Nano Polystyrene Research Articles

Impacts of root exudates on the toxic response of Chrysanthemum coronarium L. to the co-pollution of nanoplastic particles and tetracycline

Nano polystyrene (PS) particles and antibiotics universally co-exist, posing a threat to crop plants and hence human health, nevertheless, there is limited research on their combined toxic effects along with major influential factors, especially root exudates, on crop plants. This study aimed to investigate the response of Chrysanthemum coronarium L. to the co-pollution of nanoplastics and tetracycline (TC), as well as the effect of root exudates on this response. Based on a hydroponic experiment, the biochemical and physiological indices of Chrysanthemum coronarium L. were measured after 7 days of exposure. Results revealed that the co-pollution of TC and PS caused significant oxidative damage to the plants, resulting in reduced biomass. Amongst the two contaminants, TC played a more prominent role. PS could enter the root tissue, and the uptake of TC and PS by plant roots was synergetic. Malic acid, oxalic acid, and formic acid could explain 65.1% of the variation in biochemical parameters and biomass of the roots. These compounds affected the photosynthesis and biomass of Chrysanthemum coronarium L. by gradually lowering root reactive oxygen species (ROS) and leaf ROS. In contrast, the impact of rhizobacteria on the toxic response of the plants was relatively minor. These findings suggested that root exudates could alleviate the toxic response of plants to the co-pollution of TC and PS. This study enhances our understanding of the role of root exudates, providing insights for agricultural management and ensuring food safety.

Nanopolystyrene and phoxim pollution: A threat to hepatopancreas toxicity in Chinese mitten crab (Eriocheir sinensis)

Significant concerns have been raised by the widespread pollutants phoxim (PHO) and nanopolystyrene (NP) in the natural environment. This study evaluated the toxicity effects on the hepatopancreas of Eriocheir sinensis caused by NP and/or PHO at concentrations found in the environment. Subchronic exposure to NP and/or PHO triggered hepatopancreas histological damage within a 21-day exposure period. The NP, PHO, and co-exposure (NPO) groups exhibited fewer blister-like (B) cells, along with the appearance of vacuolation. Furthermore, these exposures induced impairment in the hepatic tubule mucus barrier and mechanical barrier, as evidenced by altered expression of oxidative stress-related genes, mucin-related genes, and TJ-related genes. Additionally, alterations in immunity-related genes and inflammatory cytokine genes expression were observed. The findings showed that hepatopancreas inflammation was caused by both individual and combined exposure to NP and PHO and that the inflammatory response was exacerbated by the co-exposure. The possible pathways of hepatopancreas toxicity were further investigated by transcriptomic analysis. Hepatopancreas inflammation was brought on by subchronic exposure to PHO and co-exposure; this inflammation was exacerbated by co-exposure and was backed by the activation of NF-κB signaling pathway via targeting-related genes. In summary, this research represents the initial documentation, to the best of our understanding of the detrimental effects of exposured to NP and/or PHO at levels found in the environment disrupt the hepatopancreas mucus and mechanical barrier in crustaceans, triggering inflammatory responses. These findings highlight the significance of NP and/or PHO pollution for hepatopancreas health.

Sterile inflammation induced by respirable micro and nano polystyrene particles in the pathogenesis of pulmonary diseases.

Sterile inflammation is involved in the lung pathogenesis induced by respirable particles, including micro- and nanoplastics. Their increasing amounts in the ambient and in indoor air pose a risk to human health. In two human cell lines (A549 and THP-1) we assessed the proinflammatory behavior of polystyrene nanoplastics (nPS) and microplastics (mPS) (Ø 0.1 and 1μm). Reproducing environmental aging, in addition to virgin, the cells were exposed to oxidized nPS/mPS. To study the response of the monocytes to the inflammatory signal transmitted by the A549 through the release of soluble factors (e.g. alarmins and cytokines), THP-1 cells were also exposed to the supernatants of previously nPS/mPS-treated A549. After dynamic-light-scattering (DLS) analysis and protein measurements for the assessment of protein corona in nPS/mPS, real-time PCR and enzyme-linked-immunosorbent (ELISA) assays were performed in exposed cells. The pro-inflammatory effects of v- and ox-nPS/mPS were attested by the imbalance of the Bax/Bcl-2 ratio in A549, which was able to trigger the inflammatory cascade, inhibiting the immunologically silent apoptosis. The involvement of NFkB was confirmed by the overexpression of p65 after exposure to ox-nPS and v- and ox-mPS. The fast and higher levels of IL-1β, only in THP-1 cells, underlined the NLPR3 inflammasome activation.

