Biodegradation of polystyrene nanoplastics by Achromobacter xylosoxidans M9 offers a mealworm gut-derived solution for plastic pollution.

Nanoplastics pose significant environmental problems due to their high mobility and increased toxicity. These particles can cause infertility and inflammation in aquatic organisms, disrupt microbial signaling and act as pollutants carrier. Despite extensive studies on their harmful impact on living organisms, the microbial degradation of nanoplastics is still under research. This study investigated the degradation of nanoplastics by isolating bacteria from the gut microbiome of Tenebrio molitor larvae fed various plastic diets. Five bacterial strains capable of degrading polystyrene were identified, with Achromobacter xylosoxidans M9 showing significant nanoplastic degradation abilities. Within 6 days, this strain reduced nanoplastic particle size by 92.3%, as confirmed by SEM and TEM analyses, and altered the chemical composition of the nanoplastics, indicating a potential for enhanced bioremediation strategies. The strain also caused a 7% weight loss in polystyrene film over 30 days, demonstrating its efficiency in degrading nanoplastics faster than polystyrene film. These findings might enhance plastic bioremediation strategies.

Comparison of PET tracing and biodistribution between 64Cu-labeled micro-and nano-polystyrene in a murine inhalation model.

INTRODUCTION: Recent studies showed the presence of microplastic in human lungs. There remains an unmet need to identify the biodistribution of microplastic after inhalation. In this study, we traced the biodistribution of inhaled micro-sized polystyrene (mPS) and/or nano-sized PS (nPS) using 64Cu with PET in mice. METHODS: We used 0.2-0.3-µm sized mPS and 20-nm sized nPS throughout. 64Cu-DOTA-mPS, 64Cu-DOTA-nPS and/or 64CuCl2 were used to trace the distribution in the murine inhalation model. PET images were acquired using an INVEON PET scanner at 1, 12, 24, 48, and 72 h after intratracheal instillation, and the SUVmax for interesting organs were determined, biodistribution was then determined in terms of percentage injected dose/gram of tissue (%ID/g). Ex vivo tissue-radio thin-layer chromatography (Ex vivo-radioTLC) was used to demonstrate the existence of 64Cu-DOTA-PS in tissue. RESULTS: PET image demonstrated that the amount of 64Cu-DOTA-mPS retained within the lung was significantly higher than 64Cu-DOTA-nPS until 72 h; SUVmax values of 64Cu-DOTA-mPS in lungs was 11.7 ± 5.0, 48.3 ± 6.2, 65.5 ± 2.3, 42.2 ± 13.1, and 13.2 ± 2.3 at 1, 12, 24, 48, and 72 h respectively whereas it was 31.2 ± 3.1, 17.3 ± 5.9, 10.0 ± 3.4, 8.1 ± 2.4 and 8.9 ± 3.6 for 64Cu-DOTA-nPS at the corresponding timepoints. The biodistribution data supported the PET data with a similar pattern of clearance of the radioactivity from the lung. nPS cleared rapidly post instillation in comparison to mPS within the lungs. Higher accumulation of %ID/g for nPS (roughly 2 times) were observed compared to mPS in spleen, liver, intestine, thymus, kidney, brain, salivary gland, ovary, and urinary bladder. Ex vivo-radioTLC was used to demonstrate that the detected gamma rays originated from 64Cu-DOTA-mPS or nPS. CONCLUSION: PET image demonstrated the differences in accumulations of mPS and/or nPS between lungs and other interesting organs. The information provided may be used as the basis for future studies on the toxicity of mPS and/or nPS.

Plastic Fly: What Drosophila melanogaster Can Tell Us about the Biological Effects and the Carcinogenic Potential of Nanopolystyrene.

