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Biodegradable polylactic acid (PLA) mulch has been developed to replace conventional polyethylene (PE) mulch in agriculture as a response to growing concerns about recalcitrant plastic pollution and the accumulation of microplastics (MPs) in soil. Cadmium is a significant soil pollutant in China. MPs have been shown to adsorb metals. In this study the earthworm Lumbricus terrestris was exposed to either Cd (1.0–100 mg / kg) or MPs (PE and PLA, 0.1–3 % w / w), or a combination of the two, for 28 days. Cd bioavailability significantly decreased in the presence of MPs. In particular, at the end of the experiment, PLA treatments had lower measured Cd concentrations in both earthworms (2.127–29.24 mg / kg) and pore water (below detection limits - 0.1384 mg /L) relative to PE treatments (2.720–33.77 mg / kg and below detection limits - 0.2489 mg / L). In our adsorption experiment PLA MPs adsorbed significantly more Cd than PE MPs with maximum adsorption capacities of 126.0 and 23.2 mg / kg respectively. These results suggest that the PLA MPs reduce earthworm exposure to Cd relative to PE by removing it from solution and reducing its bioavailability. [Display omitted] • Realistic levels of MP in soils did not impact earthworm mortality or weight change. • The presence of MPs decreased Cd concentrations in both earthworms and pore water. • PLA MPs decreased Cd accumulation in earthworms relative to PE MPs. • PLA MPs adsorbed significantly more Cd than PE MPs. [ABSTRACT FROM AUTHOR]

Since we rely entirely on plastics or their products in our daily lives, plastics are the invention of the hour. Polyester plastics, such as Polyethylene Terephthalate (PET), are among the most often used types of plastics. PET plastics have a high ratio of aromatic components, which makes them very resistant to microbial attack and highly persistent. As a result, massive amounts of plastic trash accumulate in the environment, where they eventually transform into microplastic (<5 mm). Rather than macroplastics, microplastics are starting to pose a serious hazard to the environment. It is imperative that these polymer microplastics be broken down. Through the use of enrichment culture, the PET microplastic-degrading bacterium was isolated from solid waste management yards. Bacterial strain was identified as Gordonia sp. CN2K by 16 S rDNA sequence analysis and biochemical characterization. It is able to use polyethylene terephthalate as its only energy and carbon source. In 45 days, 40.43 % of the PET microplastic was degraded. By using mass spectral analysis and HPLC to characterize the metabolites produced during PET breakdown, the degradation of PET is verified. The metabolites identified in the spent medium included dimer compound, bis (2-hydroxyethyl) terephthalate (BHET), mono (2-hydroxyethyl) terephthalate (MHET), and terephthalate. Furthermore, the PET sheet exposed to the culture showed considerable surface alterations in the scanning electron microscope images. This illustrates how new the current work is. [Display omitted] • Gordonia sp. CN2K, a PET degrading bacterium, which degrades 40.43% of PET in 45 days of incubation. • Degradation was affirmed by HPLC and mass spectral analysis of metabolites. • SEM images of the PET show drastic changes on the surface when compared to the control. • PCA-3,4-dioxygenase and Catechol-1,2-dioxygenase presence suggests strain CN2K mineralize PET solely for carbon and energy. • The strain CN2K is the first reported strain of this genus with the ability to degrade PET. [ABSTRACT FROM AUTHOR]

Microplastics (MPs) and okadaic acid (OA) are known to coexist in marine organisms, potentially impacting humans through food chain. However, the combined toxicity of OA and MPs remains unknown. In this study, mice were orally administered OA at 200 μg/kg bw and MPs at 2 mg/kg bw. The co-exposure group showed a significant increase in malondialdehyde (MDA) content and significant decreases in superoxide dismutase (SOD) activity and glutathione (GSH) level compared to the control, MPs and OA groups (p < 0.05). Additionally, the co-exposure group exhibited significantly higher levels of IL-1β and IL-18 compared to other groups (p < 0.05). These results demonstrated that co-exposure to MPs and OA induces oxidative stress and exacerbates inflammation. Histological and cellular ultrastructure analyses suggested that this combined exposure may enhance gut damage and compromise barrier integrity. Consequently, the concentration of OA in the small intestine of the co-exposure group was significantly higher than that in the OA group. Furthermore, MPs were observed in the lamina propria of the gut in the co-exposure group. Transcriptomic analysis revealed that the co-exposure led to increased expression of certain genes related to the NF-κB/NLRP3 pathway compared to the OA and MPs groups. Overall, this combined exposure may disrupt the intestinal barrier, and promote inflammation through the NF-κB/NLRP3 pathway. These findings provide precious information for the understanding of health risks associated with MPs and phycotoxins. [Display omitted] • Co-exposure to MPs and OA can induce oxidative stress and aggravate inflammation. • Co-exposure can enhance the accumulation of OA in the small intestine. • The MPs was observed in the lamina propria of the small intestine of co-exposed mice. • MPs and OA may induce acute intestinal toxicity in mice via NF-κB/NLRP3 pathway. [ABSTRACT FROM AUTHOR]

Microplastics (MPs), emerging as significant pollutants, have been consistently detected in aquatic environments, with the Yangtze River experiencing a particularly severe level of microplastic pollution, exceeding all other watersheds in China. Polypropylene (PP), the plastic most abundantly found in the middle and lower reaches of the Yangtze River Basin, has less comprehensive research results into its toxic effects. Consequently, the present investigation employed zebrafish as a model organism to delve into the toxicological impacts of polypropylene microplastics (PP-MPs) with a diameter of 5 μm across varying concentrations (300 mg/L and 600 mg/L). Using histopathological, microbiota profiling, and transcriptomic approaches, we systematically evaluated the impact of PP-MPs exposure on the intestine and liver of zebrafish. Histopathological analysis revealed that exposure to PP-MPs resulted in thinner intestinal walls, damaged intestinal mucosa, and hepatic cellular damage. Intestinal microbiota profiling demonstrated that, the richness, uniformity, diversity, and homogeneity of gut microbes significantly increased after the PP-MPs exposure at high concentration. These alterations were accompanied by shifts in the relative abundance of microbiota associated with intestinal pathologies, suggesting a profound impact on the intestinal microbial community structure. Concurrently, hepatic transcriptome analysis and RT-qPCR indicated that the downregulation of pathways and genes associated with cell proliferation regulation and DNA damage repair mechanisms contributed to hepatic cellular damage, ultimately exerting adverse effects on the liver. Correlation analysis between the intestinal microbiota and liver transcriptome profiles further highlighted significant associations between intestinal microbiota and the downregulated hepatic pathways. Collectively, these results provide novel insights into the subacute toxicological mechanisms of PP-MPs in aquatic organisms and highlight the need for further research on the ecological and health risks associated with PP-MPs pollution. • Polypropylene microplastic induced significant damage on gut and liver of zebrafish. • Polypropylene exposure led to Cetobacterium decrease and Rhizobiales increase in intestine. • Hepatic transcriptome analysis clarified molecular mechanisms of liver injury. • Correlated linkage between gut microbes and hepatic altered pathways was established. [ABSTRACT FROM AUTHOR]

