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There are increasing concerns regarding the rapid expansion of polystyrene nanoplastics (PS-NPs), which could impact human health. Previous studies have shown that nanoplastics can be transferred from mothers to offspring through the placenta and breast milk, resulting in cognitive deficits in offspring. However, the neurotoxic effects of maternal exposure on offspring and its mechanisms remain unclear. In this study, PS-NPs (50 nm) were gavaged to female rats throughout gestation and lactation to establish an offspring exposure model to study the neurotoxicity and behavioral changes caused by PS-NPs on offspring. Neonatal rat hippocampal neuronal cells were used to investigate the pathways through which NPs induce neurodevelopmental toxicity in offspring rats, using iron inhibitors, autophagy inhibitors, reactive oxygen species (ROS) scroungers, P53 inhibitors, and NCOA4 inhibitors. We found that low PS-NPs dosages can cause ferroptosis in the hippocampus of the offspring, resulting in a decline in the cognitive, learning, and memory abilities of the offspring. PS-NPs induced NOCA4-mediated ferritinophagy and promoted ferroptosis by inciting ROS production to activate P53-mediated ferritinophagy. Furthermore, the levels of the antioxidant factors glutathione peroxidase 4 (GPX4) and glutathione (GSH), responsible for ferroptosis, were reduced. In summary, this study revealed that consumption of PS-NPs during gestation and lactation can cause ferroptosis and damage the hippocampus of offspring. Our results can serve as a basis for further research into the neurodevelopmental effects of nanoplastics in offspring. [ABSTRACT FROM AUTHOR]

Background: Polystyrene nanoplastics (PS-NPs) are becoming increasingly prevalent in the environment with great advancements in plastic products, and their potential health hazard to animals has received much attention. Several studies have reported the toxicity of PS-NPs to various tissues and cells; however, there is a paucity of information about whether PS-NPs exposure can have toxic effects on mammalian oocytes, especially livestock. Herein, porcine oocytes were used as the model to investigate the potential effects of PS-NPs on mammalian oocytes. Results: The findings showed that different concentrations of PS-NPs (0, 25, 50 and 100 μg/mL) entering into porcine oocytes could induce mitochondrial stress, including a significant decrease in mitochondrial membrane potential (MMP), and the destruction of the balance of mitochondrial dynamic and micromorphology. Furthermore, there was a marked increase in reactive oxygen species (ROS), which led to oocyte lipid peroxidation (LPO). PS-NPs exposure induced abnormal intracellular iron overload, and subsequently increased the expression of transferrin receptor (TfRC), solute carrier family 7 member 11 (SLC7a11), and acyl-CoA synthetase long-chain family member 4 (ACSL4), which resulted in ferroptosis in oocytes. PS-NPs also induced oocyte maturation failure, cytoskeletal dysfunction and DNA damage. Cotreatment with 5 μmol/L ferrostatin-1 (Fer-1, an inhibitor of ferroptosis) alleviated the cellular toxicity associated with PS-NPs exposure during porcine oocyte maturation. Conclusions: In conclusion, PS-NPs caused ferroptosis in porcine oocytes by increasing oxidative stress and altering lipid metabolism, leading to the failure of oocyte maturation. PS-NPs could enter oocytes, caused mitochondrial dysfunction and oxidative stress, induced lipid peroxidation and ferroptosis, which eventually resulted in failure of oocyte maturation. [ABSTRACT FROM AUTHOR]

Abstract There are increasing concerns regarding the rapid expansion of polystyrene nanoplastics (PS-NPs), which could impact human health. Previous studies have shown that nanoplastics can be transferred from mothers to offspring through the placenta and breast milk, resulting in cognitive deficits in offspring. However, the neurotoxic effects of maternal exposure on offspring and its mechanisms remain unclear. In this study, PS-NPs (50 nm) were gavaged to female rats throughout gestation and lactation to establish an offspring exposure model to study the neurotoxicity and behavioral changes caused by PS-NPs on offspring. Neonatal rat hippocampal neuronal cells were used to investigate the pathways through which NPs induce neurodevelopmental toxicity in offspring rats, using iron inhibitors, autophagy inhibitors, reactive oxygen species (ROS) scroungers, P53 inhibitors, and NCOA4 inhibitors. We found that low PS-NPs dosages can cause ferroptosis in the hippocampus of the offspring, resulting in a decline in the cognitive, learning, and memory abilities of the offspring. PS-NPs induced NOCA4-mediated ferritinophagy and promoted ferroptosis by inciting ROS production to activate P53-mediated ferritinophagy. Furthermore, the levels of the antioxidant factors glutathione peroxidase 4 (GPX4) and glutathione (GSH), responsible for ferroptosis, were reduced. In summary, this study revealed that consumption of PS-NPs during gestation and lactation can cause ferroptosis and damage the hippocampus of offspring. Our results can serve as a basis for further research into the neurodevelopmental effects of nanoplastics in offspring. Graphical Abstract