Today, plastic pollution is one of the biggest threats to the environment and public health. In the tissues of exposed species, micro- and nano-fragments accumulate, leading to genotoxicity, altered metabolism, and decreased lifespan. A model to investigate the genotoxic and tumor-promoting potential of nanoplastics (NPs) is Drosophila melanogaster. Here we tested polystyrene, which is commonly used in food packaging, is not well recycled, and makes up at least 30% of landfills. In order to investigate the biological effects and carcinogenic potential of 100 µm polystyrene nanoparticles (PSNPs), we raised Oregon [R] wild-type flies on contaminated food. After prolonged exposure, fluorescent PSNPs accumulated in the gut and fat bodies. Furthermore, PSNP-fed flies showed considerable alterations in weight, developmental time, and lifespan, as well as a compromised ability to recover from starvation. Additionally, we noticed a decrease in motor activity in DNAlig4 mutants fed with PSNPs, which are known to be susceptible to dietary stressors. A qPCR molecular investigation of the larval intestines revealed a markedly elevated expression of the genes drice and p53, suggesting a response to cell damage. Lastly, we used warts-defective mutants to assess the carcinogenic potential of PSNPs and discovered that exposed flies had more aberrant masses than untreated ones. In summary, our findings support the notion that ingested nanopolystyrene triggers metabolic and genetic modifications in the exposed organisms, eventually delaying development and accelerating death and disease.

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

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

Induction of transgenerational toxicity is associated with the activated germline insulin signals in nematodes exposed to nanoplastic at predicted environmental concentrations.

Exposure to nanoplastics can induce toxicity on organisms at both parental generation (P0-G) and the offspring. However, the underlying mechanism remains unknown. Using Caenorhabditis elegans as a model organism, exposure to 20-nm polystyrene nanoparticle (PS-NP) (1-100 µg/L) upregulated the expressions of insulin ligands (INS-39, INS-3, and DAF-28), and this increase could be further detected in the offspring after PS-NP exposure. Germline ins-39, ins-3, and daf-28 RNAi induced resistance to transgenerational toxicity of PS-NP, indicating that increase in expression of these three insulin ligands mediated induction of transgenerational toxicity. These three insulin ligands transgenerationally activated function of insulin receptor DAF-2 to control transgenerational toxicity of PS-NP. Exposure to 1-100 µg/L PS-NP further upregulated DAF-2, AGE-1, and AKT-1 expressions and downregulated DAF-16 expression. During transgenerational toxicity control, DAF-16/AKT-1/AGE-1 was identified as downstream signaling cascade of DAF-2. Moreover, transcriptional factor DAF-16 activated two downstream targets of HSP-6 (a mitochondrial UPR marker) and SOD-3 (a mitochondrial SOD) to modulate transgenerational toxicity of PS-NP. Our findings indicate a crucial link between activation of insulin signaling and induction of transgenerational toxicity of nanoplastics at low concentrations in organisms.

Identification of ceRNA network to explain the mechanism of cognitive dysfunctions induced by PS NPs in mice.

Plastics breaking down of larger plastics into smaller ones (microplastics and nanoplastic) as potential threats to the ecosystem. Previous studies demonstrate that the central nervous system (CNS) is a vulnerable target of nanoplastics. However, the potentially epigenetic biomarkers of nanoplastic neurotoxicity in rodent models are still unknown. The present research aimed to determine the role of competing endogenous RNA (ceRNA) in the process of polystyrene nanoplastics (PS NPs) exposure-induced nerve injury. The study was designed to investigate whether 25 nm PS NPs could cause learning dysfunction and to elucidate the underlying mechanisms in mice. A total of 40 mice were divided into 4 groups and were exposed to PS NPs (0, 10, 25, 50 mg/kg). Chronic toxicity was introduced in mice by administration of oral gavage for 6 months. The evaluation included assessment of their behavior, pathological investigation and determination of the levels of reactive oxygen species (ROS) and DNA damage. RNA-Seq was performed to detect the expression levels of circRNAs, miRNAs and mRNAs in PFC samples of mice treated with 0 and 50 mg/kg PS NPs. The results indicated that exposure of mice to PS NPs caused a dose-dependent cognitive decline. ROS levels and DNA damage were increased in the PFC following exposure of the mice to PS NPs. A total of 987 mRNAs, 29 miRNAs and 67 circRNAs demonstrated significant differences between the 0 and 50 mg/kg PS NPs groups. Functional enrichment analyses indicated that PS NPs may induce major injury in the synaptic function. A total of 96 mRNAs, which were associated with synaptic dysfunction were identified. A competing endogenous RNA (ceRNA) network containing 27 circRNAs, 19 miRNAs and 35 synaptic dysfunction-related mRNAs was constructed. The present study provided insight into the molecular events associated with nanoplastic toxicity and induction of cognitive dysfunction.