Photoaged Nanopolystyrene Affects Neurotransmission to Induce Transgenerational Neurotoxicity in Caenorhabditis elegans.

Nanopolystyrene (NPS), a frequently employed nanoplastic, is an emerging environmental contaminant known to cause neurotoxicity in various organisms. However, the potential for transgenerational neurotoxic effects, especially from photoaged NPS (P-NPS), remains underexplored. This study investigated the aging of virgin NPS (V-NPS) under a xenon lamp to simulate natural sunlight exposure, which altered the physicochemical characteristics of the NPS. The parental generation (P0) of Caenorhabditis elegans was exposed to environmental concentrations (0.1-100 μg/L) of V-NPS and P-NPS, with subsequent offspring (F1-F4 generations) cultured under NPS-free conditions. Exposure to 100 μg/L P-NPS resulted in more pronounced deterioration in locomotion behavior in the P0 generation compared to V-NPS; this deterioration persisted into the F1-F2 generations but returned to normal in the F3-F4 generations. Additionally, maternal exposure to P-NPS damaged dopaminergic, glutamatergic, and serotonergic neurons in subsequent generations. Correspondingly, there was a significant decrease in the levels of dopamine, glutamate, and serotonin, associated with reduced expression of neurotransmission-related genes dat-1, eat-4, and tph-1 in the P0 and F1-F2 generations. Further analysis showed that the effects of P-NPS on locomotion behavior were absent in subsequent generations of eat-4(ad572), tph-1(mg280), and dat-1(ok157) mutants, highlighting the pivotal roles of these genes in mediating P-NPS-induced transgenerational neurotoxicity. These findings emphasize the crucial role of neurotransmission in the transgenerational effects of P-NPS on locomotion behavior, providing new insights into the environmental risks associated with exposure to photoaged nanoplastics.

The silent threat: Nanopolystyrene and chrysene pollutants disrupt the intestinal mucosal barrier, new insights from juvenile Siniperca chuatsi

The intestinal mucosal barrier—comprising microbial, mechanical, chemical, and immunological barriers—is critical to protection against pathogens and maintenance of host health; however, it remains unclear whether it is affected by environmental contaminants. Therefore, the present study assessed whether exposure to ambient concentrations of nanopolystyrene (NP) and chrysene (CHR)—two ubiquitous environmental pollutants in the aquatic environment—affect the intestinal mucosal barrier in juvenile Siniperca chuatsi. After exposure for 21 days, S. chuatsi exhibited intestinal oxidative stress and imbalance of intestinal microbial homeostasis. NP and/or CHR exposure also disrupted the intestinal mechanical barrier, as evidenced by the altered intestinal epithelial cell morphology, disrupted structure of intercellular tight junctions, and decreased expression of tight junction proteins. Damage to the intestinal chemical barrier manifested as thinning of the mucus layer owing to the loss and damage of goblet cells. Furthermore, the intestinal immunological barrier was impaired as indicated by the loss of intestinal intraepithelial lymphocytes and increase in pro-inflammatory cytokines, chemokines, and immunoglobulins. These findings collectively suggest that the intestinal mucosal barrier was damaged. This study is, to the best of our knowledge, the first to report that exposure to NP and/or CHR at environmentally relevant concentrations disrupts the intestinal mucosal barrier in organisms and highlight the significance of nanoplastic/CHR pollution for intestinal health.

Exposure to nanopolystyrene and phoxim at ambient concentrations causes oxidative stress and inflammation in the intestines of the Chinese mitten crab (Eriocheir sinensis)