Abstract Background Polystyrene nanoplastics (PS-NPs) are becoming increasingly prevalent in the environment with great advancements in plastic products, and their potential health hazard to animals has received much attention. Several studies have reported the toxicity of PS-NPs to various tissues and cells; however, there is a paucity of information about whether PS-NPs exposure can have toxic effects on mammalian oocytes, especially livestock. Herein, porcine oocytes were used as the model to investigate the potential effects of PS-NPs on mammalian oocytes. Results The findings showed that different concentrations of PS-NPs (0, 25, 50 and 100 μg/mL) entering into porcine oocytes could induce mitochondrial stress, including a significant decrease in mitochondrial membrane potential (MMP), and the destruction of the balance of mitochondrial dynamic and micromorphology. Furthermore, there was a marked increase in reactive oxygen species (ROS), which led to oocyte lipid peroxidation (LPO). PS-NPs exposure induced abnormal intracellular iron overload, and subsequently increased the expression of transferrin receptor (TfRC), solute carrier family 7 member 11 (SLC7a11), and acyl-CoA synthetase long-chain family member 4 (ACSL4), which resulted in ferroptosis in oocytes. PS-NPs also induced oocyte maturation failure, cytoskeletal dysfunction and DNA damage. Cotreatment with 5 μmol/L ferrostatin-1 (Fer-1, an inhibitor of ferroptosis) alleviated the cellular toxicity associated with PS-NPs exposure during porcine oocyte maturation. Conclusions In conclusion, PS-NPs caused ferroptosis in porcine oocytes by increasing oxidative stress and altering lipid metabolism, leading to the failure of oocyte maturation. Graphical Abstract PS-NPs could enter oocytes, caused mitochondrial dysfunction and oxidative stress, induced lipid peroxidation and ferroptosis, which eventually resulted in failure of oocyte maturation.

Aluminosilicates are commonly present in natural soils, contributing to their texture and composition. The fate and transport of nanoplastics within natural sediments containing aluminosilicates have not been comprehensively studied yet. To investigate the interactions between nanoplastics and sediments, polystyrene nanoplastics (PS-NPs) were injected into columns filled with zeolite under the condition of different flow rates, pH values, and ionic strengths (IS). Results show that zeolite inhibited polystyrene nanoplastics (PS-NPs) transport to different extents under different conditions. The limitation of PS-NPs transport was mainly governed by (1) the PS-NPs–zeolite interaction energy obtained via the Derjaguin–Landau–Verwey–Overbeek calculation, (2) the amphoteric sites on zeolite surface (they will possess positive charges attracting negative PS-NPs when pH < pHpzc), and (3) surface roughness leading to physical straining phenomena. In addition, the flow rate of pore water played an essential role during the PS-NPs transport. The retention of PS-NPs decreased at higher flow rates, likely due to a reduction in particle-collector contact efficiency. This study uncovers the migration mechanism of PS-NPs within zeolite, providing insights into the behavior of nanoparticles in natural porous media.Highlights: Zeolite significantly alters PS-NPs flow under diverse conditions. Amphoteric sites on zeolite surface edges affect PS-NPs transport. Increased flow rates boost PS-NPs mobility effectively. Varying ionic strength impacts PS-NPs retention notably. Different cation types crucially influence PS-NPs transport. [ABSTRACT FROM AUTHOR]

