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Plastics are novel environmental pollutants with potential threats to the ecosystem. At least 5.25 trillion plastic particles in the environment, of which nanoplastics are <100 nm in diameter. Polystyrene nanoplastics (PS-NPs) exposure damaged the spleen's immune function. Lipopolysaccharide (LPS) induced other toxicants to damage cells and organs, triggering inflammation. However, the mechanism of PS-NPs aggravated LPS-induced spleen injury remains unclear. In this study, the PS-NPs or/and LPS mice exposure model was replicated by intraperitoneal injection of PS-NPs or/and LPS, and PS-NPs or/and LPS were exposed to RAW264.7 cells. The histopathological and ultrastructural changes of the mice spleen were observed by H&E staining and transmission electron microscope. Western Blot, qRT-PCR, and fluorescent probes staining were used to detect reactive oxygen species (ROS), oxidative stress indicators, inflammatory factors, and necroptosis-related indicators in mice spleen and RAW264.7 cells. The results showed that PS-NPs or LPS induced oxidative stress, activated the MAPK pathway, and eventually caused necroptosis and inflammation in mice spleen and RAW264.7 cells. Compared with the single treatment group, the changes in PS-NPs + LPS group were more obvious. Furthermore, ROS inhibitor N-Acetyl-L-cysteine (NAC) significantly inhibited the activation of the mitogen-activated protein kinase (MAPK) signaling pathway caused by co-treatment of PS-NPs and LPS, reducing necroptosis and inflammation. The results demonstrated that PS-NPs promoted LPS-induced spleen necroptosis and inflammation in mice through the ROS/MAPK pathway. This study increases the data on the damage of PS-NPs to the organism and expands the research ideas and clues., (© 2022 Wiley Periodicals LLC.)

The use of polystyrene micro and nanoplastics in cosmetics and personal care products continues to grow every day. The harmful effects of their biological accumulation in organisms of all trophic levels including humans have been reported by several studies. While we have accumulating evidence on the impact of nanoplastics on different organ systems in humans, only a handful of reports on the impact of polystyrene nanoplastics upon direct contact with the immune system at the cellular level are avialable. The present study offers significant evidence on the cell-specific harmful impact of sulfate-modified nanoplastics (S-NPs) on human macrophages. Here we report that exposure of human macrophages to S-NPs (100 µg/mL) stimulated the accumulation of lipids droplets (LDs) in the cytoplasm resulting in the differentiation of macrophages into foam cells. The observed effect was specific for human and murine macrophages but not for other cell types, especially human keratinocytes, liver, and lung cell models. Furthermore, we found that S-NPs mediated LDs accumulation in human macrophages was accompanied by acute mitochondrial oxidative stress. The accumulated LDs were further delivered and accumulated into lysosomes leading to impaired lysosomal clearance. In conclusion, our study reveals that exposure to polystyrene nanoplastics stabilized with anionic surfactants can be a potent stimulus for dysregulation of lipid metabolism and macrophage foam cell formation, a characteristic feature observed during atherosclerosis posing a serious threat to human health. [Display omitted] • S-NPs induce accumulation of neutral lipids selectively in macrophages • Exposure to S-NPs induces acute oxidative stress • S-NPs exposed macrophages display impaired lysosomal clearance [ABSTRACT FROM AUTHOR]

[Display omitted] • Differentially charged PS-NP accumulated in brain of zebrafish larvae. • PS-NH 2 induced more serious cell apoptosis in brain than PS-COOH. • 13 altered metabolites related to NMDA2B in PS-NH 2 exposure. • 3 changed metabolites related to GPRs were increased by PS-COOH exposure. • Stronger binding between NMDA2B with PS-NH 2 than PS-COOH affected behaviors. Nanoplastics are being detected with increasing frequency in aquatic environments. Although evidence suggests that nanoplastics can cause overt toxicity to biota across different trophic levels, but there is little understanding of how materials such as differently charged polystyrene nanoplastics (PS-NP) impact fish development and behavior. Following exposure to amino-modified (positive charge) PS-NP, fluorescence accumulation was observed in the zebrafish brain and gastrointestinal tract. Positively charged PS-NP induced stronger developmental toxicity (decreased spontaneous movement, heartbeat, hatching rate, and length) and cell apoptosis in the brain and induced greater neurobehavioral impairment as compared to carboxyl-modified (negative charge) PS-NP. These findings correlated well with fluorescence differences indicating PS-NP presence. Targeted neuro-metabolite analysis by UHPLC-MS/MS reveals that positively charged PS-NP decreased levels of glycine, cysteine, glutathione, and glutamic acid, while the increased levels of spermine, spermidine, and tyramine were induced by negatively charged PS-NP. Positively charged PS-NP interacted with the neurotransmitter receptor N-methyl-D-aspartate receptor 2B (NMDA2B), whereas negatively charged PS-NP impacted the G-protein-coupled receptor 1 (GPR1), each with different binding energies that led to behavioral differences. These findings reveal the charge-specific toxicity of nanoplastics to fish and provide new perspective for understanding PS-NP neurotoxicity that is needed to accurately assess potential environmental and health risks of these emerging contaminants. [ABSTRACT FROM AUTHOR]