Response of tyramine and glutamate related signals to nanoplastic exposure in Caenorhabditis elegans.

Neurotransmission related signals are involved in the control of response to toxicants. We here focused on the tyramine and the glutamate related signals to determine their roles in regulating nanoplastic toxicity in Caenorhabditis elegans. In the range of µg/L, exposure to nanopolystyrene (100 nm) increased the expression of tdc-1 encoding a tyrosine decarboxylase required for synthesis of tyramine, and decreased the expression of eat-4 encoding a glutamate transporter. Both TDC-1 and EAT-4 could act in the neurons to regulate the nanopolystyrene toxicity. Meanwhile, neuronal RNAi knockdown of tdc-1 induced a susceptibility to nanopolystyrene toxicity, and neuronal RNAi knockdown of eat-4 induced a resistance to nanopolystyrene toxicity. In the neurons, TYRA-2 functioned as the corresponding receptor of tyramine and acted upstream of MPK-1 signaling to regulate the nanopolystyrene toxicity. Moreover, during the control of nanopolystyrene toxicity, GLR-4 and GLR-8 were identified as the corresponding glutamate receptors, and acted upstream of JNK-1 signaling and DBL-1 signaling, respectively. Our results demonstrated the crucial roles of tyramine and glutamate related signals in regulating the toxicity of nanoplastics in organisms.

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.

Assessment of nanopolystyrene toxicity under fungal infection condition in Caenorhabditis elegans.

Due to the potential of release and accumulation in the environment, nanoplastics have attracted an increasing attention. In this study, we investigated the effect of exposure to nanopolystyrene (30 nm) in nematode Caenorhabditis elegans after the fungal infection. After Candida albicans infection, exposure to nanopolystyrene (10 and 100 µg/L) for 24-h could cause the more severe toxicity on lifespan and locomotion behavior compared with fungal infection alone. The more severe activation of oxidative stress and suppression of SOD-3:GFP expression and mitochondrial unfolded protein response (mt UPR) were associated with this observed toxicity enhancement induced by nanopolystyrene exposure. Moreover, the more severe C. albicans colony formation and suppression of innate immune response as indicated by the alteration in expression of anti-microbial genes (abf-2, cnc-4, cnc-7, and fipr-22/23) further contributed to the formation of this toxicity enhancement induced by nanopolystyrene exposure. Our results demonstrated that short-term exposure to nanopolystyrene in the range of µg/L potentially enhances the adverse effects of fungal infection on organisms.

Epigenetic response to nanopolystyrene in germline of nematode Caenorhabditis elegans.

microRNAs (miRNAs) provide an epigenetic regulation mechanism for the response to environmental toxicants. mir-38, a germline miRNA, was increased by exposure to nanopolystyrene (100 nm). In this study, we further found that germline overexpression of mir-38 decreased expressions of nhl-2 encoding a miRISC cofactor, ndk-1 encoding a homolog of NM23-H1, and wrt-3 encoding a homolog of PPIL-2. Meanwhile, germline-specific RNAi knockdown of nhl-2, ndk-1, or wrt-3 caused the resistance to nanopolystyrene toxicity. Additionally, mir-38 overexpression suppressed the resistance of nematodes overexpressing germline nhl-2, ndk-1, or wrt-3 containing 3'UTR, suggesting the role of NHL-2, NDK-1, and WRT-3 as the targets of germline mir-38 in regulating the response to nanopolystyrene. Moreover, during the control of response to nanopolystyrene, EKL-1, a Tudor domain protein, was identified as the downstream target of germline NHL-2, kinase suppressors of Ras (KSR-1 and KSR-2) were identified as the downstream targets of germline NDK-1, and ASP-2, a homolog of BACE1, was identified as the downstream target of germline WRT-3. Our results raised a mir-38-mediated molecular network in the germline in response to nanopolystyrene in nematodes. Our data provided an important basis for our understanding the response of germline of organisms to nanoplastic exposure.