Abstract Plastic pollution is an emerging environmental issue, with microplastics and nanoplastics raising health concerns due to bioaccumulation. This work explored the impact of polystyrene nanoparticle (PS-NPs) exposure during prepuberty on male reproductive function post maturation in rats. Rats were gavaged with PS-NPs (80 nm) at 0, 3, 6, 12 mg/kg/day from postnatal day 21 to 95. PS-NPs accumulated in the testes and reduced sperm quality, serum reproductive hormones, and testicular coefficients. HE staining showed impaired spermatogenesis. PS-NPs disrupted the blood-testis barrier (BTB) by decreasing junction proteins, inducing inflammation and apoptosis. Transcriptomics identified differentially expressed genes related to metabolism, lysosome, apoptosis, and TLR4 signaling. Molecular docking revealed Cordycepin could compete with polystyrene for binding to TLR4. Cordycepin alleviated oxidative stress and improved barrier function in PS-NPs treated Sertoli cells. In conclusion, prepubertal PS-NPs exposure induces long-term reproductive toxicity in male rats, likely by disrupting spermatogenesis through oxidative stress and BTB damage. Cordycepin could potentially antagonize this effect by targeting TLR4 and warrants further study as a protective agent. This study elucidates the mechanisms underlying reproductive toxicity of PS-NPs and explores therapeutic strategies.

Abstract Background Nanoplastics (NPs) are emerging pollutants that pose risks to living organisms. Recent findings have unveiled the reproductive harm caused by polystyrene nanoparticles (PS-NPs) in female animals, yet the intricate mechanism remains incompletely understood. Under this research, we investigated whether sustained exposure to PS-NPs at certain concentrations in vivo can enter oocytes through the zona pellucida or through other routes that affect female reproduction. Results We show that PS-NPs disrupted ovarian functions and decreased oocyte quality, which may be a contributing factor to lower female fertility in mice. RNA sequencing of mouse ovaries illustrated that the PI3K-AKT signaling pathway emerged as the predominant environmental information processing pathway responding to PS-NPs. Western blotting results of ovaries in vivo and cells in vitro showed that PS-NPs deactivated PI3K-AKT signaling pathway by down-regulating the expression of PI3K and reducing AKT phosphorylation at the protein level, PI3K-AKT signaling pathway which was accompanied by the activation of autophagy and apoptosis and the disruption of steroidogenesis in granulosa cells. Since PS-NPs penetrate granulosa cells but not oocytes, we examined whether PS-NPs indirectly affect oocyte quality through granulosa cells using a granulosa cell–oocyte coculture system. Preincubation of granulosa cells with PS-NPs causes granulosa cell dysfunction, resulting in a decrease in the quality of the cocultured oocytes that can be reversed by the addition of 17β-estradiol. Conclusions This study provides findings on how PS-NPs impact ovarian function and include transcriptome sequencing analysis of ovarian tissue. The study demonstrates that PS-NPs impair oocyte quality by altering the functioning of ovarian granulosa cells. Therefore, it is necessary to focus on the research on the effects of PS-NPs on female reproduction and the related methods that may mitigate their toxicity.

Plastic pollution is an emerging environmental issue, with microplastics and nanoplastics raising health concerns due to bioaccumulation. This work explored the impact of polystyrene nanoparticle (PS-NPs) exposure during prepuberty on male reproductive function post maturation in rats. Rats were gavaged with PS-NPs (80 nm) at 0, 3, 6, 12 mg/kg/day from postnatal day 21 to 95. PS-NPs accumulated in the testes and reduced sperm quality, serum reproductive hormones, and testicular coefficients. HE staining showed impaired spermatogenesis. PS-NPs disrupted the blood-testis barrier (BTB) by decreasing junction proteins, inducing inflammation and apoptosis. Transcriptomics identified differentially expressed genes related to metabolism, lysosome, apoptosis, and TLR4 signaling. Molecular docking revealed Cordycepin could compete with polystyrene for binding to TLR4. Cordycepin alleviated oxidative stress and improved barrier function in PS-NPs treated Sertoli cells. In conclusion, prepubertal PS-NPs exposure induces long-term reproductive toxicity in male rats, likely by disrupting spermatogenesis through oxidative stress and BTB damage. Cordycepin could potentially antagonize this effect by targeting TLR4 and warrants further study as a protective agent. This study elucidates the mechanisms underlying reproductive toxicity of PS-NPs and explores therapeutic strategies. [ABSTRACT FROM AUTHOR]