Nanoplastics (NPs) are good carriers of persistent organic pollutants (POPs) such as polybrominated diphenyl ethers (PBDEs), and can alter their bioavailability and toxic impacts to aquatic organisms. This study highlights the single and combined toxic effects of polystyrene nanoplastics (PS-NPs) and 2,2',4,4'-tetrabromodiphenyl ether (BDE-47, one of the dominant congeners of PBDEs) on zebrafish embryos after an exposure duration of up to 120 hpf. Results showed that PS-NPs and BDE-47 co-exposure exacerbated the morphological deformities in terms of pericardial edema, yolk sac edema and curved tail in zebrafish larvae. Compared to BDE-47 single exposure, the combined exposure caused lower survival rates, shorter body lengths, and accelerated spontaneous movements. Further, PS-NPs were quickly aggregated on the surface of the embryonic chorions covered almost the entire membrane at 12 and 48 hpf, and concentration dependent accumulation was also found in the brain, mouth, trunk, gills, heart, liver and gastrointestinal tract at the larval stages. During the recovery period (7 days), PS-NPs were released from all the organs, with the highest elimination from the gastrointestinal tract. Histopathological examination revealed that co-exposure caused greater damage to retinal structures, muscle fibers and cartilage tissues. Responses of hypothalamic-pituitary-thyroid axis (CRH, TSHβ, NIS, TTR, Dio2, TG, TRα and TRβ) and reproduction (Esr2 and Vtg1) related genes were also investigated, and results showed that the co-exposure induced more significant upregulated expressions of TSHβ, TG, Doi 2, and TRβ, compared to BDE-47 single exposure. In conclusion, co-exposure to NPs and BDE-47 exacerbated developmental and thyroid toxicity in zebrafish, generally elucidating the toxicological effects mediated by complex chemical interactions between NPs with POPs in the freshwater environment., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

Plastic particles in water environment can adsorb heavy metals, leading to combined toxicity on aquatic organisms. However, current conclusions are mostly obtained based on cell population-average responses. Heterogeneity effects among cell populations in aquatic organisms remain unclear. This study firstly analyzed the basic toxic effects of 20 μg L−1, 200 μg L−1 100 nm polystyrene nanoplastics (PS-NPs), 50 μg L−1 lead (Pb), and their combined exposures on zebrafish intestine. Results found that combined exposure of 200 μg L−1 PS-NPs and 50 μg L−1 Pb induced highest MDA, 8-OHdG, and TNF-α levels. Thus 200 μg L−1 PS-NPs, 50 μg L−1 Pb and their combined exposures were chosen to analyze the heterogeneity effects on zebrafish intestine cells by single-cell RNA sequencing. A total of 38,640 zebrafish intestinal cells were obtained and identified as seven cell populations, including enterocytes, macrophages, neutrophils, B cells, T cells, enteroendocrine cells, and goblet cells. 200 μg L−1 PS-NPs exposure had the greatest influence on macrophages, while Pb exposure mostly influenced enterocytes. Results of MDA, 8-OHdG, and TNF-α analyses indicated that 20 μg L−1 and 200 μg L−1 PS-NPs increased the Pb toxicity. However, the scRNA-seq showed that the synergistic effects did not exist in most cell populations, except for goblet cells. Co-exposure of 200 μg L−1 PS-NPs and Pb caused similar transcriptome profiles with 200 μg L−1 PS-NPs exposure in macrophages, which changed immunological recognition and apoptosis processes. The Pb exposure influenced the macrophages by direct cytotoxicity. However, the Pb alone and combined exposures induced similar toxicities in the enterocytes, including the generation of oxidative stress and abnormality of lipid metabolism. This study shows the scRNA-seq is a powerful method to identify the target cell populations and corresponding toxic effects during combined exposure of pollutants. [Display omitted] • Combined effects of PS-NPs and Pb on zebrafish intestine cells were analyzed. • Seven cell populations and their transcriptome profiles were obtained. • PS-NPs and Pb exposures mostly influenced macrophages and enterocytes, respectively. • PS-NPs + Pb group induced similar toxic effects as PS-NPs group in the macrophages. • PS-NPs + Pb group induced similar toxic effects as Pb group in the enterocytes. [ABSTRACT FROM AUTHOR]

Nanoplastics (NP) (1–100 nm) are a growing global concern, and their adverse effects in marine organisms are still scarce. This study evaluated the effects of polystyrene nanoplastics (10 μg/L; 50 nm nPS) in the marine mussel Mytilus galloprovincialis after a 21 – day exposure. The hydrodynamic diameter and zeta potential of nPS were analysed, over time, in seawater and ultrapure water. A multibiomarker approach (genotoxicity (the comet assay) was assessed in mussel haemocytes, and the antioxidant enzymes (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx)), biotransformation enzyme (glutathione – S – transferase (GST)), and oxidative damage (LPO)) was assessed in gills and digestive glands to evaluate the toxicity of nPS towards mussels. In seawater, aggregation of nPS is favoured and consequently the hydrodynamic diameter increases. Genotoxicity was highly noticeable in mussels exposed to nPS, presenting a higher % tail DNA when compared to controls. Antioxidant enzymes are overwhelmed after nPS exposure, leading to oxidative damage in both tissues. Results showed that mussel tissues are incapable of dealing with the effects that this emerging stressor pursues towards the organism. The Integrated Biomarker Response index, used to summarise the biomarkers analysed into one index, shows that nPS toxicity towards mussels are both tissue and time dependent, being that gills are the tissue most compromised. [Display omitted] • Polystyrene nanoplastics aggregation/agglomeration is favoured in seawater. • Genotoxicity occurs in mussel haemolymph after NPs exposure. • NPs toxicity is tissue and time dependent. • Gills are the predominate tissue affected by nanoplastic toxicity. [ABSTRACT FROM AUTHOR]