Inhaling microplastics (MPs) and nanoplastics (NPs) in the air can damage lung function. Xenobiotics in the body can cause endoplasmic reticulum (ER) stress, and the unfolded protein response (UPR) activation alleviates ER stress. Degradation of unfolded or misfolded proteins is an important pathway for recovering cellular homeostasis. The UPR and protein degradation induced by MPs/NPs in lung tissues are not well understood. Here, we investigated the UPR and protein ubiquitination in the lungs of mice exposed to polystyrene (PS)-NPs and their possible molecular mechanisms leading to protein ubiquitination. Mice were intratracheally administered with 5.6, 17, and 51 mg/kg PS-NPs once for 24 h. Exposure to PS-NPs elevated protein ubiquitination in the lungs of mice in a dose-dependent manner. PS-NPs activated three branches of UPR including inositol-requiring protein 1α (IRE1α), eukaryotic translation initiator factor 2α (eIF2α), and activating transcription factor 6α (ATF6α) in the lungs of mice. However, activated IRE1α did not trigger X-box binding protein 1 (XBP1) mRNA splicing. Exposure to PS-NPs induced an increase in the levels of E3 ubiquitin ligase hydroxymethyl glutaryl-coenzyme A reductase degradation protein 1 (HRD1) and carboxy terminus of Hsc70 interacting protein (CHIP) in the lungs of mice and BEAS-2B cells. ATF6α siRNA inhibited the levels of HRD1 and CHIP proteins induced by PS-NPs in BEAS-2B cells. These results suggest that ATF6α plays a critical role in increasing ubiquitination of unfolded or misfolded proteins by alleviating PS-NPs induced ER stress through UPR to achieve ER homeostasis in the lungs of mice. [Display omitted] • Acute exposure to PS-NPs induces UPR in lungs of mice and BEAS-2B cells. • PS-NPs increase ubiquitination of proteins in lungs of mice and BEAS-2B cells. • ATF6α plays a key role in the ubiquitination of proteins induced by PS-NPs. [ABSTRACT FROM AUTHOR]

Polystyrene nanoplastics (PS-NPs), emerging and increasingly pervasive environmental contaminants, have the potential to cause persistent harm to organisms. Although previous reports have documented local accumulation and adverse effects in a variety of major organs after PS-NPs exposure, the impact of PS-NPs exposure on erectile function remains unexplored. Herein, we established a rat model of oral exposure to 100 nm PS-NPs for 28 days. To determine the best dose range of PS-NPs, we designed both low-dose and high-dose PS-NPs groups, which correspond to the minimum and maximum human intake doses, respectively. The findings indicated that PS-NPs could accumulate within the corpus cavernosum and high dose but not low dose of PS-NPs triggered erectile dysfunction. Moreover, the toxicological effects of PS-NPs on erectile function include fibrosis in the corpus cavernous, endothelial dysfunction, reduction in testosterone levels, elevated oxidative stress and apoptosis. Overall, this study revealed that PS-NPs exposure can cause erectile dysfunction via multiple ways, which provided new insights into the toxicity of PS-NPs. • Polystyrene nanoplastics (PS-NPs) can locally accumulate in corpus cavernosum. • PS-NPs exposure leads to erectile dysfunction via distinct mechanisms. • PS-NPs exposure causes fibrosis and impairs endothelial function in corpus cavernous. • PS-NPs exposure causes elevated oxidative stress and apoptosis in corpus cavernous. [ABSTRACT FROM AUTHOR]

There are various substances that can disrupt the homeostatic mechanisms of the body, defined as endocrine-disrupting chemicals (EDCs). The persistent nature of microplastics (MPs) is a cause for concern due to their ability to accumulate in food chains and widespread use, making their toxic effects particularly alarming. The potential of MPs for disrupting the endocrine system was observed in multiple tissues. Moreover, the adrenal gland is known to be extremely sensitive to EDCs, while with the effect of MPs on the adrenal gland has not previously been studied. This study aimed to highlight the potential polyethylene microplastics (PE-MPs) induced adreno-toxic effects rather than exploring the implicated mechanisms and concluding if melatonin (Mel) can afford protection against PE-MPs induced adreno-toxicity. To fulfill the goal, six groups of rats were used; control, Mel, PE-MPs (3.75 mg/kg), PE-MPs (15 mg/kg), PE-MPs (3.75 mg/kg) +Mel, and PE-MPs (15 mg/kg) +Mel. PE-MPs induced toxic changes in the adrenal cortex, which was evident by increased adrenal weight, histopathological examination, and ultrastructural changes detected by electron microscope. A reduction in serum cortisol and an increase in serum adrenocorticotropic hormone resulted from the adreno-toxic effects of PE-MPs. Mechanisms may include the reduction of steroidogenesis-related genes, as PE-MPs drastically reduce mRNA levels of StAR, Nr0b1, Cyp11A1, as well as Cyp11B1. Also, oxidative stress that results from PE-MPs is associated with higher rates of lipid peroxidation and decreased superoxide dismutase and glutathione. PE-MPs inflammatory effect was illustrated by elevated expression of IL-1β and NF-ķB, detected by immunohistochemical staining, in addition to increased expression of caspase-3 and mRNA of Bax, markers of proapoptotic activity. The impacts of PE-MPs were relatively dose-related, with the higher dose showing more significant toxicity than the lower one. Mel treatment was associated with a substantial amelioration of PE-MPs-induced toxic changes. Collectively, this study fills the knowledge gap about the MPs-induced adrenal cortex and elucidates various related toxic mechanisms. It also supports Mel's potential protective activity through antioxidant, anti-inflammatory, anti-apoptotic, and gene transcription regulatory effects. [Display omitted] • The first study reports polyethylene microplastics-induced adrenal toxicity in rats. • A reduction in serum cortisol and an increase in serum ACTH resulted from adreno-toxic effects of (PE)-MPs. • PE-MPs inflammatory effect was illustrated by elevated expression of IL-1β and NF-ķB. • Melatonin treatment was associated with a substantial amelioration of PE-MPs-induced toxic changes. [ABSTRACT FROM AUTHOR]

Pregnant women are a special group that is sensitive to adverse external stimuli, causing metabolic abnormalities and adverse pregnancy outcomes. Microplastics (MPs), an environmental pollutant widely used in various fields, can induce a variety of toxic responses in mammals. Recent studies verified an association between MPs and metabolic disorders. Our research built a gestational mouse model in which polystyrene microplastics (PS-MPs) of 1 μm size were consumed at concentrations of 0.1, 1, and 10 mg/L during pregnancy. Results indicated that PS-MPs induced placental malfunction and fetal growth retardation. Significant glucose disorders, decreased liver function, hepatic inflammation, and oxidative stress were also observed after PS-MPs exposure. The hepatic SIRT1/IRS1/PI3K pathway was inhibited in the 10 mg/L PS-MPs exposure group. Our study found that PS-MPs activated inflammatory response and oxidative stress by increasing hepatic lipopolysaccharide (LPS) that inhibited the hepatic SIRT1/IRS1/PI3K pathway, ultimately leading to insulin resistance, glucose metabolism disorders, and adverse pregnancy outcomes. This study provides a basis for preventing environment-related gestational diabetes and concomitant adverse pregnancy outcomes. [Display omitted] • PS-MPs have been verified to disrupt hepatic glucose metabolism during gestation. • PS-MPs caused IR by inducing hepatic inflammatory response and OS during gestation. • PS-MPs destroyed the structure of the placenta, causing FGR and intrauterine death. • SIRT1 inhibited by PS-MPs plays a role in glycometabolism and embryo implantation. [ABSTRACT FROM AUTHOR]