The environmental behavior of and risks associated with nanoplastics (NPs) have attracted considerable attention. However, compared to pristine NPs, environmental factors such as ultraviolet (UV) irradiation that lead to changes in the toxicity of NPs have rarely been studied. We evaluated the changes in morphology and physicochemical properties of polystyrene (PS) NPs before and after UV irradiation, and compared their hepatotoxicity in mice. The results showed that UV irradiation caused particle size reduction and increased the carbonyl index (CI) and negative charge on the particle surface. UV-aged PS NPs (aPS NPs) could induce the generation of hydroxyl radicals (·OH), but also further promoted the generation of ·OH in the Fenton reaction system. Hepatic pathological damage was more severe in mice exposed to aPS NPs, accompanied by a large number of vacuoles and hepatocyte balloon-like changes and more marked perturbations in blood glucose and serum lipoprotein, alanine aminotransferase and aspartate aminotransferase levels. In addition, exposure to PS NPs and aPS NPs, especially aPS NPs, triggered oxidative stress and significantly damaged the antioxidant capacity of mice liver. Compared with PS NPs, exposure to aPS NPs increased the number of altered metabolites in hepatic and corresponding metabolic pathways, especially glutathione metabolism. Our research suggests that UV irradiation can disrupt the redox balance in organisms by promoting the production of ·OH, enhancing PS NPs-induced liver damage and metabolic disorders. This study will help us understand the health risks of NPs and to avoid underestimation of the risks of NPs in nature. [Display omitted] [ABSTRACT FROM AUTHOR]

Background: Nanoplastics (NPs) are emerging pollutants that pose risks to living organisms. Recent findings have unveiled the reproductive harm caused by polystyrene nanoparticles (PS-NPs) in female animals, yet the intricate mechanism remains incompletely understood. Under this research, we investigated whether sustained exposure to PS-NPs at certain concentrations in vivo can enter oocytes through the zona pellucida or through other routes that affect female reproduction. Results: We show that PS-NPs disrupted ovarian functions and decreased oocyte quality, which may be a contributing factor to lower female fertility in mice. RNA sequencing of mouse ovaries illustrated that the PI3K-AKT signaling pathway emerged as the predominant environmental information processing pathway responding to PS-NPs. Western blotting results of ovaries in vivo and cells in vitro showed that PS-NPs deactivated PI3K-AKT signaling pathway by down-regulating the expression of PI3K and reducing AKT phosphorylation at the protein level, PI3K-AKT signaling pathway which was accompanied by the activation of autophagy and apoptosis and the disruption of steroidogenesis in granulosa cells. Since PS-NPs penetrate granulosa cells but not oocytes, we examined whether PS-NPs indirectly affect oocyte quality through granulosa cells using a granulosa cell–oocyte coculture system. Preincubation of granulosa cells with PS-NPs causes granulosa cell dysfunction, resulting in a decrease in the quality of the cocultured oocytes that can be reversed by the addition of 17β-estradiol. Conclusions: This study provides findings on how PS-NPs impact ovarian function and include transcriptome sequencing analysis of ovarian tissue. The study demonstrates that PS-NPs impair oocyte quality by altering the functioning of ovarian granulosa cells. Therefore, it is necessary to focus on the research on the effects of PS-NPs on female reproduction and the related methods that may mitigate their toxicity. Highlights: PS-NPs reduced oocyte quality and female fertility in mice. PS-NPs inhibited PI3K-AKT signaling pathway in mouse ovary and granulosa cells. PS-NPs decreased cell viability of granulosa cells by inducing apoptosis and autophagy. PS-NPs suppressed steroidogenesis of granulosa cells. PS-NPs reduced oocyte quality by causing granulosa cell dysfunction. [ABSTRACT FROM AUTHOR]