In animal species, the brain-gut axis is a complex bidirectional network between the gastrointestinal (GI) tract and the central nervous system (CNS) consisting of numerous microbial, immune, neuronal, and hormonal pathways that profoundly impact organism development and health. Although nanoplastics (NPs) have been shown to cause intestinal and neural toxicity in fish, the role of the neurotransmitter and intestinal microbiota interactions in the underlying mechanism of toxicity, particularly at environmentally relevant contaminant concentrations, remains unknown. Here, the effect of 44 nm polystyrene nanoplastics (PS-NPs) on the brain-intestine-microbe axis and embryo-larval development in zebrafish ( Danio rerio ) was investigated. Exposure to 1, 10, and 100 μg/L PS-NPs for 30 days inhibited growth and adversely affected inflammatory responses and intestinal permeability. Targeted metabolomics analysis revealed an alteration of 42 metabolites involved in neurotransmission. The content of 3,4-dihydroxyphenylacetic acid (DOPAC; dopamine metabolite formed by monoamine oxidase activity) was significantly decreased in a dose-dependent manner after PS-NP exposure. Changes in the 14 metabolites correlated with changes to 3 microbial groups, including Proteobacteria , Firmicutes , and Bacteroidetes , as compared to the control group. A significant relationship between Firmicutes and homovanillic acid (0.466, Pearson correlation coefficient) was evident. Eight altered metabolites (l-glutamine (Gln), 5-hydroxyindoleacetic acid (5-HIAA), serotonin, 5-hydroxytryptophan (5-HTP), l-cysteine (Cys), l-glutamic acid (Glu), norepinephrine (NE), and l-tryptophan (l-Trp)) had a negative relationship with Proteobacteria although histamine (His) and acetylcholine chloride (ACh chloride) levels were positively correlated with Proteobacteria . An Associated Network analysis showed that Firmicutes and Bacteroidetes were highly correlated (0.969). Furthermore, PS-NPs accumulated in the gastrointestinal tract of offspring and impaired development of F1 (2 h post-fertilization) embryos, including reduced spontaneous movements, hatching rate, and length. This demonstration of transgenerational deficits is of particular concern. These findings suggest that PS-NPs cause intestinal inflammation, growth inhibition, and restricted development of zebrafish, which are strongly linked to the disrupted regulation within the brain-intestine-microbiota axis. Our study provides insights into how xenobiotics can disrupt the regulation of brain-intestine-microbiota and suggests that these end points should be taken into account when assessing environmental health risks of PS-NPs to aquatic organisms.

Mucin (Mu), a biological substance extracted from jellyfish ( Aurelia aurita ), was used to reduce the toxic effect of polystyrene nanoplastics (PS-NP) combined with phenanthrene (Phe) in the aquatic environment of zebrafish ( Danio rerio ), among other aquatic organisms. Mu showed a high binding capacity, as it bound to 92.84% and 92.87% of the PS-NPs (concentration of 2.0 mg/L) after 0.5 h and 8 h, respectively. A zebrafish embryo development test was conducted to check for any reduction in toxicity by Mu. When exposed to PS-NP + Mu and PS-NP + Phe + Mu, respectively, the hatching rates were 88.33 ± 20.21% and 93.33 ± 2.89%, respectively; these results were not significantly different from those of the control group. However, the hatching rate with the addition of Mu increased, compared to that of the PS-NP (71.83 ± 13.36%) and Phe (37.50 ± 19.83%) treatments, and the morphological abnormality rate decreased. The presence of Mu was also found to obstruct the absorption of PS-NP and PS-NP + Phe by the zebrafish. When zebrafish embryos were exposed to PS-NP at a concentration of 5.0 mg/L, the hatching rate differed significantly from that of the control group, and the expression of CAT and p53 genes increased significantly, but the expression of Bcl-2 decreased significantly. An mRNA sequence analysis revealed that the gene expression levels of the test group containing Mu were similar to those of the control group. These results infer that Mu can be used as a biological material to collect and remove PS-NPs from aquatic environments and reduce toxicity.

Recently, the effects of nanoplastics (NPs) on aquatic organisms have attracted much attention; however, research on the toxicity of NPs to microalgae has been insufficient. In the present study, the effects of polystyrene nanoplastics (nano-PS, 50 nm) on growth inhibition, chlorophyll content, oxidative stress, and algal toxin production of the marine toxigenic dinoflagellate Amphidinium carterae Hulburt were investigated. Chlorophyll synthesis was promoted by nano-PS on day 2 but was inhibited on day 4; high concentrations of nano-PS (≥50 mg/L) significantly inhibited the growth of A. carterae. Moreover, despite the combined effect of superoxide dismutase (SOD) and glutathione (GSH), high reactive oxygen species (ROS) level and malondialdehyde (MDA) content were still induced by nano-PS (≥50 mg/L), indicating severe lipid peroxidation. In addition, the contents of extracellular and intracellular hemolytic toxins in nano-PS groups were significantly higher than those in control groups on days 2 and 8, except that those of extracellular hemolytic toxins in the 100 mg/L nano-PS group decreased on day 8 because of severe adsorption of hemolytic toxins to the nano-PS. Hence, the effects of nano-PS on A. carterae are closely linked to nano-PS concentration and surface properties and exposure time. These findings provide a deep understanding of the complex effects of NPs on toxigenic microalgae and present valuable data for assessing their environmental risks. [ABSTRACT FROM AUTHOR]