Polystyrene nanoplastics (PS-NPs) have been reported to accumulate in the testes and constitute a new threat to reproductive health. However, the exact effects of PS-NPs exposure on testicular cells and the underlying mechanisms remain largely unknown. The C57BL/6 male mice were orally administered with PS-NPs (80 nm) at different dosages (0, 10, and 40 mg/kg/day) for 60 days, and GC-1 cells were treated with PS-NPs in this study. Enlarged seminiferous tubule lumens and a loose and vacuolated layer of spermatogenic cells were observed in PS-NPs-exposed mice. Spermatogenic cells which may be one of the target cells for this reproductive damage, were decreased in the mice from PS-NPs group. PS-NPs caused spermatogenic cells to undergo senescence, manifested as elevated SA-β-galactosidase activity and activated senescence-related signaling p53-p21/Rb-p16 pathways, and induced cell cycle arrest. Mechanistically, Gene Ontology (GO) enrichment suggested the key role of reactive oxygen species (ROS) in PS-NPs-induced spermatogenic cell senescence, and this result was confirmed by measuring ROS levels. Moreover, ROS inhibition partially attenuated the senescence phenotype of spermatogenic cells and DNA damage. Using the male health atlas (MHA) database, Sirt1 was filtrated as the critical molecule in the regulation of testicular senescence. PS-NPs induced overexpression of the main ROS generator Nox2, downregulated Sirt1, increased p53 and acetylated p53 in vivo and in vitro, whereas these disturbances were partially restored by pterostilbene. In addition, pterostilbene intervention significantly alleviated the PS-NPs-induced spermatogenic cell senescence and attenuated ROS burst. Collectively, our study reveals that PS-NPs exposure can trigger spermatogenic cell senescence mediated by p53-p21/Rb-p16 signaling by regulating the Sirt1/ROS axis. Importantly, pterostilbene intervention may be a promising strategy to alleviate this damage. • Nanoplastics induced reproductive damage in male mice. • Nanoplastics triggered spermatogenic cell senescence. • Sirt1/ROS axis was involved in the nanoplastic induced spermatogenic cell senescence. • Pterostilbene intervention may be a promising strategy to alleviate nanoplastic damage. [ABSTRACT FROM AUTHOR]

Microplastics (MPs) pose a clear threat to aquatic organisms affecting their health. Their impact on liver homeostasis, as well as on the potential onset of nonalcoholic fatty liver disease (NAFLD), is still poorly investigated and remains almost unknown. The aim of this study was to evaluate the outcomes of subchronic exposure to polystyrene MPs (PS-MPs; 1–20 μm; 0, 25, or 250 mg/kg b.w./day) on lipid metabolism, inflammation, and oxidative balance in the liver of gilthead seabreams (Sparus aurata Linnaeus, 1758) exposed for 21 days via contaminated food. PS-MPs induced an up-regulation of mRNA levels of crucial genes associated with lipid synthesis and storage (i.e., PPARy, Srebp1, Fasn) without modifications of genes involved in lipid catabolism (i.e., PPARα , HL, Pla2) or transport and metabolism (Fabp1) in the liver. The increase of CSF1R and pro-inflammatory cytokines gene expression (i.e., TNF-α and IL-1β) was also observed in exposed fish in a dose-dependent manner. These findings were confirmed by hepatic histological evaluations reporting evidence of lipid accumulation, inflammation, and necrosis. Moreover, PS-MPs caused the impairment of the hepatic antioxidant defense system through the alteration of its enzymatic (catalase, superoxide dismutase, and glutathione reductase) and non-enzymatic (glutathione) components, resulting in the increased production of reactive oxygen species (ROS) and malondialdehyde (MDA), as biomarkers of oxidative damage. The alteration of detoxifying enzymes was inferred by the decreased Ethoxyresorufin-O-deethylase (EROD) activity and the increased activity of glutathione-S-transferase (GST) at the highest PS-MP dose. The study suggests that PS-MPs affect the liver health of gilthead seabream. The liver dysfunction and damage caused by exposure to PS-MPs result from a detrimental interplay of inflammation, oxidative damage, and antioxidant and detoxifying enzymatic systems modifications, altering the gut-liver axis homeostasis. This scenario is suggestive of the involvement of MP-induced effects in the onset and progression of hepatic lipid dysfunction in gilthead seabream. [Display omitted] • Subchronic exposure to PS-MPs affected liver health in gilthead seabreams. • PS-MPs increased lipid synthesis and accumulation in the liver. • PS-MPs caused inflammation and oxidative stress in the liver. • PS-MPs contributes to the onset and progression of hepatic metabolic dysfunctions. [ABSTRACT FROM AUTHOR]

Nanoplastic contamination has been of intense concern by virtue of the potential threat to human and ecosystem health. Animal experiments have indicated that exposure to nanoplastics (NPs) can deposit in the liver and contribute to hepatic injury. To explore the mechanisms of hepatotoxicity induced by polystyrene-NPs (PS-NPs), mice and AML-12 hepatocytes were exposed to different dosages of 20 nm PS-NPs in this study. The results illustrated that in vitro and in vivo exposure to PS-NPs triggered excessive production of reactive oxygen species and repressed nuclear factor erythroid-derived 2-like 2 (NRF2) antioxidant pathway and its downstream antioxidase expression, thus leading to hepatic oxidative stress. Moreover, PS-NPs elevated the levels of NLRP3, IL-1β and caspase-1 expression, along with an activation of NF-κB, suggesting that PS-NPs induced hepatocellular inflammatory injury. Nevertheless, the activaton of NRF2 signaling by tert-butylhydroquinone mitigated PS-NPs-caused oxidative stress and inflammation, and inbihited NLRP3 and caspase-1 expression. Conversely, the rescuing effect of NRF2 signal activation was dramatically supressed by treatment with NRF2 inhibitor brusatol. In summary, our results demonstrated that NRF2-NLRP3 pathway is involved in PS-NPs-aroused hepatotoxicity, and the activation of NRF2 signaling can protect against PS-NPs-evoked liver injury. These results provide novel insights into the hepatotoxicity elicited by NPs exposure. [Display omitted] • PS-NPs exposure resulted in hepatic inflammatory injury. • PS-NPs treatment suppressed NRF2-dependent antioxidant pathway in the liver. • PS-NPs could enter into AML-12 cells and impose hepatotoxicity. • Activation of NRF2 signaling relieved PS-NPs-induced oxidative stress and inflammation. [ABSTRACT FROM AUTHOR]

Microplastics (MPs) and benzo[ a ]pyrene (B[ a ]P) are prevalent environmental pollutants. Numerous studies have extensively reported their individual adverse effects on organisms. However, the combined effects and mechanisms of exposure in mammals remain unknown. Thus, this study aims to investigate the potential effects of oral administration of 0.5μm polystyrene (PS) MPs (1 mg/mL or 5 mg/mL), B[ a ]P (1 mg/mL or 5 mg/mL) and combined (1 mg/mL or 5 mg/mL) on 64 male SD rats by gavage method over 6-weeks. The results demonstrate that the liver histopathological examination showed that the liver lobules in the combined (5 mg/kg) group had blurred and loose boundaries, liver cord morphological disorders, and significant steatosis. The levels of AST, ALT, TC, and TG in the combined dose groups were significantly higher than those in the other groups, the combined (5 mg/kg) group had the lowest levels of antioxidant enzymes and the highest levels of oxidants. The expression of Nrf2 was lowest and the expression of P38, NF-κB, and TNF-α was highest in the combined (5 mg/kg) group. In conclusion, these findings indicate that the combination of PSMPs and B[ a ]P can cause the highest levels of oxidative stress and elicit markedly enhanced toxic effects, which cause severe liver damage. [Display omitted] • Combined exposure to PSMPs and B[ a ]P enhances liver damage. • Combined exposure to PSMPs and B[ a ]P induces oxidative stress in the liver. • Combined exposure to PSMPs and B[ a ]P increases the expression of oxidative stress proteins. • Combined exposure to PSMPs and B[ a ]P leads to abnormal liver metabolism. • The P38 signaling pathway is the major pathway in liver injury. [ABSTRACT FROM AUTHOR]