Nanoplastics, as emerging environmental pollutants, can transport contaminants across marine environments, polluting pristine ecosystems and being ingested by marine organisms. This transfer poses a severe threat to global aquatic ecosystems and potentially impacts human health through the food chain. Neurobehavioral and reproductive toxicity are critical areas of concern because they directly affect the survival, health, and population dynamics of aquatic species, which can have cascading effects on the entire ecosystem. Using zebrafish as a model organism, we investigated the toxic effects of environmental concentrations of polystyrene nanoplastics (PS-NPs). Behavioral assessments, including the novel tank test and open field test, demonstrated significant neurobehavioral changes, indicating increased anxiety and depressive behaviors. A pathological analysis of brain and gonadal tissues, along with evaluations of neurobehavioral and reproductive toxicity biomarkers, revealed that exposure to PS-NPs leads to brain tissue lesions, inflammatory responses, oxidative stress activation, hormone level disruptions, and gonadal damage. Real-time quantitative PCR studies of reproductive gene expression further showed that PS-NPs disrupt the endocrine regulation pathways of the brain-pituitary-gonadal (BPG) axis, causing reproductive toxicity with sex-specific differences. These findings provide crucial insights into the impacts of nanoplastics on aquatic organisms and their ecological risks, offering theoretical support for future environmental protection and pollutant management efforts. [ABSTRACT FROM AUTHOR]

Background: Nanoplastics can be considered a novel contaminant for the environment because of their extensive applications in modern society, which represents a possible threat to humans. Nevertheless, the negative effect of polystyrene nanoplastics (PS‐NPs) on male reproduction, fertility, and progeny outcomes is not well known. Thus, the aim of the present work was to calculate the median lethal dose (LD50) and investigate the consequences of exposure to PS‐NPs (25 nm) on male reproductive toxicity. Methods: This investigation first determined the LD50 of PS‐NPs in male Wistar rats, and then in a formal study, 24 rats were distributed into three groups (n = 8): the control group; the low‐dose group (3 mg/kg bw); and the high‐dose group (10 mg/kg bw) of PS‐NPs administered orally for 60 days. On the 50th day of administration, the fertility test was conducted. Results: The LD50 was determined to be 2500 mg/kg. PS‐NP administration induced significant alternations, mainly indicating mortality in the high‐dose group, a significant elevation in body weight gain, declined sperm quality parameters, altered reproductive hormonal levels, thyroid endocrine disruption, an alternation of the normal histo‐architecture and the histo‐morphometric analysis of the testes, and impaired male fertility. Conclusion: Altogether, the current findings provide novel perspectives on PS‐NP general toxicity with specific reference to male reproductive toxicity. [ABSTRACT FROM AUTHOR]

Globally, plastic pollution threatens human health, particularly affecting the hearts of offspring exposed to maternal environmental factors early in development. Few studies have specifically addressed sex-specific cardiac injury in offspring resulting from maternal exposure to polystyrene nanoplastics (PS-NPs). This study investigates the potential cardiac injury in offspring following maternal exposure to 1 mg/L PS-NPs. Pregnant C57BL/6J mice were exposed to PS-NPs until 3 weeks postpartum to establish a maternal exposure model. Heart tissues were collected and weighed, and the transcriptomes of the offspring hearts were sequenced and analyzed using high-throughput RNA sequencing. Immunohistochemical staining was performed to assess the effects of PS-NPs on cardiac immune infiltration, fibrosis, and apoptosis in the offspring. PS-NPs caused a significant reduction in heart and body weight in female offspring compared to males. Additionally, PS-NPs induced sex-specific transcriptional reprogramming and metabolic disruptions in the offspring. PS-NPs also induced significant fibrosis, apoptosis, and increased CD68+ macrophage infiltration in offspring hearts. Notably, PS-NPs induced distinct cardiovascular diseases in the offspring. Fluid shear stress and atherosclerosis were significantly enriched in PS-NP-treated male offspring, while viral myocarditis was predominantly enriched in PS-NP-treated females. Our findings suggest that PS-NPs induce cardiotoxicity in offspring by disrupting metabolism, impairing immunity, and triggering fibrosis and apoptosis, with sex-specific differences. This study provides novel insights and a foundation for understanding sex-specific pharmacological differences and interventions in PS-NP-induced cardiovascular disease in offspring.

Nanoplastics are ubiquitous in our daily lives, raising concerns about their potential impact on the human brain. Many studies reported that nanoplastics permeate the blood-brain barrier and influence cellular processes in mouse models. However, the neurotoxic effects of ingesting nanoplastics on human brain remain poorly understood. Here, we treated cerebral organoids with polystyrene nanoplastics to model the effects of nanoplastic exposure on human brain. Importantly, we found that mitochondria might be the significant organelles affected by polystyrene nanoplastics using immunostaing and RNA-seq analysis. Subsequently, we observed the increased cell death and decreased cell differentiation in our cerebral organoids. In conclusion, our findings shed insights on the mechanisms underlying the toxicity of nanoplastics on human brain organoids, providing an evaluation system in detection potential environmental toxicity on human brain.