Nanopolystyrene (NP) and phoxim (PHO) are common environmental pollutants in aquatic systems. We evaluated the toxic effects of exposure to ambient concentrations of NP and/or PHO in the intestines of the Chinese mitten crab (Eriocheir sinensis). Our study showed that histopathological changes were observed in the intestines. Specifically, NP and/or PHO exposure increased intraepithelial lymphocytes. Furthermore, NP and/or PHO exposure induced oxidative stress, as evidenced by a significant decrease in superoxide dismutase activity (SOD), peroxidase activity (POD), and total antioxidant capacity (T-AOC). Pro-inflammatory gene expression and transcriptome analysis demonstrated that NP and/or PHO exposure induced the intestinal inflammatory response. Transcriptome results showed that NP and/or PHO exposure upregulated the NF-κB signaling pathway, which is considered a key pathway in the inflammatory response. Additionally, the expression of pro-inflammatory genes significantly increased after a single exposure to NP or PHO, but it exhibited a significant decrease after the co-exposure. The downregulation of these genes in the co-exposure group likely suggested that the co-exposure mitigated intestinal inflammation response in E. sinensis. Collectively, our findings mainly showed that NP and/or PHO exposure at ambient concentrations induces oxidative stress and inflammatory response in the intestines of E. sinensis.

Nanoplastics and chrysene pollution: Potential new triggers for nonalcoholic fatty liver disease and hepatitis, insights from juvenile Siniperca chuatsi

Nanopolystyrene (NP) and chrysene (CHR) are ubiquitous contaminants in the natural environment; however, research on their hepatotoxicity and associated adverse effects remains relatively inadequate. The present study aimed to investigate the hepatotoxic effects of NP and/or CHR at environmentally relevant concentrations, as well as the underlying molecular mechanisms, in juvenile Siniperca chuatsi (mandarin fish). After a 21-day exposure period, the livers of exposed S. chuatsi exhibited macrostructural and microstructural damage accompanied by oxidative stress. Importantly, our study provides the first evidence that NP exposure leads to the development of nonalcoholic fatty liver disease (NAFLD) and hepatitis in S. chuatsi. Similarly, CHR exposure has also been found, for the first time, to cause hepatic sinusoidal dilatation (HSD) and hepatitis. Exposure to the combination of NP and CHR alleviated the symptoms of NAFLD, HSD, and hepatitis. Furthermore, our comprehensive multi-omic analysis revealed that the pathogenesis of NP-induced NAFLD was mainly due to induction of the triglyceride synthesis pathway and inhibition of the very-low-density lipoprotein secretion process. CHR induced HSD primarily through a reduction in vasoprotective ability and smooth muscle contractility. Hepatitis was induced by activation of the JAK-STAT/NF-kappa B signaling pathways, which upregulated the expression of inflammation-specific genes. Collectively, results of this study offer novel insight into the multiple hepatotoxicity endpoints of NP and/or CHR exposure at environmentally relevant concentrations in organisms, and highlight the importance of nanoplastic/CHR pollution for liver health.

Toxic effects of nanopolystyrene and cadmium on the intestinal tract of the Chinese mitten crab (Eriocheir sinensis)

Nanopolystyrene (NP) and cadmium (Cd) are ubiquitous contaminants in aquatic systems. The present study aimed to investigate the toxic effects of exposure to ambient concentrations of NP and/or Cd on the intestinal tract of the Chinese mitten crab (Eriocheir sinensis). Exposure to NP and/or Cd induced oxidative stress, as evidenced by a significant increase in lipid peroxide content (LPO), total antioxidant capacity (T-AOC), and peroxidase activity (POD), and significant decreases in superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) activities in E. sinensis. In addition, exposure to NP and/or Cd imbalanced the homeostasis of the intestinal microbiota, as demonstrated by the significantly increased abundance of Spiroplasma. Transcriptomic and metabolomic analyses were performed to investigate the mechanisms underlying intestinal toxicity. Our results showed that ferroptosis, ABC transporters, phosphotransferase system, apoptosis, and leukocyte transendothelial migration were disturbed after exposure to NP and/or Cd. In particular, Cd exposure affected mucin type O-glycan biosynthesis, purine metabolism, and neuroactive ligand-receptor interaction. Intriguingly, co-exposure to NP and Cd might mitigate intestinal toxicity by decreasing oxidative stress and affecting these pathways. Taken together, our study clearly demonstrates that exposure to NP and/or Cd at environmentally relevant concentrations causes intestinal toxicity in E. sinensis.

