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Nanoplastic pollution has become one of the most pressing environmental issues, and its bioaccumulation in aquatic environment also causes a great difficulty in treatment. Therefore, this work investigated the microbial dynamics of mainstream anaerobic ammonia oxidizing (anammox) process to treat the wastewater containing typical nanoplastics, as well as the fate and regulation mechanism of polystyrene nanoparticles (PS-NPs) with different concentrations. The results showed that 0.1–0.5 mg L-1 of PS-NPs had no significant effect on the nitrogen removal efficiency (NRE). When the concentration of PS-NPs increased from 0.5 mg L-1 to 2 mg L-1, the NRE of R 1 with PS-NPs decreased from 94.9 ± 2.3 % to 77.0 ± 1.6 %, while the control reactor R 0 maintained a stable NRE. Notably, the relative abundance of Ca. Kuenenia decreased from 17.4 % to 14.8 %, and that of Ca. Brocadia slightly decreased from 5.9 % to 5.0 % in R 1. In addition, PS-NPs induced oxidative stress in anammox consortia, leading to the significant increase in reactive oxygen species (ROS) and lactate dehydrogenase (LDH) as well as cell membrane damage. PS-NPs also downregulated the content of heme c and further inhibited anammox activity. Based on the molecular docking simulation and western blotting, cold shock proteins (CSPs) could bind to PS-NPs and reduce the performance of anammox processes at low temperatures. [Display omitted] • High concentrations of PS-NPs affected the mainstream anammox performance. • PS-NPs induced oxidative stress, cell membrane damage and decreased heme c content. • PS-NPs inhibited anammox activity by regulating cold shock proteins. • PS-NPs reduced two anammox bacteria abundance, but increased Nitrospira abundance. • Mainstream anammox process had the potential to treat NPs-containing wastewater. [ABSTRACT FROM AUTHOR]

The impact of plastic pollution on living organisms have gained significant research attention. However, the effects of nanoplastics (NPs) on retina remain unclear. This study aimed to investigate the effect of long-term polystyrene nanoparticles (PS-NPs) exposure on mouse retina. Eight weeks old C57BL/6 J mice were exposed to PS-NPs at the diameter of 100 nm and concentration of 10 mg/L in drinking water for 3 months. PS-NPs were able to penetrate the blood-retina barrier, accumulated at retinal tissue, caused increased oxidative stress level and reduced scotopic electroretinal responses without remarkable structural damage. PS-NPs exposure caused cytotoxicity and reactive oxygen species accumulation in cultured photoreceptor cell. PS-NPs exposure increased oxidative stress level in retinal pigment epithelial (RPE) cells, leading to changes of gene and protein expression indicative of compromised phagocytic activity and cell junction formation. Long-term PS-NPs exposure also aggravated light-induced photoreceptor cell degeneration and retinal inflammation. The transcriptomic profile of PS-NPs-exposed, light-challenged retinal tissue shared similar features with those of age-related macular degeneration (AMD) patients in the activation of complement-mediated phagocytic and proinflammatory responses. Collectively, these findings demonstrated the oxidative stress- and inflammation-mediated detrimental effect of PS-NPs on retinal function, suggested that long-term PS-NPs exposure could be an environmental risk factor contributing to retinal degeneration. [Display omitted] • Long-term PS-NPs exposure causes retinal ROS accumulation and decreases electroretinal responses in mice. • PS-NPs exposure affects gene and protein expression of photoreceptor cells and retinal pigment epithelial cells. • Long-term PS-NPs exposure exacerbates the retinal degenerative effect of light challenge. • Chronic MPs/NPs exposure could be a detrimental environmental factor contributing to retinal degeneration. [ABSTRACT FROM AUTHOR]

The widespread use of plastics and the rapid development of nanotechnology bring convenience to our lives while also increasing the environmental burden and increasing the risk of exposure of organisms to nanoparticles (NPs). While recent studies have revealed an association between nanoparticles and liver injury, the intrinsic mechanism of NP exposure-induced liver damage remains to be explored. Here, we found that polystyrene nanoparticle (PSNP) exposure resulted in a significant increase in local neutrophil infiltration and neutrophil extracellular trap (NET) formation in the liver. Analysis of a coculture system of PBNs and AML12 cells revealed that PSNP-induced NET formation positively correlates with the reactive oxygen species (ROS)-NLRP3 axis. Inhibition of ROS and genetic and pharmacological inhibition of NLRP3 in AML12 can both alleviate PSNP-induced NET formation. In turn, exposure of mice to deoxyribonuclease I (DNase Ⅰ)-coated PSNPs disassembled NET in vivo , neutrophil infiltration in the liver was reduced, the ROS-NLRP3 axis was inhibited, and the expression of cytokines was markedly decreased. Collectively, our work reveals a mechanism of NET formation in PSNP exposure-induced liver inflammation and highlights the possible role of DNase Ⅰ as a key enzyme in degrading NET and alleviating liver inflammation. [Display omitted] • PS-NPs exposure aggravates LPS-induced liver inflammation in mice. • PS-NPs exposure-induced liver inflammation relies on NET formation. • NET formation induced by PS-NPs exposure is regulated by ROS-NLRP3 axis. • DNase Ⅰ-coated PS-NPs alleviates liver inflammation by blocking NETs. [ABSTRACT FROM AUTHOR]