Intestinal mir-794 responds to nanopolystyrene by linking insulin and p38 MAPK signaling pathways in nematode Caenorhabditis elegans.

Caenorhabditis elegans is sensitive to toxicity of environmental pollutants. The alteration in expression of mir-794, a microRNA (miRNA) molecule, mediated a protective response to nanopolystyene (100 nm) at predicted environmental concentration (1 µg/L) in nematodes. However, the underlying molecular basis for mir-794 function in regulating the response to nanopolystyrene remains largely unclear. In this study, we found that intestinal overexpression of mir-794 caused the susceptibility to nanopolystyrene toxicity, suggesting that mir-794 acted in the intestine to regulate the response to nanopolystyrene. Intestinal overexpression of mir-794 further decreased the expressions of daf-16 encoding a FOXO transcriptional factor in insulin signaling pathway, skn-1 encoding a Nrf transcriptional factor in p38 MAPK signaling pathway, and mdt-15 encoding a lipid metabolic sensor acting downstream of SKN-1 in nanopolystyrene exposed nematodes. Meanwhile, intestinal overexpression of mir-794 could suppress the resistance of nematodes overexpressing intestinal daf-16, skn-1, or mdt-15 containing the corresponding 3' untranslated region (3' UTR) to nanopolystyrene toxicity. Therefore, DAF-16, SKN-1, and MDT-15 acted as the downstream targets of intestinal mir-794 to regulate the response to nanopolystyrene. In the intestine, DAF-16 functioned synergistically with SKN-1 or MDT-15 to regulate the response to nanopolystyrene. Our results suggested that the intestinal mir-794 provided an important epigenetic regulation mechanism to control the response to nanopolystyrene by linking insulin and p38 MAPK signaling pathways in nematodes.

Nanopolystyrene at predicted environmental concentration enhances microcystin-LR toxicity by inducing intestinal damage in Caenorhabditis elegans.

We employed nematode Caenorhabditis elegans to determine the combinational effect between nanopolystyrene at predicted environmental concentration and microcystin-LR (MC-LR). Prolonged exposure to nanopolystyrene (1 µg/L) increased MC-LR (0.1 µg/L) toxicity in reducing brood size and locomotion behavior and in inducing oxidative stress. Moreover, the adsorption of MC-LR by nanopolystyrene particles played an important role in inducing the enhancement in MC-LR toxicity by nanopolystyrene particles. Additionally, only exposure to resuspension of nanopolystyrene (1 µg/L) caused the increased intestinal permeability in MC-LR (0.1 µg/L) exposed nematodes. Our data indicates the potential of nanopolystyrene at predicted environmental concentration in enhancing MC-LR toxicity on environmental organisms.

Combinational effect of titanium dioxide nanoparticles and nanopolystyrene particles at environmentally relevant concentrations on nematode Caenorhabditis elegans.

The possible adverse effects of nanoplastics have received the great attention recently; however, their effects at environmentally relevant concentration on organisms are still largely unclear. We here employed Caenorhabditis elegans to investigate the combinational effects of titanium dioxide nanoparticles (TiO2-NPs) and nanopolystyrene particles at environmentally relevant concentrations on organisms. In wild-type nematodes, prolonged exposure to nanopolystyrene particles (1 µg/L) could enhance the toxicity of TiO2-NPs (1 µg/L) in decreasing locomotion behavior and in inducing intestinal reactive oxygen species (ROS) production. Meanwhile, combinational exposure to TiO2-NPs (1 µg/L) and nanopolystyrene particles (1 µg/L) altered the molecular basis for oxidative stress in wild-type nematodes. Moreover, prolonged exposure to nanopolystyrene particles (0.1 µg/L) could further enhance the toxicity of TiO2-NPs (1 µg/L) in decreasing locomotion behavior and in inducing intestinal ROS production in sod-3 mutant nematodes. Our data suggest the potential role of nanopolystyrene particles at environmentally relevant concentrations in enhancing the toxicity of ENMs in the environment.