Polystyrene microplastics (PS-MPs) are new types of environmental pollutant that have garnered significant attention in recent years since they were found to cause damage to the human respiratory system when they are inhaled. The pulmonary fibrosis is one of the serious consequences of PS-MPs inhalation. However, the impact and underlying mechanisms of PS-MPs on pulmonary fibrosis are not clear. In this study, we studied the potential lung toxicity and PS-MPs-developed pulmonary fibrosis by long-term intranasal inhalation of PS-MPs. The results showed that after exposing to the PS-MPs, the lungs of model mouse had different levels of damage and fibrosis. Meanwhile, exposing to the PS-MPs resulted in a markedly decrease in glutathione (GSH), an increase in malondialdehyde (MDA), and iron overload in the lung tissue of mice and alveolar epithelial cells (AECs). These findings suggested the occurrence of PS-MP-induced ferroptosis. Inhibitor of ferroptosis (Fer-1) had alleviated the PS-MPs-induced ferroptosis. Mechanically, PS-MPs triggered cell ferroptosis and promoted the development of pulmonary fibrosis via activating the cGAS/STING signaling pathway. Inhibition of cGAS/STING with G150/H151 attenuated pulmonary fibrosis after PS-MPs exposure. Together, these data provided novel mechanistic insights of PS-MPs-induced pulmonary fibrosis and a potential therapeutic paradigm. [Display omitted] • Polystyrene microplastics (PS-MPs) exposure caused pulmonary fibrosis through triggering ferroptosis. • Inhibition of ferroptosis with Fer-1 attenuated PS-MPs induced pulmonary fibrosis. • PS-MPs induced alveolar epithelial cell ferroptosis through activating cGAS/STING signaling pathway. • cGAS/STING and ferroptosis might be potential therapeutic targets for intervening pulmonary fibrosis induced by PS-MPs. [ABSTRACT FROM AUTHOR]

Microplastics, plastic particles 5 mm or less in size, are abundant in the environment; hence, the exposure of humans to microplastics is a great concern. Usually, the surface of microplastics found in the environment has undergone degradation by external factors such as ultraviolet rays and water waves. One of the characteristics of changes caused by surface degradation of microplastics is the introduction of oxygen-containing functional groups. Surface degradation alters the physicochemical properties of plastics, suggesting that the biological effects of environmentally degraded plastics may differ from those of pure plastics. However, the biological effects of plastics introduced with oxygen-containing functional groups through degradation are poorly elucidated owing to the lack of a plastic sample that imitates the degradation state of plastics found in the environment. In this study, we investigated the degradation state of microplastics collected from a beach. Next, we degraded a commercially available polyethylene (PE) particles via vacuum ultraviolet (VUV) irradiation and showed that chemical surface state of PE imitates that of microplastics in the environment. We evaluated the cytotoxic effects of degraded PE samples on immune and epithelial cell lines. We found that VUV irradiation was effective in degrading PE within a short period, and concentration-dependent cytotoxicity was induced by degraded PE in all cell lines. Our results indicate that the cytotoxic effect of PE on different cell types depends on the degree of microplastic degradation, which contributes to our understanding of the effects of PE microplastics on humans. [Display omitted] • Surface of microplastics in the environment was chemically degraded. • Vacuum ultraviolet irradiation was performed to chemically degrade polyethylene (PE). • Experimentally degraded PE product imitated the environmentally degraded PE. • Degraded PE microplastics induced cytotoxicity to immune and epithelial cells. [ABSTRACT FROM AUTHOR]

Microplastics (MPs), which are prevalent and increasingly accumulating in aquatic environments. Other pollutants coexist with MPs in the water, such as pesticides, and may be carried or transferred to aquatic organisms, posing unpredictable ecological risks. This study sought to assess the adsorption of lambda-cyhalothrin (LCT) by virgin and aged polyethylene MPs (VPE and APE, respectively), and to examine their influence on LCT's toxicity in zebrafish, specifically regarding acute toxicity, oxidative stress, gut microbiota and immunity. The adsorption results showed that VPE and APE could adsorb LCT, with adsorption capacities of 34.4 mg∙g−1 and 39.0 mg∙g−1, respectively. Compared with LCT exposure alone, VPE and APE increased the acute toxicity of LCT to zebrafish. Additionally, exposure to LCT and PE-MPs alone can induce oxidative stress in the zebrafish gut, while combined exposure can exacerbate the oxidative stress response and intensify intestinal lipid peroxidation. Moreover, exposure to LCT or PE-MPs alone promotes inflammation, and combined exposure leads to downregulation of the myd88-nf-κb related gene expression, thus impacting intestinal immunity. Furthermore, exposure to APE increased LCT toxicity to zebrafish more than VPE. Meanwhile, exposure to PE-MPs and LCT alone or in combination has the potential to affect gut microbiota function and alter the abundance and diversity of the zebrafish gut flora. Collectively, the presence of PE-MPs may affect the toxicity of pesticides in zebrafish. The findings emphasize the importance of studying the interaction between MPs and pesticides in the aquatic environment. • Microplastics adsorb Lambda-cyhalothrin and become the carrier of Lambda-cyhalothrin. • Microplastics enhanced the acute toxicity of Lambda-cyhalothrin to zebrafish. • Combined exposure inhibited oxidative stress and exacerbates lipid peroxidation. • Single and combined exposures led to changes in intestinal flora richness as well as diversity. • Combined exposure produced immunotoxicity. [ABSTRACT FROM AUTHOR]

Endogenous immune defenses provide an intrinsic barrier against external entity invasion. Microplastics in the environment, especially those at the nanoscale (nanoplastics or NPs), may pose latent health risks through direct exposure. While links between nanoplastics and inflammatory processes have been established, detailed insights into how they may perturb the innate immune mechanisms remain uncharted. Employing murine and macrophage (RAW264.7) cellular models subjected to polystyrene nanoplastics (PS-NPs), our investigative approach encompassed an array of techniques: Cell Counting Kit-8 assays, flow cytometric analysis, acridine orange/ethidium bromide (AO/EB) fluorescence staining, cell transfection, cell cycle scrutiny, genetic manipulation, messenger RNA expression profiling via quantitative real-time PCR, and protein expression evaluation through western blotting. The results showed that PS-NPs caused RAW264.7 cell apoptosis, leading to cell cycle arrest, and activated the cGAS-STING pathway. This resulted in NF-κB signaling activation and increased pro-inflammatory mediator expression. Importantly, PS-NPs-induced activation of NF-κB and its downstream inflammatory cascade were markedly diminished after the silencing of the STING gene. Our findings highlight the critical role of the cGAS-STING pathway in the immunotoxic effects induced by PS-NPs. We outline a new mechanism whereby nanoplastics may trigger dysregulated innate immune and inflammatory responses via the cGAS/STING pathway. • PS-NPs can activate innate immunity. • 2.PS-NPs can induce inflammatory response through cGAS-STING pathway. • After macrophages knocked down the STING gene, the inflammatory response induced by PS-NPs was inhibited. [ABSTRACT FROM AUTHOR]