Histopathological, physiological, and multi-omics insights into the hepatotoxicity mechanism of nanopolystyrene and/or diclofenac in Mylopharyngodon piceus

Nanopolystyrene (NP) and diclofenac (DCF) are common environmental contaminants in the aquatic ecosystem; therefore, the present study aimed to investigate the hepatotoxicity of NP and/or DCF exposure on aquatic organisms and the underlying mechanisms. Juvenile Mylopharyngodon piceus were used as a model organism to study the effects of NP and/or DCF exposure at environmentally relevant concentrations for 21 days. Subchronic exposure to NP and/or DCF resulted in liver histological damage. In the NP group, the presence of large lipid droplets was observed, whereas the DCF group exhibited marked hepatic sinusoidal dilatation accompanied by inflammation. Additionally, this exposure induced liver oxidative stress, as evidenced by the changes in several physiological parameters, including catalase (CAT), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), total antioxidant capacity (T-AOC), reactive oxygen species (ROS), and malondialdehyde (MDA). Integrated transcriptomic and metabolomic analysis was performed to further investigate the molecular mechanism underlying hepatotoxicity. Multi-omics analysis demonstrated, for the first time to our knowledge, that NP induced hepatic steatosis mainly through activating the glycerol-3-phosphate pathway and inhibiting VLDL assembly by targeting several key enzyme genes including GPAT, DGAT, ACSL, APOB, and MTTP. Furthermore, NP exposure disrupted arachidonic acid metabolism, which induced the release of inflammatory factors and inhibited the release of anti-inflammatory factors, ultimately causing liver inflammation in M. piceus. In contrast, DCF induced interleukin production and downregulated KLF2, causing hepatic sinusoidal dilatation with inflammation in juvenile M. piceus, which is consistent with the finding of JAK–STAT signaling pathway activation. In addition, the upregulated AMPK signaling pathway in the DCF group suggested perturbation of energy metabolism. Collectively, these findings provide novel insights into the molecular mechanism of the multiple hepatotoxicity endpoints of NP and/or DCF exposure in aquatic organisms.

Nano polystyrene induced changes in anxiety and learning behaviour are mediated through oxidative stress and gene disturbance in mouse brain regions

It is widely reported now that nanoplastic particles have potential neurotoxic effects and may disturb central nervous system (CNS) function. However, the mechanism behind these toxic effects still needs to be elucidated. In the current study, we investigated the effects of polystyrene nanoplastics (PS-NPs) on changes in learning, memory, and anxiety-related behavior in mice based on some selected biochemical, molecular, and histopathological changes in three important brain regions (Cortex, Hypothalamus, and Hippocampus). Male mice were orally administered daily with two doses of 50 nm PS-NPs (0.2 mg/ml and 1 mg/ml) for 8 weeks. We observed decreased expression of neurotransmitter-related genes (VAChT, GAD, and SYP) in the cortex, hypothalamus, and hippocampus areas of the mouse brain. Other biochemical variables including, antioxidant enzymes, biomarkers for oxidative stress, and acetylcholinesterase activity showed significant alterations in all three brain regions. Molecular and neurochemical data thus suggest significant neurobehavioral changes following sub-chronic exposure to PS-NPs which may lead to enhanced anxiety-related and spatial learning and memory-related impairments by affecting limbic areas of the brain.

Environmentally persistent free radicals on photoaged nanopolystyrene induce neurotoxicity by affecting dopamine, glutamate, serotonin and GABA in Caenorhabditis elegans

Microplastics are widely detected in the environment and induce toxic effects in various organisms. However, the properties and toxicity associated with environmentally persistent free radicals (EPFRs) in photoaged nanopolystyrene (NPS) remain largely unknown. We investigated the generation of EPFRs on photoaged NPS and their neurotoxicity and underlying mechanism in Caenorhabditis elegans. The results suggested that photoaging induces the generation of EPFRs and reactive oxygen species (O2•−, •OH, and 1O2), which altered the physicochemical properties (morphology, crystallinity, and functional groups) of NPS. Acute exposure to 1 μg/L of NPS-60 (NPS with light irradiation time of 60 d) significantly decreased locomotion behaviors and neurotransmitter contents (e.g., glutamate, serotonin, dopamine, and γ-aminobutyric acid). Treatment with N-acetyl-L-cysteine (NAC) by radical quenching test significantly reduced EPFRs levels on the aged NPS, and the toxicity of NAC-quenching NPS was decreased in nematodes compared to those in photoaged NPS. EPFRs also caused dysfunction of neurotransmission-related gene expression in C. elegans. Thus, EPFRs generated on photoaged NPS contributed to neurotoxicity by affecting dopamine, glutamate, serotonin, and γ-aminobutyric acid neurotransmission. The study highlights the potential risks of photoaged NPS and the contributions of EPFRs to toxicity.