Nanopolystyrene size effect and its combined acute toxicity with halogenated PAHs on Daphnia magna.

Nanoplastics (NPs, diameter <1 µm) not only have toxicity but also change the toxicity of other pollutants in water. To date, the nanopolystyrene (nano-PS) size effect and its combined toxicity with halogenated polycyclic aromatic hydrocarbons (HPAHs) remain unclear. In this study, the single toxicity, combined toxicity, and mode of action of the binary mixture of polystyrene (PS) and HPAH were examined. At the same time, the nano-PS size effect on combined toxicity was also discussed. According to our results, the 48 h acute toxicity test results showed that 30 nm PS was highly toxic (EC50-48 h = 1.65 mg/L), 200 nm PS was moderately toxic (EC50-48 h = 17.8 mg/L), and 1 µm PS was lowly toxic (EC50-48 h = 189 mg/L). The NP toxicity decreased with increasing size. HPAHs were highly toxic substances to Daphnia magna (EC50-48 h = 0.12-0.22 mg/L). The mode of action of PS and HPAHs was antagonistic according to the toxicity unit method (TU), additive index method (AI), and mixture toxicity index method (MTI). The size effect of nano-PS operates via two mechanisms: the inherent toxicity of nano-PS and the sorption of pollutants by nano-PS. The former impacts the combined toxicity more than the latter. In the binary mixed system, the larger the particle size and the higher the proportion of NPs in the system, the less toxic the system was. Linear interpolation analysis can be used to predict the combined toxicity of a mixed system with any mixing ratio.

The photosynthetic toxicity of nano-polystyrene to Microcystis aeruginosa is influenced by surface modification and light intensity.

It is known that nanoplastics can cause membrane damage and production of reactive oxygen species (ROS) in cyanobacteria, negatively impacting their photosynthetic reactions and growth. However, the synergistic effect of light intensity on nanoplastics' toxicity to cyanobacteria is rarely investigated. Here, we investigated the impact of nano-polystyrene particles (PS) and amino-modified nano-polystyrene particles (PS-NH2) on cyanobacterium Microcystis aeruginosa cultivated under two light intensities. We discovered that PS-NH2 was more toxic to M. aeruginosa compared to PS with more damage of cell membranes by PS-NH2. The membrane damage was found by scanning electron microscope and atomic force microscopy. Under low light, PS-NH2 inhibited the photosynthesis of M. aeruginosa by decreasing the PSII quantum yield, photosynthetic electron transport rate and pigment content, but increasing non-photochemical quenching and Car/chl a ratio to cope with this stress condition. Moreover, high light appeared to increase the toxicity of PS-NH2 to M. aeruginosa by increasing its in vitro and intracellular ROS content. Specifically, on the one hand, high visible light (without UV) and PS-NH2 induced more in vitro singlet oxygen, hydroxyl radical and superoxide anion measured by electron paramagnetic resonance spectrometer in vitro, which could be another new toxic mechanism of PS-NH2 to M. aeruginosa. On the other hand, high light and PS-NH2 might increase intracellular ROS by inhibiting more photosynthetic electron transfer and accumulating more excess energy and electrons in M. aeruginosa. This research broadens our comprehension of the toxicity mechanisms of nanoplastics to cyanobacteria under varied light conditions and suggests a new toxic mechanism of nanoplastics involving in vitro ROS under visible light, providing vital information for assessing ecotoxicological effects of nanoplastics in the freshwater ecosystem.

Insights into the interaction mechanism of ofloxacin and functionalized nano-polystyrene.