Analysis of microplastics in the environment requires polymer characterization as a confirmation step for suspected microplastic particles found in a sample. Material characterization is costly and can take a long time per particle. When microplastic particle counts are high, many researchers cannot characterize every particle in their sample due to time or monetary constraints. Moreover, characterizing every particle in samples with high plastic particle counts is unnecessary for describing the sample properties. We propose an a priori approach to determine the number of suspected microplastic particles in a sample that should be randomly subsampled for characterization to accurately assess the polymer distribution in the environmental sample. The proposed equation is well-founded in statistics literature and was validated using published microplastic data and simulations for typical microplastic subsampling routines. We report values from the whole equation but also derive a simple way to calculate the necessary particle count for samples or subsamples by taking the error to the power of negative two. Assuming an error of 0.05 (5 %) with a confidence interval of 95 %, an unknown expected proportion, and a sample with many particles (> 100k), the minimum number of particles in a subsample should be 386 particles to accurately characterize the polymer distribution of the sample, given the particles are randomly characterized from the full population of suspected particles. Extending this equation to simultaneously estimate polymer, color, size, and morphology distributions reveals more particles (620) would be needed in the subsample to achieve the same high absolute error threshold for all properties. The above proposal for minimum subsample size also applies to the minimum count that should be present in samples to accurately characterize particle type presence and diversity in a given environmental compartment. [Display omitted] • A priori assessment of required microplastic counts in samples should be conducted. • No fewer than 96 microplastic particles should be in a (sub)sample. • No more than 620 microplastic particles are typically needed in a (sub)sample. • The exact value needed can be fine tuned with equations we describe. [ABSTRACT FROM AUTHOR]

Many laboratory studies demonstrated that the exposure to microplastics causes testosterone deficiency and spermatogenic impairment in mammals; however, the mechanism underlying this process remains still unclear. In this study, we investigated the effects of polystyrene microplastics (PS-MP) on the proliferation and functionality of cultured Leydig (TM3) and Sertoli (TM4) cells, focusing on the mitochondrial compartment and its association with the endoplasmic reticulum (ER). The in vitro exposure to PS-MP caused a substantial reduction in cellular viability in TM3 and TM4 cells. In TM3 cells PS-MP inhibited the protein levels of StAR and of steroidogenic enzymes 3β-HSD and 17β-HSD, and in TM4 cells PS-MP inhibited the protein levels of the androgen receptors other than the activity of lactate dehydrogenase (LDH). PS-MP inhibited the functions of TM3 and TM4, as evidenced by the decrease of the phosphorylation of ERK1/2 and Akt in both cell lines. The oxidative stress caused by PS-MP decreased antioxidant defense in TM3 and TM4 cells, promoting autophagic and apoptotic processes. Furthermore, we found mitochondrial dysfunction and activation of ER stress. It is known that mitochondria are closely associated with ER to form the Mitochondrial-Associated Endoplasmic Reticulum Membranes (MAM), the site of calcium ions transfer as well as of lipid biosynthesis-involved enzymes and cholesterol transport from ER to the mitochondria. For the first time, we studied this aspect in PS-MP-treated TM3 and TM4 cells and MAMs dysregulation was observed. This study is the first to elucidate the intracellular mechanism underlying the effects of PS-MPs in somatic testicular cells, corroborating that PS-MP might be one of the causes of an increase in male infertility through the impairment of steroidogenesis in Leydig cells and of the nurse function of Sertoli cells. Thus, our findings contributed with new information to the mechanism underlying the effects of PS-MP on the male reproductive system. [Display omitted] • PS-MP caused a substantial reduction in cellular viability in TM3 and TM4 cells. • PS-MP inhibited the protein levels of StAR, 3β-HSD, and 17β-HSD in TM3 cells. • PS-MP inhibited the of AR expression protein levels and LDH activity in TM4 cells. • PS-MP promoted autophagy and apoptosis in the TM3 and TM4 cells. • PS-MP induced mitochondrion-endoplasmic reticulum dysregulation. [ABSTRACT FROM AUTHOR]

Ingestion of microplastics can lead to deleterious consequences for organisms, as documented by numerous laboratory studies. The current knowledge is based on a multitude of effect studies, conducted with conventional fossil-based and non-degradable plastics. However, there is a lack of information about the acceptance and the effects of novel bio-based and biodegradable plastics. Biodegradable plastics are considered an alternative to conventional plastics and are showing rapidly growing production rates. Biodegradable plastics can disperse into the environment in the same way as conventional plastics do, becoming available to marine organisms. This study aims to provide new insights into the uptake and effects of biodegradable microplastics on marine invertebrates. Rockpool shrimp, Palaemon elegans, were fed with algal flakes coated with polylactic acid (PLA), polyhydroxybutyrate-co-valerate (PHBV) and conventional low-density polyethylene (LDPE) microparticles. Live observations showed that all of the different types of microplastics were ingested. After dissection of the shrimp, less LDPE particles were found in the stomachs than PLA and PHBV particles. This indicates a longer retention time of biodegradable microplastics compared to conventional microplastics. Presumably, less LDPE particles were ingested or evacuated from the stomach, probably by regurgitation. The ingestion of microparticles of all types of plastics induced enzymatic activity of short-chain carboxylesterases in the midgut glands of the shrimp. However, only PLA induced enzymatic activity of medium-chain carboxylesterases. Palaemon elegans showed no oxidative stress response after ingestion of microparticles, irrespective of polymer type. From our results we conclude that biodegradable plastics might have different effects than conventional plastics. The longer retention times of biodegradable plastics might enhance exposure to leaching additives and other harmful substances. Our study provides new insights into how biodegradable plastics might affect aquatic fauna and indicate that the use of biodegradable plastics needs to be reconsidered to some extent. [Display omitted] • Higher numbers of biodegradable microplastics are found in the stomach of the shrimp. • All microplastics induce enzyme activities of short-chained carboxylesterases. • Ingestion of PLA results in the strongest induction of carboxylesterase activities. • Use of biodegradable plastics as less harmful alternative needs to be reconsidered. [ABSTRACT FROM AUTHOR]

Microplastics (MPs)/nanoplastics (NPs), as a source and vector of pathogenic bacteria, are widely distributed in the natural environments. Here, we investigated the combined effects of polystyrene NPs (PS-NPs) and lipopolysaccharides (LPS) on testicular function in mice for the first time. 24 male mice were randomly assigned into 4 groups, control, PS-NPs, LPS, and PS-NPs + LPS, respectively. Histological alterations of the testes were observed in mice exposed to PS-NPs, LPS or PS-NPs + LPS. Total sperm count, the levels of testosterone in plasma and testes, the expression levels of steroidogenic acute regulatory (StAR) decreased more remarkable in testes of mice treated with PS-NPs and LPS than the treatment with LPS or PS-NPs alone. Compared with PS-NPs treatment, LPS treatment induced more sever inflammatory response in testes of mice. Moreover, PS-NPs combined with LPS treatment increased the expression of these inflammatory factors more significantly than LPS treatment alone. In addition, PS-NPs or LPS treatment induced oxidative stress in testes of mice, but their combined effect is not significantly different from LPS treatment alone. These results suggest that PS-NPs exacerbate LPS-induced testicular dysfunction. Our results provide new evidence for the threats to male reproductive function induced by both NPs and bacterial infection in human health. [Display omitted] • Coexposure to PS-NPs and LPS aggravated the decrease of sperm count in mice. • PS-NPs and LPS induced oxidative stress in the testis of mouse. • PS-NPs exacerbated LPS-induced decrease in StAR expression and testosterone level. • PS-NPs exacerbated LPS-induced expression of inflammatory factors in mouse testis. • PS-NPs enhanced LPS-induced activation of NF-κB in mouse testis. [ABSTRACT FROM AUTHOR]