Translocation of 14C-polystyrene nanoplastics into fish during a very-low concentration dietary exposure

Assessing the dietary accumulation of nanoplastics in animals following very-low exposure concentrations is restricted due to analytical limitations. This study adapted a method for synthesising semi-stable 14C-PS NPs (through styrene polymerisation) in small volumes for deployment in environmental studies. The method was developed with non-labelled material where the final polystyrene product had a primary particle size of 35 ± 8 nm (as measured by transmission electron microscopy). This method was then applied to 14C-labelled styrene to produce radiolabelled polystyrene nanoplastics (14C-PS NPs). The 14C-PS NPs were added (top-dressed) to a commercially available fish feed, with a measured concentration of 27.9 ± 2.1 kBq kg−1 (n = 5), equating to 5.9 μg polystyrene kg−1 feed. Fish (rainbow trout; Oncorhynchus mykiss) were fed this diet at a ration of 2% body weight per day for a period of two weeks. On day 3, 7 and 14, the fish were sampled for the mid intestine, hind intestine, kidney and liver, and measured for tissue radioactivity (determined by liquid scintillation counting). Some background activity was detected in the control samples (e.g., 1–16 and 4–11 Bq g−1 in the hind intestine and liver, respectively) which is due to natural background fluorescence. By the end of the experiment, the hind intestine and liver had significantly elevated radioactivity (25.3 and 15.0 Bq g−1, respectively) compared to the control, indicating the accumulation of nano polystyrene. In the liver, this equated to 1.8 μg polystyrene g−1 dry weight. This study confirms the accumulation of nano particles in vertebrates at low, environmentally relevant concentration, and highlights radiolabelling as a methodological approach suitable for exploring the bioaccumulation of nanoplastics and potential impacts.

Impacts of exposure to nanopolystyrene and/or chrysene at ambient concentrations on neurotoxicity in Siniperca chuatsi

Health risks caused by widespread environmental pollutants such as nanopolystyrene (NP) and chrysene (CHR) in aquatic ecosystems have aroused considerable concern. The present study established juvenile Mandarin fish (Siniperca chuatsi) models of NP and/or CHR exposure at ambient concentrations for 21 days to systematically investigate the underlying neurotoxicity mechanisms. The results showed that single and combined exposure to NP and CHR not only reduced the density of small neuronal cells in the grey matter layer of the optic tectum, but also induced brain oxidative stress according to physiological parameters including CAT, GSH-Px, SOD, T-AOC, and MDA. The co-exposure alleviated the histopathological damage, compared to NP and CHR single exposure group. These results indicate that NP and/or CHR causes neurotoxicity in S. chuatsi, in accordance with decreased acetylcholinesterase activity and altered expression of several marker genes of nervous system functions and development including c-fos, shha, elavl3, and mbpa. Transcriptomics analysis was performed to further investigate the potential molecular mechanisms of neurotoxicity. We propose that single NP and co-exposure induced oxidative stress activates MMP, which degrades tight junction proteins according to decreased expression of claudin, JAM, caveolin and TJP, ultimately damaging the integrity of the blood-brain barrier in S. chuatsi. Remarkably, the co-exposure exacerbated the blood-brain barrier disruption. More importantly, single NP and co-exposure induced neuronal apoptosis mainly activates the expression of apoptosis-related genes through the death receptor apoptosis pathway, while CHR acted through both death receptor apoptosis and endoplasmic reticulum apoptosis pathways. Additionally, subchronic CHR exposure caused neuroinflammation, supported by activation of TNF/NF-κB and JAK-STAT signaling pathways via targeting-related genes, while the co-exposure greatly alleviated the neuroinflammation. Collectively, our findings illuminate the underlying neurotoxicity molecular mechanisms of NP and/or CHR exposure on aquatic organisms.

Modeling and Experiments of Droplet Evaporation with Micro or Nano Particles in Coffee Ring or Coffee Splat.