Nano-plastics (NPs), an emerging contaminant in the environment, have a larger specific surface area and can act as a carrier of other contaminants. Thus, insights into the interaction mechanisms between NPs and other pollutants are crucial for the assessment of environmental impacts of NPs in the ecosystems. In this study, the interaction mechanism between NPs and ofloxacin (OFL) were investigated via kinetics, fluorescence quenching, and two-dimensional correlation spectroscopy (2DCOS). The adsorption kinetics of OFL on carboxyl-modified polystyrene (PS-COOH) and amine modified polystyrene (PS-NH2) closely fitted the pseudo-second-order kinetics model (R2 = 0.99). Adsorption kinetics indicated that chemical adsorption is dominant mechanism, and the Fourier Transform Infrared Spectrometer (FT-IR) and X-ray photoelectron spectroscopy (XPS) results showed that the electronic interaction, π-π, and H-binding were also involved in the adsorption process. OFL showed strong fluorescence quenching in the presence of NPs. Stern-Volmer quenching was negatively related with the temperature, which was dominated by the static type of quenching. 2DCOS indicated that the π-π conjugation was dominant in the interaction process, and the interaction process was dependent on the solution pH and salinity. Overall, this work provides new insights into the interaction mechanism of NPs and antibiotics in the aquatic ecosystems.

Comprehensive Analysis of lncRNA-mRNA Expression Profiles in Depression-like Responses of Mice Related to Polystyrene Nanoparticle Exposure.

Plastics in the environment can break down into nanoplastics (NPs), which pose a potential threat to public health. Studies have shown that the nervous system constitutes a significant target for nanoplastics. However, the potential mechanism behind nanoplastics' neurotoxicity remains unknown. This study aimed to investigate the role of lncRNA in the depressive-like responses induced by exposure to 25 nm polystyrene nanoplastics (PS NPs). Forty mice were divided into four groups administered doses of 0, 10, 25, and 50 mg/kg via gavage for 6 months. After conducting behavioral tests, RNA sequencing was used to detect changes in mRNAs, miRNAs, and lncRNAs in the prefrontal cortex of the mice in the 0 and 50 mg/kg PS NPs groups. The results revealed that mice exposed to chronic PS NPs developed depressive-like responses in a dose-dependent manner. It was demonstrated that 987 mRNAs, 29 miRNAs, and 116 lncRNAs were significantly different between the two groups. Then, a competing endogenous RNA (ceRNA) network containing 6 lncRNAs, 18 miRNAs, and 750 mRNAs was constructed. Enrichment results suggested that PS NPs may contribute to the onset of depression-like responses through the activation of axon guidance, neurotrophin-signaling pathways, and dopaminergic synapses. This study provided evidence of the molecular relationship between PS NPs and depression-like responses.

Enhanced toxicity of 2,2-bis(chloromethyl) trimethylene bis[bis(2-chloroethyl) phosphate] (V6) by nanopolystyrene particles towards HeLa cells.

2,2-bis(chloromethyl) trimethylene bis[bis(2-chloroethyl) phosphate] (V6) has been widely used as an additive in a variety of plastics due to its extremely low toxicity. However, we showed in the study that once mixed with nanopolystyrene particles (NPs), the nontoxic V6 could exhibit significant toxicity to HeLa cells. The enhanced toxicity was much higher than the toxicity of NPs alone and was related to the size of NPs. The mixture of V6 and small polystyrene NPs (10 nm and 15 nm in radius) showed obvious toxicity to HeLa cells. The toxicity increased with the concentrations of both V6 and NPs. On the contrary, the mixture of V6 and larger NPs (25 nm, 50 nm, 100 nm, and 500 nm in radius) showed almost no toxicity even at extremely high concentrations (NPs: 100 mg/L; V6: 50 mg/L). The small NPs could enter the cells and accumulated in cytoplasm. However, the larger NPs did not distribute inside the cells. NPs efficiently adsorbed V6 on the surface. The mechanism of the enhanced toxicity was attributed to the increased intracellular reactive oxygen species (ROS) production and the regulation of gene expression concerning apoptosis and ROS scavenging. Our study not only showed that a safe chemical V6 could be turned to be toxic by NPs, but also pointed out a potential risk caused by the joint toxicity of 'safe' chemicals and plastic particles with small size.