Many studies have proved the impacts of nanoplastic pollution in freshwaters on aquatic organisms and ecosystems. To explore toxic mechanisms of nanoplastics on stream functioning, we conducted a microcosm experiment to investigate the effects of polystyrene nanoparticles (PS NPs, 1–100 μg L−1) on the process of leaf litter decomposition mediated by the microbial community. The chronic exposure to PS NPs at 1 and 100 μg L−1 caused significant decreases in leaf litter decomposition and nutrient (carbon and nitrogen) releases. During the ecological process, some extracellular enzymes (i.e., β-glucosidase, glycine-aminopeptidase, and phenol oxidase) rather than fungal biomass were suppressed. Besides, decreases in the relative abundance of Anguillospora and Setophaeosphaeria weakened their functions in leaf litter decomposition. Thus, the microcosm experiment showed that PS NPs inhibited stream leaf decomposition by modulating the microbial metabolic activity and fungal community structure. Overall, the results of this study provide evidence for the consequences of nanoplastic pollution on freshwater microbial community and stream ecosystem functioning, which is conducive to evaluate the potential risks of nanoplastics in aquatic environments. [Display omitted] • Nanoplastics at 1 and 100 μg L−1 slowed litter decomposition rate. • Nanoplastics enhanced fungal biomass but suppressed enzyme activities. • Fungal community structure was affected through decreasing hub genera percentage. • Fungal hyphae were damaged by nanoplastic pollution. • Inhibitions on litter decay were due to metabolic activity and fungal community. [ABSTRACT FROM AUTHOR]

Caenorhabditis elegans is a useful animal model to assess nanoplastic toxicity. Using polystyrene nanoparticles (PS-NPs) as the example of nanoplastics, we found that exposure to PS-NPs (1–100 μg/L) from L1-larvae for 6.5 days increased expression of cbp-1 encoding an acetyltransferase. The susceptibility to PS-NPs toxicity was observed in cbp-1(RNAi) worms, suggesting that CBP-1-mediated histone acetylation regulation reflects a protective response to PS-NPs. The functions of CBP-1 in intestine, neurons, and germline were required for formation of this protective response. In intestinal cells, CBP-1 controlled PS-NPs toxicity by modulating functions of insulin and p38 MAPK signaling pathways. In neuronal cells, CBP-1 controlled PS-NPs toxicity by affecting functions of DAF-7/TGF-β and JNK MAPK signaling pathways. In germline cells, CBP-1 controlled PS-NPs toxicity by suppressing NHL-2 activity, and NHL-2 further regulated PS-NPs toxicity by modulating insulin communication between germline and intestine. Therefore, our data suggested that the CBP-1-mediated histone acetylation regulation in certain tissues is associated with the induction of protective response to PS-NPs in C. elegans. [Display omitted] • Alteration in CBP-1, an acetyltransferase, mediated protective response to PS-NPs. • CBP-1-mediated signaling cascades in intestine, neuron, and germline were identified. • Germline-intestine communication of insulin was required for protective response. • Our data suggests association of acetylation regulation with protective response to PS-NPs. [ABSTRACT FROM AUTHOR]

• The biological effects of PSNPs depend on the leukocyte cell line used. • Phagocytic cellular function (shown by the THP-1 cell line) likely offer resistance to PSNPs treatment. • PSNPs can cause genotoxicity through different mechanisms of DNA damage. • Assessing toxicity of PSNPs in different cell lines is crucial to elaborate a relevant risk assessment In recent years the terms "micro-/nanoplastics" (MNPLs) have caught special attention due to the increasing levels by which humans are exposed. Among MNPLs, polystyrene nanoparticles (PSNPs) are one of the most represented MNPLs in the environment. These tiny particles may enter into the human body, translocate through human barriers, interacting with blood and lymphatic immune cells, and reaching secondary organs. By using three different human leukocytic cell lines: Raji-B (B-lymphocytes), TK6 (lymphoblasts) and THP-1 (monocytes), we pursued to determine the effects of these PSNPs on the immune cell population. With this aim, the three cell lines were exposed to spherical PSNPs of about 50 nm of diameter and cytotoxicity, cellular uptake, reactive oxygen species (ROS) production, and genotoxicity were assessed at different time-points. Results show differences in all the measured endpoints, among the selected cell lines. Thus, whilst the monocytic THP-1 cells showed the highest particle internalization, no adverse effects were observed in such cells. On the other side, although Raji-B and TK6 showed lesser PSNPs uptake, mild toxicity, ROS production and genotoxicity were detected. These results highlight the importance of the cell line selection when the biological effects of PSNPs are evaluated. [ABSTRACT FROM AUTHOR]