Microplastic (MP) are an emerging environmental pollutant, which has toxic effects on organisms, and it has received extensive attention currently. Studying the transcriptomic and metabolic responses of mice to nanoplastic-contaminated water is critical for understanding molecular-level toxicity of nanoplastics (NPs), but there are few studies on this topic. To analyze the effects of different concentrations of polystyrene (PS) nanoplastic-contaminated water on mice at the transcriptome and metabolism of spleens to study the molecular toxicity. Here, testing of histopathology of spleen of female mice was performed after drinking water containing 0.1 μm PS-NPs (1 mg/mL and 50 mg/mL) at different concentrations for 49 days, respectively. The spleen tissue samples were subjected to metabolome and transcriptome sequencing. Four differentially expressed genes were randomly chosen for qRT-PCR to confirm the correctness of transcriptome sequencing. Common Kyoto encyclopedia of genes and genomes (KEGG) pathway analysis showed that a large number of differential genes and differential metabolites mainly focused on immune, inflammation, neurodegenerative disease, cardiovascular disease, nervous, etc. in the organism systems module; lipid, amino acid, taurine and hypotaurine metabolisms, etc. in the metabolism module; signaling translation, signaling molecules and interaction, and neuroactive ligand-receptor interaction, etc. in the environmental information processing. The results showed that pathway analysis at transcriptome and metabolome levels confirmed that the immune system of mice was affected after drinking water contaminated with polystyrene nanoplastics.

The excessive usage of nanoplastics (NPs) has posed a serious threat to the ecological environment and human health, which can enter the brain and then result in neurotoxicity. However, research on the neurotoxic effects of NPs based on different exposure routes and modifications of functional groups is lacking. In this study, the neurotoxicity induced by NPs was studied using polystyrene nanoplastics (PS-NPs) of different modifications (PS, PS-COOH, and PS-NH2). It was found that PS-NH2 through intranasal administration (INA) exposure route exhibited the greatest accumulation in the mice brain after exposure for 7 days. After the mice were exposed to PS-NH2 by INA means for 28 days, the exploratory ability and spatial learning ability were obviously damaged in a dose-dependent manner. Further analysis indicated that these damages induced by PS-NH2 were closely related to the decreased ability of glymphatic system to clear β-amyloid (Aβ) and phosphorylated Tau (P-Tau) proteins, which was ascribed to the loss of aquaporin-4 (AQP4) polarization in the astrocytic endfeet. Moreover, the loss of AQP4 polarization might be regulated by the NF-κB pathway. Our current study establishes the connection between the neurotoxicity induced by PS-NPs and the glymphatic system dysfunction for the first time, which will contribute to future research on the neurotoxicity of NPs.

Excessive nanoplastics not only pose a direct threat to the environment but also have the propensity to adsorb and interact with other pollutants, exacerbating their impact. The coexistence of nanoplastics and heavy metals in soils is a prevalent phenomenon. However, limited research existed about the joint effects of the two contaminants on soil organisms. In this paper, we ascertained the combined toxicity of polystyrene nanoplastics (PS-NPs) and copper (Cu2+) on soil organisms (Caenorhabditis elegans) at quantities that were present in the environment, further exploring whether the two toxicants were synergistic or antagonistic. The outcomes manifested that single exposure to low-dose PS-NPs (1 μg/L) would not cause significant damage to nematodes. After treatment with PS-NPs and Cu2+, the locomotion ability of nematode was impaired, accompanied by an elevation in reactive oxygen species (ROS) level and a biphasic response in antioxidant enzyme activity. Moreover, combined exposure to PS-NPs and Cu2+ induced the mRNA up-regulation of vit-6, cyp-35a2, hsp-16.2, age-1, and cep-1, both of which were stress-related genes. The comparative analysis between groups (with or without PS-NPs) revealed that the combined exposure group resulted in significantly greater toxic effects on nematodes compared with Cu2+ exposure alone. Furthermore, the addition of PS-NPs influenced the metabolic profiles of Caenorhabditis elegans under Cu2+ stress, with numerous differential metabolites associated with oxidative damage or defense mechanism. Overall, these findings manifested that PS-NPs at the expected environmental concentration elevated Cu2+ toxicity on nematodes.