In recent years, nanoplastics (NPs) and triclosan (TCS, a pharmaceutical and personal care product) have emerged as environmental pollution issues, and their combined presence has raised widespread concern regarding potential risks to organisms. However, the combined toxicity and mechanisms of NPs and TCS remain unclear. In this study, we investigated the toxic effects of polystyrene NPs and TCS and their mechanisms on KGN cells, a human ovarian granulosa cell line. We exposed KGN cells to NPs (150 μg/mL) and TCS (15 μM) alone or together for 24 hours. Co-exposure significantly reduced cell viability. Compared with exposure to NPs or TCS alone, co-exposure increased reactive oxygen species (ROS) production. Interestingly, co-exposure to NPs and TCS produced synergistic effects. We examined the activity of superoxide dismutase (SOD) and catalase (CAT), two antioxidant enzymes; it was significantly decreased after co-exposure. We also noted an increase in the lipid oxidation product malondialdehyde (MDA) after co-exposure. Furthermore, co-exposure to NPs and TCS had a more detrimental effect on mitochondrial function than the individual treatments. Co-exposure activated the NRF2–KEAP1–HO-1 antioxidant stress pathway. Surprisingly, the expression of SESTRIN2, an antioxidant protein, was inhibited by co-exposure treatments. Co-exposure to NPs and TCS significantly increased the autophagy-related proteins LC3B-II and LC3B-Ⅰ and decreased P62. Moreover, co-exposure enhanced CASPASE-3 expression and inhibited the BCL-2/BAX ratio. In summary, our study revealed the synergistic toxic effects of NPs and TCS in vitro exposure. Our findings provide insight into the toxic mechanisms associated with co-exposure to NPs and TCS to KGN cells by inducing oxidative stress, activations of the NRF2-KEAP1-HO-1 pathway, autophagy, and apoptosis. • Nanoplastics (NPs) and triclosan (TCS) can synergistically induce cytotoxicity in KGN cells. • The combined exposure of NPs and TCS resulted in oxidative stress, autophagy, and apoptosis in KGN cells. • The combined exposure to NPs and TCS synergistically activates the NRF2-KEAP1-HO-1 signaling pathway. • The downregulation of SESTRIN2 expression affects the oxidation-antioxidant status. [ABSTRACT FROM AUTHOR]

Anthropogenic influences such as plastic pollution are causing serious environmental problems. While effects of microplastics on marine organisms are well studied, less is known about effects of plastic particles on terrestrial organisms such as plants. We investigated the effects of microplastic particles on different growth and metabolic traits of savoy cabbage (Brassica oleracea var. sabauda). Sections of seedlings exposed to polystyrene particles were analysed by coherent Raman scattering microscopy. These analyses revealed an uptake of particles in a size range of 0.5 µm to 2.0 µm into cells of the hypocotyl. Furthermore, plants were grown in substrate amended with polyethylene and polystyrene particles of different sizes (s 1 : 200–500 µm; s 2 : 100–200 µm; s 3 : 20–100 µm; s 4 : < 100 µm, with most particles < 20 µm; s 5 : < 20 µm) and in different concentrations (c 1 = 0.1%, c 2 = 0.01%, c 3 = 0.001%). After several weeks, shoot and root biomass were harvested. Leaves were analysed for their carbon to nitrogen ratio, while amino acid and glucosinolate composition were measured using high performance liquid chromatography. Plastic type, particle size and concentration showed distinct effects on certain plant traits. Shoot biomass was interactively influenced by size and concentration of polyethylene, while root biomass was not modified by any of the plastic exposure treatments. Likewise, the composition and total concentrations of leaf amino acids were not affected, but the leucine concentration was significantly increased in several of the plastic-exposed plants. Glucosinolates were also slightly altered, depending on the particle size. Some of the observed effects may be independent of plastic uptake, as larger particles were not taken up but still could affect plant traits. For example, in the rhizosphere plastic particles may increase the water holding capacity of the soil, impacting some of the plant traits. In summary, this study shows how important the plastic type, particle size and concentration are for the uptake of microplastics and their effects on plant traits, which may have important implications for crops, but also for ecosystems. [Display omitted] • Coherent Raman scattering microscopy revealed a polystyrene uptake into seedlings. • Effects of plastics on plants were type-, size- and concentration-dependent. • Foliar leucine concentrations were partly increased due to plastic exposure. • Foliar glucosinolates were by trend altered, in dependence of plastic particle size. [ABSTRACT FROM AUTHOR]

Microplastics (MPs) are widely identified as emerging hazards causing considerable eco-toxicity in terrestrial ecosystems, but the impacts differ in different ecosystem functions among different chemical compositions, morphology, sizes, concentrations, and experiment duration. Given the close relationships and trade-offs between plant and soil systems, probing the "whole ecosystem" instead of individual functions must yield novel insights into MPs affecting terrestrial ecosystems. Here, a comprehensive meta-analysis was employed to reveal an unambiguous response of the plant-soil-microbial system to MPs. Results showed that in view of plant, soil, and microbial functions, the general response patterns of plant and soil functions to MPs were obviously opposite. For example, polyethylene (PE) and polyvinyl chloride (PVC) MPs highly increased plant functions, while posed negative effects on soil functions. Polystyrene (PS) and biodegradable (Bio) MPs decreased plant functions, while stimulating soil functions. Additionally, low-density polyethylene (LDPE), PE, PS, PVC, Bio, and granular MPs significantly decreased soil microbial functions. These results clearly revealed that MPs alter the equilibrium of the plant-soil-microbial system. More importantly, our results further revealed that MPs tended to increase ecosystem multifunctionality, e.g., LDPE and PVC MPs posed positive effects on ecosystem multifunctionality, PE, PS, and Bio MPs showed neutral effects on ecosystem multifunctionality. Linear regression analysis showed that under low MPs size (<100 µm), ecosystem multifunctionality was gradually reduced with the increased size of MPs. The response of ecosystem multifunctionality showed a concave shape pattern along the gradient of experimental duration which was lower than 70 days. More importantly, there was a threshold (i.e., 5% w/w) for the effects of MPs concentration on ecosystem multifunctionality, i.e., under low concentration (< 5% w/w), ecosystem multifunctionality was gradually increased with the increased concentration of MPs, while ecosystem multifunctionality was gradually decreased under high concentration (i.e., > 5% w/w). These findings emphasize the importance of studying the effects of MPs on plant-soil-microbial systems and help us identify ways to reduce the eco-toxicity of MPs and maintain environmental safety in view of an ecology perspective. [Display omitted] • MPs posed opposite effects on plant and soil functions. • Soil microbial functions endured more severe damage from MPs. • MPs are likely to cause positive effects on ecosystem multifunctionality. • Impacts of MPs on EMF are type, size, concentration and duration dependency. [ABSTRACT FROM AUTHOR]