Experimental and numerical experiments were carried out to study the coffee rings or coffee splats formed by droplet evaporation with micro or nano polystyrene sphere particles (Dp = 10 μm or 100 nm). Particle image velocimetry (PIV) and a high-resolution camera were used in this experiment, along with a temperature-controlled heater and a data-acquisition computer. The results showed that a nano particle could form a homogeneous coffee splat, instead of the common coffee ring formed when using micro particles. In order to account for this phenomenon, this paper developed a complex multiphase model, one which included the smooth particle hydrodynamics (SPH) fluid model coupled with the van der Waals equation of state for droplet evaporation, the rigid particle model of finite-size micro particles, and the point-particle model of the nanometer particles. The numerical simulation was operated on a GPU-based algorithm and tested by four validation cases. A GPU could calculate 533 times the speed of a single-core CPU for about 300,000 particles. The results showed that, for rigid solid particles, the forms emerged spontaneously on the wall, and their structure was mainly affected by the boundary wettability, and less affected by the fluid flow and thermal condition. When the wall temperature was low, it was easier for the particles to be deposited on the contact line. At high wall temperature, the coffee ring effect would be weakened, and the particles were more likely to be deposited in the droplet center. The hydrophilic surface produced a larger coffee ring compared to the hydrophobic surface. The experimental and numerical results proved that particle size could play a significant role during the particle deposition, which may be a possible route for producing uniform-distributed and nano-structure coatings.

Nano polystyrene microplastics could accumulate in Nile tilapia (Oreochromis niloticus): Negatively impacts on the intestinal and liver health through water exposure

Microplastics (MPs) have become a significant concern for their potential toxicity. However, the correlation between the size of plastic particles and their toxicity remains inconclusive. Here, we investigate the toxic effects of different sizes (80 nm, 800 nm, 8 µm and 80 µm) polystyrene MPs (PS-MPs) on the model organism Nile tilapia (Oreochromis niloticus). The results of bioluminescent imaging indicate that the 80 nm PS-MPs are more likely to invade the body. H&E staining shows severe damage on the intestinal villi and distinct hepatic steatosis in the 80 nm group. EdU labeling shows that the proliferation activity of intestinal and liver cells reduces significantly in the 80 nm group. The gut microbiome analysis shows a severe imbalance of gut microbiota homeostasis in the 80 nm group. The analysis of liver transcriptomics and metabolomics shows that the liver lipid metabolism is disordered in the 80 nm group. In conclusion, this study confirms that the 80 nm PS-MPs are more likely to induce intestinal and liver toxicity. All the above lay the foundation for further study on the pathological damage of MPs to other organisms.

Endocrine disrupting effect and reproductive toxicity of the separate exposure and co-exposure of nano-polystyrene and diethylstilbestrol to zebrafish

The co-occurrence of nanoplastics and other pollutants in the environment has gotten a lot of attention, but information on the biological toxicity of their co-exposure was limited. This study aims to reveal the endocrine disrupting effect and reproductive toxicity of nano-polystyrene (NPS) and diethylstilbestrol (DES) to zebrafish under separate and combined exposure. Results indicated that NPS and DES exposure in isolation reduced the hepatosomatic index and gonadosomatic index, and altered the cell maturity in gonads in both cases. Even worse, the co-exposure of NPS and DES exacerbated the damage to the liver and gonads of fish. The two pollutants individually inhibited the secretion of sex hormones and vitellogenin. The inhibition effect of DES was especially dose-dependent, while NPS had weaker effect than DES. Their combined action on the secretion of sex hormones and vitellogenin exhibited additive effect. However, NPS did not affect the content of thyroid hormones in fish, and also had no significant effect on the reduction of thyroid hormone caused by DES exposure. Furthermore, their co-exposure decreased the cumulative eggs from 1031 to 306, and the spawning number from 12 to 8. The fertilization rate and hatchability rete of eggs were reduced by 30.9% and 40.4%, respectively. The abnormality rate of embryos was 65.0%, significantly higher than in separate DES and NPS groups (55.7% and 30.8% respectively). The abnormal development of offspring was mainly pericardial cyst, spinal curvature, and growth retardation.

Exposure to nanopolystyrene and its 4 chemically modified derivatives at predicted environmental concentrations causes differently regulatory mechanisms in nematode Caenorhabditis elegans