Presence of nanoplastics within aqueous media has raised concerns about their adverse impacts on aquatic organisms. This study evaluated toxic effects of amino-functionalized polystyrene nanoplastics (PS–NH 2) with diameters of 90 (PS–NH 2 -90), 200 (PS–NH 2 -200) and 300 (PS–NH 2 -300) nm on green microalgae Chlorella vulgaris. A dose-dependent toxicity response by PS-NH 2 -90 and/or PS-NH 2 -200 on biomass and photosynthetic pigment (chlorophyll a) end-points of C. vulgaris was observed. Whereas varied concentrations of PS-NH 2 -300 had no significant toxic effect on biomass and chlorophyll a end-points compared to control groups (p > 0.05). A comparison of toxicity of similar concentrations of PS-NH 2 -90, PS-NH 2 -200 and PS-NH 2 -300 showed small-sized PS-NH 2 were more toxic than large-sized PS-NH 2 (toxicity of PS-NH 2 increased in the order PS-NH 2 -300 < PS-NH 2 -200 < PS-NH 2 -90). With decreasing PS-NH 2 size, greater morphological changes and loss of original shape were observed, so that algal density/size reduced, and cell aggregations increased. Since PS-NH 2 have high affinity to C. vulgaris due to electrostatic interaction with polysaccharide wall of algae, this could be as the main reason for formation of large aggregates at high concentrations of PS-NH 2 compared to low concentrations of PS-NH 2 used in algae medium. At high concentrations, PS-NH 2 may act as intermediaries for connection of algal cells and therefore formation of aggregates. Field emission scanning electron microscopy images confirmed that high amounts of PS-NH 2 -90 were found to be embedded and adsorbed on algal cells, thereby limiting transfer of materials, gas exchange and energy between the aqueous medium and algal cells. These data may have serious ecological health implications, as C. vulgaris are important primary producers responsible for producing oxygen in aquatic environments. [Display omitted] • Dose-dependent toxicity of PS-NH 2 nanoplastics with 90, 200 and 300 nm diameters were evaluated on Chlorella vulgaris. • Small-sized PS-NH 2 were more toxic than large-sized PS-NH 2 to C. vulgaris. • With decreasing PS-NH 2 size, greater morphological changes were observed. • PS-NH 2 -90 nanoplastics embedded and sorbed onto algal cells. • PS-NH 2 -300 nanoplastics had no toxic effect on C. vulgaris biomass and chlorophyll a. [ABSTRACT FROM AUTHOR]

The increasing accumulation of plastic waste and the widespread presence of its derivatives, micro- and nanoplastics (MNPLs), call for an urgent evaluation of their potential health risks. In the environment, MNPLs coexist with other known hazardous contaminants and, thus, an interesting question arises as to whether MNPLs can act as carriers of such pollutants, modulating their uptake and their harmful effects. In this context, we have examined the interaction and joint effects of two relevant water contaminants: arsenic and polystyrene nanoplastics (PSNPLs), the latter being a model of nanoplastics. Since both agents are persistent pollutants, their potential effects have been evaluated under a chronic exposure scenario and measuring different effect biomarkers involved in the cell transformation process. Mouse embryonic fibroblasts deficient for oxidative DNA damage repair mechanisms, and showing a cell transformation status, were used as a sensitive cell model. Such cells were exposed to PSNPLs, arsenic, and a combination PSNPLs/arsenic for 12 weeks. Interestingly, a physical interaction between both pollutants was demonstrated by using TEM/EDX methodologies. Results also indicate that the continuous co-exposure enhances the DNA damage and the aggressive features of the initially transformed phenotype. Remarkably, co-exposed cells present a higher proportion of spindle-like cells within the population, an increased capacity to grow independently of anchorage, as well as enhanced migrating and invading potential when compared to cells exposed to arsenic or PSNPLs alone. This study highlights the need for further studies exploring the long-term effects of contaminants of emerging concern, such as MNPLs, and the importance of considering the behavior of mixtures as part of the hazard and human risk assessment approaches.

Nowadays, plastic pollution and in particular nano(micro)plastics is considered as an issue of global concern in environmental samples. The present work was conducted to clarify the oxidative stress of polystyrene nanoplastics (PS-NPs) exposure and physiological response of male Wistar rats. Animals were treated orally with PS-NPs at four doses (1, 3, 6, and10 mg/kg-day) for 5 weeks. Results demonstrated the accumulation of PS-NPs through whole body scanning and also a dose-dependent increase in the production of reactive oxygen species (ROS). Alterations in antioxidant responses including serum levels of catalase (CAT) and total glutathione content were noticed, but not superoxide dismutase (SOD), pointing towards the perturbation of redox state induced by exposure conditions. Biochemical parameters viz. glucose, cortisol, lipase, lactate, lactate dehydrogenase (LDH), alkaline phosphatase, gamma-glutamyl transpeptidase (GGT), triglycerides, and urea showed a significant increase, while total protein, albumin, and globulin levels showed an appreciable decline. The pattern of associations noticed with AChE activity and biochemical responses in our study suggests the possibility that a neurobehavioral effect or dysfunctions in energy metabolism may be the potential modes of action, possibly through stress response as well as liver function. Perturbations of creatinine and uric acid levels are indeed plausible biological explanations for the association with kidney dysfunction. Although we provided a new scientific clue for exploring the biological consequences of NPs which might induce effects such as oxidative stress relating to the induction of antioxidant enzymes, the results warrant additional research with a larger sample size., (© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Agroecosystems represent more and more a huge long-term sink for plastic compounds which inevitably undergo fragmentation, generating micro- and nano-plastics, with potential adverse effects on soil chemistry and living organisms. The present work was focused on the short-term effects of two different concentrations of polystyrene nanoplastics (PSNPs) (0.1 or 1 g L -1 suspensions) on rice seedlings starting from seed germination, hypothesizing that possible acute effects on seedlings could depend on oxidative damage trigged by PSNPs internalization. As shown by TEM analysis, PSNPs were absorbed by roots and translocated to the shoots, affected root cell ultrastructure, the germination process, seedling growth and root mitotic activity, inducing cytogenetic aberration. Treatments were not correlated with increase in oxidative stress markers, but rather with a different pattern of their localization both in roots and in shoots, impairing H 2 O 2 homeostasis and membrane damage, despite the adequate antioxidant response recorded. The harmful effects of PSNPs on cell biology and physiology of rice seedlings could be caused not only by a direct action by the PSNPs but also by changes in the production/diffusion of ROS at the tissue/cellular level., (Copyright © 2022 Elsevier Masson SAS. All rights reserved.)