First approach to assess the effects of nanoplastics on the soil species Folsomia candida: A mixture design with bisphenol A and diphenhydramine.

The terrestrial environment is one of the main recipients of plastic waste. However, limited research has been performed on soil contamination by plastics and even less assessing the effects of nanoplastics (NPls). Behind the potential toxicity caused per se, NPls are recognized vectors of other environmental harmful contaminants. Therefore, the main aim of the present study is to understand whether the toxicity of an industrial chemical (bisphenol A - BPA) and a pharmaceutical (diphenhydramine - DPH) changes in the presence of polystyrene NPls to the terrestrial invertebrate Folsomia candida. Assessed endpoints encompassed organismal (reproduction, survival and behavior) and biochemical (neurotransmission and oxidative stress) levels. BPA or DPH, 28 d single exposures (1 to 2000 mg/kg), induce no effect on organisms' survival. In terms of reproduction, the calculated EC50 (concentration that causes 50% of the effect) and determined LOEC (lowest observed effect concentration) were higher than the environmental concentrations, showing that BPA or DPH single exposure may pose no threat to the terrestrial invertebrates. Survival and reproduction effects of BPA or DPH were independent on the presence of NPls. However, for avoidance behavior (48 h exposure), the effects of the tested mixtures (BPA + NPls and DPH + NPls) were dependent on the NPls concentration (at 0.015 mg/kg - interaction: no avoidance; at 600 mg/kg - no interaction: avoidance). Glutathione S-transferase activity increased after 28 d exposure to 100 mg/kg DPH + 0.015 mg/kg NPls (synergism). The increase of lipid peroxidation levels found after the exposure to 0.015 mg/kg NPls (a predicted environmental concentration) was not detected in the mixtures (antagonism). The results showed that the effects of the binary mixtures were dependent on the assessed endpoint and the tested concentrations. The findings of the present study show the ability of NPls to alter the effects of compounds with different natures and mechanisms of toxicity towards soil organisms, showing the importance of environmental risk assessment considering mixtures of contaminants.

High doses of nano-polystyrene aggravate the oxidative stress, DNA damage, and the cell death in onions.

Plastic pollution has been reported to negatively impact global biodiversity and ecosystem health. However, the molecular mechanisms of nano-plastics in plants are unidentified, especially their negative impacts on genomic stability. This study for the first time showed that nano-polystyrene leads to cell death in plants by subjugating the cellular antioxidant defence mechanisms through the aggravated production of ROS, which in turn could induce the DNA damage impairing the genetic regulation of the corresponding DNA repair pathway. To validate the proposed hypothesis, the DNA damage potential of nano-polystyrene and the expression levels of key genetic regulators of the DNA damage repair pathway (such as - CYCA/B, CDKA, SOG1, MYB transcription factors, and RAD51) have been assessed in onion roots after 72 h exposure with three ecologically relevant concentrations (25, 50, and 100 µg ml-1) of 100 nm nano-polystyrene. In addition, imbalance in redox homeostasis (oxidative stress), cell viability, and nuclear aberrations such as - the frequency of micronucleus and bi-nucleate cells that are directly linked to the DNA damages have been checked to point out the cause and effect of nano-polystyrene-induced DNA damage. Results showed a significant increase in oxidative stress in each treatment concentrations of nano-polystyrene. However, ROS generated at 100 µg ml-1 nano-polystyrene dose subdues the antioxidant defence system and induces cell death. These observations may be ascribed to the accumulation damaged DNA and the down-regulation of repair pathway-associated genes, as observed in this treatment group. Conversely, the observed DNA damage and the reduced expressions of genes would be a mere consequence of reduced cellular viability.