completion of cancer patients. Previous studies have demonstrated that environmental pollutant microplastics led to various kinds of injury in the gut, but its effects on RIII are still uncovered. In this study, we fed the C57BL/6J mice with distilled water or 50 µg/d polystyrene microplastics (PSMPs) for 17 days and exposed the mice to total abdominal irradiation (TAI) at day 14. Then the severity of RIII was examined by performing histopathological analysis and microbial community analysis. The results demonstrated that PSMPs significantly aggravated RIII in small intestine rather than colon of mice upon TAI. PSMPs increased levels of the histopathological damage and the microbial community disturbance in mice small intestine, shown by the overabundance of Akkermansiaceae and the decrease of microflora including Lactobacillaceae, Muribaculaceae and Bifidobacteriaceae. In conclusion, our results suggested that more microplastics exposure might led to more severe RIII, which should be considered in patients' daily diet adjustment and clinical radiotherapy plan evaluation. Furthermore, this study also called for the further researches to uncover the underlying mechanism and develop novel strategies to attenuate RIII in mice intestine.

Polystyrene nanoplastics-induced intestinal barrier disruption via inflammation and apoptosis in zebrafish larvae (Danio Rerio).

Plastics are one of the most pervasive materials on Earth, to which humans are exposed daily. Polystyrene (PS) is a common plastic packaging material. However, the impact of PS on human health remains poorly understood. Therefore, this study aimed to identify intestinal damage induced by PS nanoplastics (PS-NPs) in zebrafish larvae which have a high homology with humans. Four days post fertilization (dpf), zebrafish larvae were exposed to 0-, 10-, and 50-ppm PS-NPs for 48 h Initially, to ascertain if 100 nm PS-NPs could accumulate in the gastrointestinal (GI) tract of zebrafish larvae, the larvae were exposed to red fluorescence-labeled PS-NPs, and at 6 dpf, the larvae were examined using a fluorescence microscope. Analysis of the fluorescence intensity revealed that the GI tract of larvae exposed to 50-ppm exhibited a significantly stronger fluorescence intensity than the other groups. Nonfluorescent PS-NPs were then used in further studies. Scanning electron microscopy (SEM) confirmed the spherical shape of the PS-NPs. Fourier-transform infrared spectroscopy (FT-IR) analysis revealed chemical alterations in the PS-NPs before and after exposure to larvae. The polydispersity index (PDI) value derived using a Zetasizer indicated a stable dispersion of PS-NPs in egg water. Whole-mount apoptotic signal analysis via TUNEL assay showed increased apoptosis in zebrafish larval intestines exposed to 50-ppm PS-NPs. Damage to the intestinal tissue was assessed by Alcian blue (AB) and hematoxylin and eosin (H&E) staining. AB staining revealed increased mucin levels in the zebrafish larval intestines. Thin larval intestinal walls with a decrease in the density of intestinal epithelial cells were revealed by H&E staining. The differentially expressed genes (DEGs) induced by PS-NPs were identified and analyzed. In conclusion, exposure to PS-NPs may damage the intestinal barrier of zebrafish larvae due to increased intestinal permeability, and the in vivo gene network may change in larvae exposed to PS-NPs.

Fragile Guts Make Fragile Brains: Intestinal Epithelial Nrf2 Deficiency Exacerbates Neurotoxicity Induced by Polystyrene Nanoplastics.

Oral ingestion is the primary route for human exposure to nanoplastics, making the gastrointestinal tract one of the first and most impacted organs. Given the presence of the gut-brain axis, a crucial concern arises regarding the potential impact of intestinal damage on the neurotoxic effects of nanoplastics (NPs). The intricate mechanisms underlying NP-induced neurotoxicity through the microbiome-gut-brain axis necessitate further investigation. To address this, we used mice specifically engineered with nuclear factor erythroid-derived 2-related factor 2 (Nrf2) deficiency in their intestines, a strain whose intestines are particularly susceptible to polystyrene NPs (PS-NPs). We conducted a 28-day repeated-dose oral toxicity study with 2.5 and 250 mg/kg of 50 nm PS-NPs in these mice. Our study delineated how PS-NP exposure caused gut microbiota dysbiosis, characterized by Mycoplasma and Coriobacteriaceae proliferation, resulting in increased levels of interleukin 17C (IL-17C) production in the intestines. The surplus IL-17C permeated the brain via the bloodstream, triggering inflammation and brain damage. Our investigation elucidated a direct correlation between intestinal health and neurological outcomes in the context of PS-NP exposure. Susceptible mice with fragile guts exhibited heightened neurotoxicity induced by PS-NPs. This phenomenon was attributed to the elevated abundance of microbiota associated with IL-17C production in the intestines of these mice, such as Mesorhizobium and Lwoffii, provoked by PS-NPs. Neurotoxicity was alleviated by in vivo treatment with anti-IL-17C-neutralizing antibodies or antibiotics. These findings advanced our comprehension of the regulatory mechanisms governing the gut-brain axis in PS-NP-induced neurotoxicity and underscored the critical importance of maintaining intestinal health to mitigate the neurotoxic effects of PS-NPs.