Microplastics (MPs) and nanoplastics (NPs) in the environment pose significant risks to organisms of different trophic levels. While the toxicity of MPs and NPs have been extensively investigated, it remains unknown whether these particles affect microbial transformation of organic pollutants. Here, we show that 20 and 100 nm polystyrene NPs (PS-NPs) can inhibit the transformation of tetrabromobisphenol A (TBBPA) by Gram-positive bacterium Rhodococcus jostii in a concentration-dependent manner. We found that smaller PS-NPs were more inhibitory than larger ones and that both PS-NPs affected biotransformation in several ways. PS-NPs adsorbed TBBPA on their surface and reduced the bioavailable concentration of TBBPA for transformation by R. jostii . Furthermore, PS-NPs induced oxidative stress, increased membrane permeability, and downregulated O -methyltransferase enzymes that transform TBBPA into their methylated derivatives. Our results demonstrate that PS-NPs can impact microbial transformation of organic pollutants, and these effects should be accounted for in future environmental risk assessments.

There is a growing concern regarding the toxic effects of nanoplastics (NPs) on aquatic and marine organism, while relatively few studies about their toxicity evaluation on mammals are conducted. In the present study, we observed accumulation of polystyrene NPs (PS NPs) in mice spleen, lung, kidney, small intestine, large intestine, testis, and brain after oral exposure to PS NPs (~100 nm, 10 mg/mL, 100 μL) for 28 days, and NPs were identified to induce cell apoptosis, inflammation, and structure disorder in these tissues. We also found that PS NPs could bring about hematological system injury and lipid metabolism disorder. Further in vitro studies identified that PS NPs could be absorbed by the intestinal epithelial Caco-2 cells by macropinocytosis and clathrin-mediated endocytosis, and induced disruption of tight junction between Caco-2 cells. Moreover, we found that it was easier for PS-NH 2 and PS-COOH to enter into Caco-2 cells, which may be associated with observed stronger toxicity of PS-NH 2 and PS-COOH NPs. In summary, this study demonstrated that NPs exposure brings about toxic effects to mice. This study could provide new insights regarding the distribution of NPs in humans, and helps us to evaluate the potential physiological risks of NPs to human beings. [Display omitted] • We systematically examined the distribution pattern of polystyrene nanoplastics in mice. • We evaluated the physiologic effects of nanoplastics in mice. • We investigated the molecular mechanism underlying the internalization of nanoplastics into Caco-2 cells. • We compared toxic effects of nanoplastics with different surface modifications on mice and Caco-2 cells. [ABSTRACT FROM AUTHOR]

Polystyrene nanoplastics (PS-NPs) are known to impair the function of the digestive system, intestinal flora, immune system, and nervous system of marine organisms. We tested whether PS-NPs influence viral infection of orange-spotted grouper (Epinephelus coioides). We found that grouper spleen (GS) cells took up PS-NPs at exposure concentrations of 5, 50, and 500 μg/mL and experienced cytotoxicity at 50 and 500 μg/mL concentrations. At 12 h after exposure to 50 μg/mL of PS-NPs, the replication of Singapore grouper iridovirus (SGIV) and red-spotted grouper nervous necrosis virus (RGNNV) increased in GS cells after their invasion. Juvenile fish exposed to 300 and 3000 μg/L of PS-NPs for 7 d showed PS-NPs uptake to the spleen and vacuole formation in brain tissue. Moreover, PS-NPs exposure accelerated SGIV replication in the spleen and RGNNV replication in the brain. PS-NP exposure also decreased the expression of toll-like receptor genes and interferon-related genes before and after virus invasion in vitro and in vivo , thus reducing the resistance of cells and tissues to viral replication. This is the first report that PS-NPs have toxic effects on GS cells and spleen and brain tissues, and it provides new insights into assessing the impact of PS-NPs on marine fish. [Display omitted] • PS-NPs were cytotoxic to grouper spleen (GS) cells. • PS-NPs exposure accelerated virus invasion in GS cells. • PS-NPs exposure accelerated virus invasion into the spleen and brain. • PS-NP exposure decreased the expression of interferon-related genes before and after virus invasion in vitro and in vivo. [ABSTRACT FROM AUTHOR]