A surge in the number of anthropogenic pollutants has been caused by increasing industrial activities. Nanoplastics are spotlighted as a new aquatic pollutant that are a threat to microbes and larger organisms. Our previous study showed that the subinhibitory concentrations of aquatic pollutants such as phenol and formalin act as signaling molecules and modulate global gene expression and metabolism. In this study, we aimed to investigate the impact of a new type of anthropogenic contaminant, polystyrene (PS) nanoplastics, on the expression of key virulence factors in zoonotic pathogen Edwardsiella piscicida and the assessment of potential changes in the susceptibility of zebrafish as a model host. The TEM data indicated a noticeable change in the cell membrane indicating that PS particles were possibly entering the bacterial cells. Transcriptome analyses performed to identify the differentially expressed genes upon PS exposure revealed that the genes involved in major virulence factor type VI secretion system (T6SS) were down-regulated. However, the expression of T6SS-related genes was recovered from the PS adapted E. piscicida when nanoplastics are free. This demonstrated the hypervirulence of pathogen in infection assays with both cell lines and in vivo zebrafish model. Therefore, this study provides experimental evidence elucidating the direct regulatory impact of nanoplastics influx into aquatic ecosystems on fish pathogenic bacteria, notably influencing the expression of virulence factors. [Display omitted] • Changes of morphology and down-regulating gene expression of type VI secretion system upon PS exposure. • Increased cell invasion ability of E. piscicida adapted to nanoplastics. • Restoration of T6SS-related gene expression under nanoplastic-free conditions leading to elevated host mortality rates. • Need for appropriate management of environmental plastics to mitigate impact on pathogens and host organisms. [ABSTRACT FROM AUTHOR]

Micro/nanoplastics (MNPs) have emerged as a significant environmental concern due to their widespread distribution and potential adverse effects on human health and the environment. In this study, to integrate exposure and toxicity pathways of MNPs, a comprehensive review of the occurrence, toxicokinetics (absorption, distribution, and excretion [ADE]), and toxicity of MNPs were investigated using the aggregate exposure pathway (AEP) and adverse outcome pathway (AOP) frameworks. Eighty-five papers were selected: 34 papers were on detecting MNPs in environmental samples, 38 papers were on the ADE of MNPs in humans and fish, and 36 papers were related to MNPs toxicity using experimental models. This review not only summarizes individual studies but also presents a preliminary AEP-AOP framework. This framework offers a comprehensive overview of pathways, enabling a clearer visualization of intricate processes spanning from environmental media, absorption, distribution, and molecular effects to adverse outcomes. Overall, this review emphasizes the importance of integrating exposure and toxicity pathways of MNPs by utilizing AEP-AOP to comprehensively understand their impacts on human and ecological organisms. The findings contribute to highlighting the need for further research to fill the existing knowledge gaps in this field and the development of more effective strategies for the safe management of MNPs. [Display omitted] • Exposure and toxicity pathways of micro/nanoplastics (MNPs) were visually integrated. • MNPs are omnipresent in all environmental media, foods, and in human organs. • Toxicokinetic studies were revealed systemic distribution of MNPs throughout the organs. • Polyethylene was common in the environment, while polystyrene predominated in toxicity studies. • Oxidative stress and inflammation were most frequently observed toxicity of MNPs. [ABSTRACT FROM AUTHOR]

Due to microplastics (MPs) being widely distributed in soil, the use of advanced oxidation to remediate organic-contaminated soils may accelerate the aging of MPs in soil and impact the release of di-(2-ethylhexyl) phthalate (DEHP), a potential carcinogen used as a plasticizer in plastics, from MPs. In this study, persulfate oxidation (PO) and temperature treatment (TT) were used to treat biodegradable and petroleum-based MPs, including polylactic acid (PLA), polyvinyl chloride (PVC), and polystyrene (PS). The methods used for evaluating the characteristics changes of MP were X-ray diffraction (XRD) analysis and water contact angle measurement. The effects of aging on DEHP release from MPs were investigated via soil incubation. The results showed PO and TT led to increased surface roughness, oxygen-containing functional group content, and hydrophilicity of the MPs with prolonged aging, consequently accelerating the release of DEHP from the MPs. Interestingly, PLA aged faster than PVC and PS under similar conditions. After 30 days of PO treatment, DEHP release from PLA into the soil increased 0.789-fold, exceeding the increase from PVC (0.454-fold) and PS (0.287-fold). This suggests that aged PLA poses a higher ecological risk than aged PVC or PS. Furthermore, PO treatment resulted in the oxidation and degradation of DEHP on the MP surface. After 30 days of PO treatment, the DEHP content in PLA, PVC, and PS decreased by 19.1%, 25.8%, and 23.5%, respectively. Specifying the types of MPs studied and the environmental conditions would provide a more precise context for the results. These findings provide novel insights into the fate of biodegradable and petroleum-based MPs and the potential ecotoxicity arising from advanced oxidation remediation in contaminated soils. [Display omitted] • Aging accelerated di(2-ethylhexyl) phthalate (DEHP) release from microplastics (MPs). • Aging enhanced the ecotoxicity of biodegradable and petroleum-based MPs in soil. • The ecotoxicity of biodegradable MPs was higher than that of petroleum-based MPs. • Persulfate oxidation reduced DEHP extractable content in MPs via DEHP degradation. [ABSTRACT FROM AUTHOR]

Biodegradable plastics (BPs) are widely used as alternatives to non-BPs due to their inherent ability to undergo facile degradation. However, the ecotoxicological impact of biodegradable microplastics (MPs) rarely remains scientific documented especially to aquatic ecosystem and organisms compared to conventional microplastics. Therefore, this study aimed to investigate the ecotoxicity of biodegradable polylactic acid (PLA) MPs to Daphnia magna with that of conventional polyethylene (PE) MPs with and without ultraviolet (UV) treatment (4 weeks). The acute toxicity (48 h) of PLA MPs was significantly higher than that of PE MPs, potentially attributable to their elevated bioconcentration resulting from their higher density. UV treatment notably reduced the particle size of PLA MPs and induced new hydrophilic functional groups containing oxygen. Thus, the acute lethal toxicity of PLA MPs exhibited noteworthy increase, compared to before UV treatment after UV treatment, which was greater than that of UV-PE MPs. In addition, UV-PLA MPs showed markedly elevated reactive oxygen species concentration in D. magna compared to positive control. However, there was no significant increase in the level of lipid peroxidation, possibly due to successful defense by antioxidant enzymes (superoxide dismutase and catalase). These findings highlight the ecotoxicological risks of biodegradable MPs to aquatic organisms, which require comprehensive long-term studies. [Display omitted] • PLA MPs showed higher bioconcentration and acute toxicity in D. magna than PE MPs. • UV treatments degraded PLA MPs and produced hydrophilic functional groups on their surface. • UV-PLA MPs showed higher acute lethal and sublethal toxicity than that of PLA before UV treatments. [ABSTRACT FROM AUTHOR]