Nanoplastics represented by nanopolystyrene (NPS) and its chemically modified derivatives are environmentally ecotoxicological hotpots in recent years, but their toxicity and underlying mechanisms have not been fully identified. Here we employed Caenorhabditis elegans as an animal model to systematically compare the toxicity between nanopolystyrene and its 4 chemically modified derivatives (PS-PEG, PS-COOH, PS-SOOOH and PS-NH2) at predicted environmental concentrations. Our study demonstrated that compared with PS exposed group, PS-NH2 exposure (15 μg/L) caused a significant decline in lifespan by suppressed DAF-16/insulin signaling and shortened body length by inhibiting DBL-1/TGF β signaling. Different from PS-NH2 exposed group, PS-SOOOH exposure (15 μg/L) could not cause changes in lifespan, but shortened body length by inhibiting DBL-1/TGF β signaling. In addition, PS-COOH, PS-SOOOH or PS-NH2 exposure (1 μg/L or 15 μg/L) caused more serious toxicity in reducing locomotion behavior and causing gut barrier deficit. Hence the rank order in toxicity of PS-NH2＞PS-SOOOH＞PS-COOH＞PS＞PS-PEG was identified. Furthermore, we also presented evidence to support the contention that the observed toxic effects on nematodes were linked to oxide stress and activation of anti-oxidative molecules for reversing the adverse effects induced by nanopolystyrene and its 4 chemically modified derivatives. Our data highlighted nanoplastics may be charge-dependently toxic to environmental organisms, and the screened low toxic modification may support polystyrene nanoparticles continued application for daily consumer goods and biomedicine.

Nano Polystyrene of Different Sizes Causes Apoptosis by Inducing Mitochondrial Damage in Caco-2 Cells

Nano Polystyrene of Different Sizes Causes Apoptosis by Inducing Mitochondrial Damage in Caco-2 Cells

Dysregulated mir-76 mediated a protective response to nanopolystyrene by modulating heme homeostasis related molecular signaling in nematode Caenorhabditis elegans

The underlying mechanisms of microRNAs (miRNAs) in regulating nanoplastic toxicity are still largely unclear in organisms. In nanopolystyrene (NPS) exposed Caenorhabditis elegans, the expression of mir-76 (a neuronal miRNA) was significantly decreased, and the mir-76 mutant was resistant to the toxicity of NPS. The aim of this study was to determine the molecular basis of mir-76 in controlling NPS toxicity in nematodes. The mir-76 mutation increased expression of glb-10 encoding a globin protein in NPS (1 μg/L) exposed nematodes. Exposure to NPS (1–100 μg/L) increased the glb-10 expression, and the glb-10(RNAi) worm was susceptible to NPS toxicity in inducing reactive oxygen species (ROS) production and in decreasing locomotion behavior. Using ROS production and locomotion behavior as endpoints, mutation of glb-10 inhibited resistance of mir-76 mutant to NPS toxicity, and neuronal overexpression of mir-76 inhibited the resistance to NPS toxicity in nematodes overexpressing neuronal glb-10 containing 3’ untranslated region (3’UTR). Thus, GLB-10 functioned as a target of mir-76 in the neurons to regulate the NPS toxicity. Moreover, a signaling cascade of HRG-7-HRG-5 required for the control of heme homeostasis was identified to function downstream of neuronal GLB-10 to regulate the NPS toxicity. In this signaling cascade, the neuronal HRG-7 regulated the NPS toxicity by antagonizing function of intestinal HRG-5. Furthermore, in the intestine, HRG-5 controlled NPS toxicity by inhibiting functions of hypoxia-inducible transcriptional factor HIF-1 and transcriptional factor ELT-2. Our results highlight the crucial function of heme homeostasis related signaling in regulating the NPS toxicity in organisms.

Comparison of transgenerational reproductive toxicity induced by pristine and amino modified nanoplastics in Caenorhabditis elegans

Certain modifications can aggravate the toxicity of nanoplastics. However, the influence of surface amino modification on transgenerational impairment induced by nanoplastics remains largely unclear. Pristine nanopolystyrene (NPS) and amino modified NPS (NPS-NH2) were used to determine their transgenerational toxicity in Caenorhabditis elegans. Exposure to 100 μg/L pristine NPS in parents (P0) cause a decrease in reproductive capacity in the F1–F3 generations and the damage on gonad development in the F1–F2 generations. In contrast, exposure to 10 μg/L NPS-NH2 caused toxicity on reproductive capacity and gonad development in the F1 generation. The toxic effects of NPS-NH2 on reproductive capacity and gonad development in the F1–F3 generations were more severe than those of pristine NPS. Moreover, amino modification could increase transgenerational toxicity of NPS in inducing apoptosis of germline and in affecting expressions of ced-1, ced-4, and ced-9. Our data demonstrate that surface modification of NPS with amino groups enhances transgenerational reproductive toxicity of NPS in C. elegans.