• Paternal transfer of TDCIPP and NPPs was observed in zebrafish offspring. • NPPs enhance bioaccumulation and transfer of TDCIPP to offspring. • Thyroid hormones were further decreased by co-exposure in F0 and F1 generations. • Most thyroid-toxic biomarker expressions down-regulate in the co-exposure group. • Parental coexposure impaired survival and growth of offspring larvae. Plastic is a globally recognized superwaste that can affect human health and wildlife when it accumulates and is amplified in the food chain. Microplastics (plastic particles < 5 mm) and nanoplastics (plastic particles < 100 nm) can interact with organic pollutants already present in the aquatic environment, potentially acting as carriers for pollutants entering organisms and thus influencing the bioavailability and toxicity of those pollutants. In this study, we investigated the transfer kinetics and transgenerational effects of exposure to tris(1,3-dichloro-2-propyl) phosphate (TDCIPP) and polystyrene nanoplastics (PS-NPs) in F1 offspring. At 90 days postfertilization, zebrafish (Danio rerio) strain AB was exposed to either TDCIPP (0, 0.47, 2.64, or 12.78 μg/L) or PS-NPs (10 mg/L) or their combination for 120 days. The results showed that TDCIPP and PS-NPs accumulated in the gut, gill, head, and liver of the zebrafish in a sex-dependent manner. The presence of PS-NPs promoted the bioaccumulation of TDCIPP in the adult fish and increased the parental transfer of TDCIPP to their offspring. We demonstrate that parental exposure to TDCIPP alone or in combination with PS-NPs induces thyroid disruption in adults, and then leads to thyroid endocrine disruption in their larval offspring. Reduced thyroxine (T4) and 3,5,3′-triiodothyronine (T3) levels contributed to the observed transgenerational thyroid dysfunction, which inhibited developmental growth and disturbed the transcription of genes and expression of proteins involved in the hypothalamic–pituitary–thyroid (HPT) axis in the F1 larvae. The increased transfer of TDCIPP to the offspring in the presence of PS-NPs also enhanced transgenerational thyroid endocrine disruption, demonstrated by a further reduction in T4 and the upregulation of thyroglobulin (tg), uridine diphosphate-glucuronosyltransferase (ugt1ab), thyroid-stimulating hormone (tshβ), and thyroid hormone receptor (trα) expression in the F1 larvae compared with the effects of parental TDCIPP exposure alone. Overall, our results indicate that the presence of PS-NPs modifies the bioavailability of TDCIPP and aggravates transgenerational thyroid disruption in zebrafish. [ABSTRACT FROM AUTHOR]

With increasing plastic production and consumption, large amounts of polystyrene nanoplastics are accumulated in soil due to improper disposal causing pollution and deleterious effects to environment. However, little information is available about how to alleviate the adverse impacts of nanoplastics on crops. In this study, the involvement of melatonin in modulating nanoplastic uptake, translocation, and toxicity in wheat plant was investigated. The results demonstrated that exogenous melatonin application reduced the nanoplastic uptake by roots and their translocation to shoots via regulating the expression of genes associated with aquaporin, including the upregulation of the TIP2-9, PIP2, PIP3, and PIP1.2 in leaves and TIP2-9, PIP1-5, PIP2, and PIP1.2 in roots. Melatonin activated the ROS scavenging system to maintain a better redox homeostasis and ameliorated the negative effects of nanoplastics on carbohydrate metabolism, hence ameliorated the plant growth and enhanced the tolerance to nanoplastics toxicity. This process was closely related to the exogenous melatonin application induced melatonin accumulation in leave. These results suggest that melatonin could alleviate the adverse effects of nanoplastics on wheat, and exogenous melatonin application might be used as a promising management strategy to sustain crop production in the nanoplastic-polluted soils., (© 2021 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

[Display omitted] • Polystyrene nanoplastics induce haemolysis and acute oxidative stress. • Polystyrene nanoplastics impair lysosomes in macrophages in vitro. • Exposure to sulfate modified polystyrene nanoplastics induces foam cell formation. • 3- Methyl Adenine reduces viability of nanoplastics exposed cells. • Sulfate modified polystyrene nanoplastics disrupt lipid metabolism in BV2 cells. Micro and nanoplastics are one of the major emerging environmental contaminants. Their impact on human health is less explored. There are several in vitro studies on their cellular uptake and accumulation, where micro and nanoplastics were mostly reported to be non-cytotoxic. The effects caused by the direct contact of nanoplastics with the immune system, especially at the cellular level is less known. Here we report that RAW 264.7 macrophages undergo differentiation into lipid laden foam cells when exposed to polystyrene nanoplastics (50 μg/mL). We found that exposure of RAW 264.7 macrophages to sulfate-modified polystyrene nanoplastics results in the accumulation of lipid droplets in the cytoplasm leading to foam cell formation. Exposure to high concentration of polystyrene nanoplastics (100 and 200 μg/mL) results in increased reactive oxygen species and impair lysosomes in macrophages. The exposure of BV2 microglial cells to polystyrene nanoplastics (50 μg/mL) induces lipid accumulation. In addition, our results indicate the role of polystyrene nanoplastics in altering the lipid metabolism in murine macrophages in vitro. In the present study we reported that polystyrene nanoplastics stabilized with anionic surfactants can be potent stimuli for lipotoxicity and foam cell formation leading to the pathogenesis of atherosclerosis posing major threat for animal and human health. [ABSTRACT FROM AUTHOR]