Micro/nanoplastics (M/NPs) in water have raised global concern due to their potential environmental risks. To reestablish a M/NPs free world, enormous attempts have been made toward employing chemical technologies for their removal in water. This review comprehensively summarizes the advances in chemical degradation approaches for M/NPs elimination. It details and discusses promising techniques, including photo-based technologies, Fenton-based reaction, electrochemical oxidation, and novel micro/nanomotors approaches. Subsequently, critical influence factors, such as properties of M/NPs and operating factors, are analyzed in this review specifically. Finally, it concludes by addressing the current challenges and future perspectives in chemical degradation. This review will provide guidance for scientists to further explore novel strategies and develop feasible chemical methods for the improved control and remediation of M/NPs in the future. [Display omitted] • This review summarized the recent chemical degradation methods for M/NPs. • Photo-based approaches pose great potential for M/NPs degradation. • The mechanism, limitations, and influence factors of each technologies are reviewed. • Challenges and perspectives about M/NPs chemical degradation are summarized. [ABSTRACT FROM AUTHOR]

The global production and consumption of plastics, as well as their deposition in the environment, are experiencing exponential growth. In addition, mismanaged plastic waste (PW) losses into drainage channels are a growing source of microplastic (MP) pollution concern. However, the complete understanding of their environmental implications throughout their life cycle is yet to be fully understood. Determining the potential extent to which MPs contribute to overall ecotoxicity is possible through the monitoring of PW release and MP removal during remediation. Life cycle assessments (LCAs) have been extensively utilized in many comparative analyses, such as comparing petroleum-based plastics with biomass and single-use plastics with multi-use alternatives. These assessments typically yield unexpected or paradoxical results. Nevertheless, there is still a paucity of reliable data and tools for conducting LCAs on plastics. On the other hand, the release and impact of MP have so far not been considered in LCA studies. This is due to the absence of inventory-related data regarding MP releases and the characterization factors necessary to quantify the effects of MP. Therefore, this review paper conducts a comprehensive literature review in order to assess the current state of knowledge and data regarding the environmental impacts that occur throughout the life cycle of plastics, along with strategies for plastic management through LCA. • Life cycle assessment (LCA) is a standardized tool designed to aid decision-making. • LCA evaluates the environmental impacts of products throughout their life cycle. • Waste management alternatives for bio-based and conventional plastics are distinct. • Several approaches have been used to mitigate microplastics (MPs). • Existing LCA studies do not address environmental or human health impacts of MPs. [ABSTRACT FROM AUTHOR]

Nanoplastics (NPs) are widely detected in food and drinking water, and human exposure to NPs is ubiquitous. The digestive tract is the main route of exposure to NPs in humans, and the esophagus is one of the main target organs for NPs exposure. However, the toxicological effects of polystyrene nanoplastics (PS-NPs) on the esophagus are not fully understood. Here, we used two esophageal cell lines as models to explore the effects of NPs exposure on esophageal cells and the underlying molecular mechanisms. Western blot analysis, indirect immunofluorescence assay, and enzyme-linked immunosorbent assay revealed that NPs exposure caused inflammatory responses and cell death. Mechanistic investigations showed that PS-NPs exposure induced iron overload in esophageal cells, leading to the accumulation of mitochondrial reactive oxygen species and promoting inflammatory responses and cell death. Additionally, PS-NPs treatment suppressed mitochondrial autophagy, which exacerbated NP-induced cell inflammation and death. Collectively, our experimental findings provide new evidence for the toxicological effects of PS-NPs and offer new insights and avenues for future research. • PS-NPs could be internalized into esophageal cells. • NPs leads to inflammation and death of the esophageal cells. • NPs shows its toxicology effects through regulation of mitochondrial iron overload. [ABSTRACT FROM AUTHOR]

Microplastics are detrimental to the environment. However, the combined effects of microplastics and arsenic (As) remain unclear. In this study, we investigated the combined effects of polystyrene (PS) microplastics and As on HepG2 cells. The results showed that PS microplastics 20, 50, 200, and 500 nm in size were taken up by HepG2 cells, causing a decrease in cellular mitochondrial membrane potential. The results of lactate dehydrogenase release and flow cytometry showed that PS microplastics, especially those of 50 nm, enhanced As-induced apoptosis. In addition, transcriptome analysis revealed that TP53, AKT1, CASP3, ACTB, BCL2L1, CASP8, XIAP, MCL1, NFKBIA, and CASP7 were the top 10 hub genes for PS that enhanced the role of As in HepG2 cell apoptosis. Our results suggest that nano-PS enhances As-induced apoptosis. Furthermore, this study is important for a better understanding of the role of microplastics in As-induced hepatotoxicity. [Display omitted] • Polystyrene microplastics exacerbated arsenic-induced hepatocytotoxicity. • Nano polystyrene microplastics had the greatest impact on arsenic toxicity. • The TP53 gene plays an important regulatory role in the enhanced hepatotoxicity of arsenic by Polystyrene microplastics. [ABSTRACT FROM AUTHOR]

Polyethylene microplastics (PE-MPs) are one of the environmental contaminants that instigate oxidative stress (OS) in various organs of the body, including testes. Kaempferide (KFD) is a plant-derived natural flavonol with potential neuroprotective, hepatoprotective, anti-cancer, anti-oxidant and anti-inflammatory properties. Therefore, the present study was designed to evaluate the alleviative effects of KFD against PE-MPs-prompted testicular toxicity in rats. Fourty eight adult male albino rats were randomly distributed into 4 groups: control, PE-MPs-administered (1.5 mgkg-1), PE-MPs (1.5 mgkg-1) + KFD (20 mgkg-1) co-treated and KFD (20 mgkg-1) only treated group. PE-MPs intoxication significantly (P < 0.05) lowered the expression of Nrf-2 and anti-oxidant enzymes, while increasing the expression of Keap-1. The activities of anti-oxidants i.e., catalase (CAT), glutathione reductase (GSR), superoxide dismutase (SOD), hemeoxygene-1 (HO-1) and glutathione peroxidase (GPx) were reduced, besides malondialdehyde (MDA) and reactive oxygen species (ROS) contents were increased significantly (P < 0.05) following the PE-MPs exposure. Moreover, PE-MPs exposure significantly (P < 0.05) reduced the sperm motility, viability and count, whereas considerably (P < 0.05) increased the dead sperm number and sperm structural anomalies. Furthermore, PE-MPs remarkably (P < 0.05) decreased steroidogenic enzymes and Bcl-2 expression, while increasing the expression of Caspase-3 and Bax. PE-MPs exposure significantly (P < 0.05) reduced the levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH) and testosterone, whereas inflammatory indices were increased. PE-MPs exposure also induced significant histopathological damages in the testes. Nevertheless, KFD supplementation significantly (P < 0.05) abrogated all the damages induced by PE-MPs. The findings of our study demonstrated that KFD could significantly attenuate PE-MPs-instigated OS and testicular toxicity, due to its anti-oxidant, anti-inflammatory, androgenic and anti-apoptotic potential. [Display omitted] • PE-MPs exposure disturbed biochemical, spermatogenic and histological profiles in male albino rats. • Kaempferide increased Nrf-2 & anti-oxidant enzymes expression and decreased Keap-1 expression. • Kaempferide elevated anti-oxidant enzyme activities and decreased the levels of MDA and ROS. • Kaempferide escalated the expression of steroidogenic enzymes and hormone levels. • Kaempferide regulated the levels of inflammatory and apoptotic markers as well as histological profile. [ABSTRACT FROM AUTHOR]