Effects of polystyrene microplastic composite with florfenicol on photosynthetic carbon assimilation of rice (Oryza sativa L.) seedlings: Light reactions, carbon reactions, and molecular metabolism.

The effects of co-exposure to antibiotics and microplastics in agricultural systems are still unclear. This study investigated the effects of florfenicol (FF) and polystyrene microplastics (PS-MPs) on photosynthetic carbon assimilation in rice seedlings. Both FF and PS-MPs inhibited photosynthesis, while PS-MPs can alleviate the toxicity of FF. Chlorophyll synthesis genes (HEMA, HEMG, CHLD, CHLG, CHLM, and CAO) were down-regulated, whereas electron transport chain genes (PGR5, PGRL1A, PGRL1B, petH, and ndhH) were up-regulated. FF inhibited linear electron transfer (LET) and activated cyclic electron transfer (CET), which was consistent with the results of the chlorophyll fluorescence parameters. The photosynthetic carbon assimilation pathway was altered, the C3 pathway enzyme Ribulose1,5-bisphosphatecarboxylase/oxygenase (RuBisCO) was affected, C4 enzyme ((phosphoenolpyruvate carboxykinase (PEPCK), pyruvate orthophosphate dikinase (PPDK), malate dehydrogenase (MDH), and phosphoenolpyruvate carboxylase (PEPC))) and related genes were significantly up-regulated, suggesting that the C3 pathway is converted to C4 pathway for self-protection. The key enzymes involved in photorespiration, glycolate oxidase (GO) and catalase (CAT), responded positively, photosynthetic phosphorylation was inhibited, and ATP content and H+-ATPase activity were suppressed, nutrient content (K, P, N, Ca, Mg, Fe, Cu, Zn, Mn, and Ni) significantly affected. Transcriptomic analysis showed that FF and PS-MPs severely affected the photosynthetic capacity of rice seedlings, including photosystem I, photosystem II, non-photochemical quenching coefficients, and photosynthetic electron transport.

Polystyrene microplastics induce molecular toxicity in Simocephalus vetulus: A transcriptome and intestinal microorganism analysis.

The global prevalence and accumulation of plastic waste is leading to pollution levels that cause significant damage to ecosystems and ecological security. Exposure to two concentrations (1 and 5 mg/L) of 500 nm polystyrene (PS)-nanoplastics (NPs) for 14 d was evaluated in Simocephalus vetulus using transcriptome and 16 s rRNA sequencing analyses. PS-NP exposure resulted in stress-induced antioxidant defense, disturbed energy metabolism, and affected the FoxO signaling pathway, causing neurotoxicity. The expression of Cyclin D1 (CCND), glucose-6-phosphatase (G6PC) and phosphoenolpyruvate carboxykinase (PCK) genes was decreased compared to the control, whereas the expression of caspase3 (CASP3), caspase7 (CASP7), Superoxide dismutase (SOD), Heat shock protein 70 (HSP70), MPV17, and Glutathione S-transferase (GST) genes was increased, thus, suggesting that NP ingestion triggered oxidative stress and disrupted energy metabolism.. PS-NPs were present in the digestive tract of S. vetulus after 14 days of exposure. In addition, the abundance of the Proteobacteria and opportunistic pathogens was elevated after PS-NPs exposure. The diversity and homeostasis of the S. vetulus gut microbiota were disrupted and the stability of intestinal barrier function was impaired. Multiomic analyses highlighted the molecular toxicity and microbial changes in S. vetulus after exposure to NPs, providing an overview of how plastic pollution affects freshwater organisms and ecosystems.

Exposure to polystyrene nanoplastics causes immune damage, oxidative stress and intestinal flora disruption in salamander (Andrias davidianus) larvae.

The toxic effects of nanoparticles have been increasingly investigated, but there has been limited research on amphibians, especially those of conservation value. This study examined the effects of different concentrations (0, 0.04, 0.2, 1, 5 mg/L) of polystyrene nanoplastics (PS-NPs, 80 nm) on the short-term exposure (7 d) of Andrias davidianus. Results demonstrated the concentration-dependent enrichment of PS-NPs in the intestine. Histological lesions displayed increased hepatic macrophages with cellular rupture, broken intestinal villi, decreased cuprocytes and crypt depression. Antioxidant- and inflammation-related enzyme activities were analysed, and it was found that hepatic and intestinal MDA content and CAT activity were highest in the N-1 group and SOD activity was highest in the N-0.2 group (p < 0.05). AKP activity continued to decline, and iNOS activity was highest in the N-0.2 group (p < 0.05). il-10, tgf-ß, bcl-w and txnl1 were significantly downregulated in the N-0.2 group, while il-6 and il-8 were markedly upregulated in the N-0.2 group (p < 0.05). Exposing to PS-NPs decreased probiotic bacteria (Cetobacterium, Akkermansia) and increased pathogenic bacteria (Lachnoclostridium). Our results suggest that NPs exposure can have deleterious effects on salamanders, which predicts that NPs contamination may lead to continued amphibian declines. Therefore, we strongly recommend that attention be paid to amphibians, especially endangered species, in the field of NPs.