Here we investigated the acute effects (12 h exposure) of three polystyrene nanoplastics (PS NPs, including PS, PS−COOH and PS−NH 2) on extracellular polymeric substance (EPS) composition of activated sludge. Three PS NPs exhibited the significant inhibition in total EPS and protein (PRO) production. The functional groups involved in the interactions between PS NPs and EPS were C-(C, H), and those between PS-NH 2 NPs and EPS were C O and O–C–O. In addition, the dewaterability of activated sludge were optimized by three PS NPs, especially PS-NH 2 NPs. Three PS NPs caused nonnegligible cellular oxidative stress and cell membrane damage in activated sludge (PS NPs exposure concentration: 100 mg/L). Among them, the cell membrane damage caused by PS-NH 2 was the most significant. Overall, the degree of influence on EPS and cytotoxicity of activated sludge varies with the surface functional groups of PS NPs. [Display omitted] • Compared the effects of PS NPs with surface modification on EPS of activated sludge. • Three PS NPs inhibited the total production of EPS and protein after 12 h exposure. • C-(C, H) was involved in the interactions between PS NPs and EPS. • C=O and O-C-O were involved in the interactions between PS-NH 2 NPs and EPS. • Three PS NPs induced obvious increases in ROS generation and LDH release. The surface functional groups of PS NPs lead to different cytotoxicity mechanisms and influence on EPS composition and structure of activated sludge. [ABSTRACT FROM AUTHOR]

Plastic particles, which are formed from routinely used plastics and their fragments, have become a new pollutant raising widespread concern about their potential effects. Several studies have been conducted to examine their toxicity, but the effects of nano-sized plastic fragments on freshwater organisms remain largely unclear and need to be further investigated. In this study, larval tilapia were first exposed to 100 nm polystyrene nanoparticles (PS-NPs, 20 mg/L) for seven days and then returned to freshwater without PS-NPs for another seven days in order to determine the toxic effects of PS-NPs at both transcriptomic and metabolomic levels. A total of 203 significantly changed metabolites, and 2,152 differentially expressed unigenes were identified between control and PS-NP treatment groups, control and recovery groups, as well as treatment and recovery groups. Our data suggested that PS-NPs induced abnormal metabolism of glycolipids, energy, and amino acids in tilapia after short-term exposure. Additionally, PS-NPs caused disturbed signaling, as suggested by the transcriptomic results. Different transcriptomic and metabolomic levels between the treatment group and recovery group indicated a persistent impact of PS-NPs on tilapia. The presence of adhesion molecule-related differentially expressed genes (DEGs) suggested that PS-NPs might cause early inflammatory responses. Notably, the detection of chemical stimulus involved in the sensory perception of smell was the most severely impacted biological process. Our work systemically studied the ecotoxicity of nano-sized plastics in aquatic creatures at the molecular and genetic levels, serving as a basis for future investigations on the prevention and treatment of such pollutants. [Display omitted] • Nanoparticle toxicity was evaluated by metabolomics and transcriptome analysis. • Polystyrene nanoparticle induces signaling and metabolism disorders in tilapia. • Nanoparticle causes enduring damage on feeding and sensing behaviors of tilapia. Both transcriptome and metabolome profiles revealed that PS-NPs (100 nm, 20 mg/L) disturbed the metabolism of glycolipids, energy, and amino acids in tilapia. [ABSTRACT FROM AUTHOR]

Nanoplastics, a kind of emerging pollutant in natural environments, have now drawn tremendous attention worldwide. Flocculation with Mg/Al-layered double hydroxides (LDH) precursor solutions has showed great potential for removing negatively charged nanoparticles from water. In this study, the flocculation behavior and mechanism for the removal of polystyrene nanoplastics (PSNP) with Mg/Al flocs or Mg/Al LDH were systematically analyzed and investigated. During the process of flocculation, it was observed that in situ Mg/Al LDH can be gradually formed with increasing pH, in addition, PSNP were captured or attached to the surface of LDH with a turning point around pH of 5.0. In acidic solutions with pH < 5.0, the negative surface charges of PSNP were diminished mainly due to the high concentrations of hydrogen ions and the positive charges from Mg and Al ions. In a moderately alkaline solution, Mg and Al ions gradually formed crystals capturing PSNP. Electrostatic adsorption and intermolecular force are the main mechanisms via which PSNP are captured on Mg/Al flocs. Herein, PSNP removal efficiencies from water were more than 90.0%. As the problem of plastic pollution becomes more severe, in situ LDH growth flocculation can provide an efficient way for the removal of PSNP. ga1 • Mg/Al dual flocculation showed a great potential for removing PSNP from water. • PSNP captured on Mg/Al flocs depends on electrostatic and intermolecular force. • Mechanisms of PSNP removed by Mg/Al dual flocculation at different pH were deciphered. • Crystals formed with the increase of pH and that Mg/Al LDH was formed at pH 9–10. • We provide a new idea for the removal of PSNP from water. [ABSTRACT FROM AUTHOR]

• Protein corona formation was related to the surface properties of PSNPs. • BSA significantly improved the stability of PS-Bare and PS-COOH in electrolytes. • Protein corona structure was visualized by negative-stained TEM. • Anion displayed contrary effects on the stability of oppositely charged PSNPs. • PSNPs would suspend in fresh water for a long time due to NOM corona formation. Nanosized plastics are considered as being a class of contaminants of emerging concern. The interaction between nanoplastics and proteins may significantly influence the environmental behavior and fate of nanoplastics. Here, we employed time-resolved dynamic light scattering to explore the aggregation kinetics and stability of polystyrene nanoparticles (PSNPs) exposed to a model globular protein (bovine serum albumin, BSA) in the presence of a number of typical electrolytes (NaCl, CaCl 2 , and Na 2 SO 4). With the increase of the BSA concentration, the amount of BSA adsorbed on the surface of negatively charged PS-Bare (non-modified) and PS-COOH (carboxyl-modified) increased, resulting in higher dispersibility in comparison to the treatment without BSA. This stabilization effect derived from the protein corona structure was revealed by combining characterization techniques and visualized by transmission electron microscopy. Upon addition of NaCl and CaCl 2 , the aggregation of positively charged PS-NH 2 (amino-modified) was inhibited by the BSA addition possibly due to the screening of the attractive patch-charge force and the competition for adsorption of cations between PS-NH 2 and the protein. When Na 2 SO 4 was present in the suspension, BSA addition significantly increased PS-NH 2 aggregation rate due to patch-charge attraction and the high performance of SO 4 2− in attaching to particles and charge neutralization. These findings shed light on the interactions between PSNPs and proteins, which were shown to vary with the composition of the surface coatings of PSNPs. The newly gained knowledge will help us to forecast the transport and fate of PSNPs in natural aqueous systems. Image, graphical abstract [ABSTRACT FROM AUTHOR]

• Polystyrene-nanoplastics (PS-NPs) enhance antioxidant activity and activate carbon metabolism. • The difference in root-related gene expressions is induced by PS-NPs. • Jasmonate and lignin biosynthesis are inhibited by PS-NPs treatments. • Exogenous JA application alleviates potential adverse effects of PS-NPs on rice seedlings. Potential adverse effects of nanoplastics (NPs) on marine organisms have received increased attention in recent years. In contrast, few data are available on terrestrial plants, especially on the mechanisms for transport of NPs in plants and phytotoxicity (at both phenotypic and molecular levels) of plants induced by NPs. To address this knowledge gap, we conducted a microcosm study in which hydroponically-cultured rice (Oryza sativa L.) seedlings were exposed to polystyrene (PS)-NPs at 0, 10, 50, and 100 mg L−1 for 16 d and examined for morphological and physiological phenotypes and transcriptomics. Laser confocal scanning micrographs confirmed PS-NPs were uptaken by rice roots, greatly benefitted from the transport activity of aquaporin in rice roots. The significant enhancement (p < 0.05) of antioxidant enzyme activities reflected the oxidative stress response of rice roots upon exposure to PS-NPs. Treatment by PS-NPs decreased root length and increased lateral root numbers. Carbon metabolism was activated (e.g., increased carbon and soluble sugar contents) whereas jasmonic acid and lignin biosynthesis were inhibited. The present study demonstrated the likelihood for transport of PS-NPs in rice roots and induced phytotoxicity by PS-NPs, which should inspire further investigations into the potential human health risks from rice consumption. [ABSTRACT FROM AUTHOR]

Effects of nanoplastics at low level on the marine primary producer are largely unclear. To assess the potential risk of nanoplastic pollution, this study exposed marine green microalgae Platymonas helgolandica to 20, 200, and 2000 μg/L 70-nm polystyrene nanoplastics for 6 days. Nanoplastics significantly inhibited the growth of P. helgolandica during the first 4 days of exposure, and elevated heterocyst frequency was observed in 200 and 2000 μg/L exposure groups in the early exposure stage. Exposure to 200 and 2000 μg/L nanoplastics for 4 days increased the membrane permeability and mitochondrial membrane potential, and decreased light energy used in photochemical processes of microalgae. Moreover, clear morphological changes, including surface folds, fragmentation, aggregation cluster, and rupture, in the microalgae exposed to nanoplastics were observed under scanning electron microscope and transmission electron microscope. These results demonstrate that nanoplastics could reduce the microalgal vitality by the damage on cell morphology and organelle function. Unlabelled Image • Nanoplastic exposure induced high heterogeneity and mortality in the first 3 days. • The growth was inhibited in the first 3 days, but stimulated after 5 days of exposure. • Nanoplastics increased membrane permeability and mitochondrial membrane potential. • Nanoplastics decreased light energy used for photochemical processes of microalgae. • Exposure to 200 and 2000 μg/L nanoplastics damaged cell and organelle morphology. [ABSTRACT FROM AUTHOR]

Intensive use of engineered nanoparticles (NPs) in daily products ineluctably results in their release into aquatic systems and consequently into drinking water resources. Therefore, understanding NPs behavior in various waters from naturel to mineral waters is crucial for risk assessment evaluation and the efficient removal of NPs during the drinking water treatment process. In this study, the impact of relevant physicochemical parameters, such as pH, water hardness, and presence of natural organic matter (NOM) on the surface charge properties and aggregation abilities of both NPs and nanoplastic particles is investigated. TiO2, CeO2, and Polystyrene (PS) nanoplastics are selected, owing to their large number applications and contrasting characteristics at environmental pH. Experiments are performed in different water samples, including, ultrapure water, three bottled mineral waters, Lake Geneva, and drinking water produced from Lake Geneva. Our findings demonstrate that both water hardness and negatively charged natural organic matter concentrations, which were measured via dissolved organic carbon determination, are playing important roles. At environmental pH, when negatively charged nanoparticles are considered, specific cation adsorption is promoting aggregation so long as NOM concentration is limited. On the other hand, NOM adsorption is expected to be a key process in NPs destabilization when positively charged PS nanoplastics are considered. [ABSTRACT FROM AUTHOR]