The study on the influence of Natural Organic Matter (NOM) over the individual and combined effects of different nanomaterials on marine species is pertinent. The current study explores the role of Extracellular Polymeric Substances (EPS) in influencing the individual and combined toxic effects of polystyrene nanoplastics (PSNPs) viz. aminated (NH2-PSNPs), carboxylated (COOH-PSNPs), and plain PSNPs and TiO2 NPs in the marine crustacean, Artemia salina. A. salina was interacted with pristine PSNPs, pristine TiO2 NPs, EPS incubated PSNPs, EPS incubated TiO2 NPs, binary mixture of PSNPs and TiO2 NPs, and EPS adsorbed binary mixture of PSNPs and TiO2 NPs for 48 h. The present study proves that, when compared to the pristine toxicity of PSNPs and TiO2 NPs, the coexposure of TiO2 NPs with PSNPs resulted in increased toxicity. The adsorption of algal EPS on the NMs (both in their pristine and combined forms) significantly increased the toxic nature of the NMs against A. salina. It was observed that with an increase in the hydrodynamic diameter of the particles, the mortality, oxidative stress, and ingestion of the NMs by A. salina increased. The uptake of Ti by A. salina from 8 mg/L TiO2 NPs, EPS adsorbed 8 mg/L TiO2 NPs, 8 mg/L TiO2 NPs + NH2-PSNPs and the EPS adsorbed mixture of 8 mg/L TiO2 NPs, 8 mg/L TiO2 NPs + NH2-PSNPs was observed to be 0.043, 0.047, 0.186, and 0.307 mg/g of A. salina. The adsorption of algal EPS on the NMs (both in their pristine and combined forms) significantly increased the toxic nature of the NMs against A. salina. The major outcomes from the current study highlight the role of EPS in exacerbating the toxicity of NMs in marine crustaceans.

Abstract Background With rapid increase in the global use of various plastics, microplastics (MPs) and nanoplastics (NPs) pollution and their adverse health effects have attracted global attention. MPs have been detected out in human body and both MPs and NPs showed female reproductive toxicological effects in animal models. Miscarriage (abnormal early embryo loss), accounting for 15-25% pregnant women worldwide, greatly harms human reproduction. However, the adverse effects of NPs on miscarriage have never been explored. Results In this study, we identified that polystyrene (PS) plastics particles were present in women villous tissues. Their levels were higher in villous tissues of unexplained recurrent miscarriage (RM) patients vs. healthy control (HC) group. Furthermore, mouse assays further confirmed that exposure to polystyrene nanoplastics (PS-NPs, 50 nm in diameter, 50 or 100 mg/kg) indeed induced miscarriage. In mechanism, PS-NPs exposure (50, 100, 150, or 200 µg/mL) increased oxidative stress, decreased mitochondrial membrane potential, and increased apoptosis in human trophoblast cells by activating Bcl-2/Cleaved-caspase-2/Cleaved-caspase-3 signaling through mitochondrial pathway. The alteration in this signaling was consistent in placental tissues of PS-NPs-exposed mouse model and in villous tissues of unexplained RM patients. Supplement with Bcl-2 could efficiently suppress apoptosis in PS-NPs-exposed trophoblast cells and reduce apoptosis and alleviate miscarriage in PS-NPs-exposed pregnant mouse model. Conclusions Exposure to PS-NPs activated Bcl-2/Cleaved-caspase-2/Cleaved-caspase-3, leading to excessive apoptosis in human trophoblast cells and in mice placental tissues, further inducing miscarriage. Graphical Abstract

In recent years, the adverse effects of nanoplastics (NPs) and pyriproxyfen on aquatic environments have attracted widespread attention. However, research on their combined exposure to aquatic organisms could be more extensive. This work evaluated the acute and chronic toxic effects of polystyrene NPs (PS-NPs) and pyriproxyfen on Daphnia magna (D. magna) under their combined exposure conditions. The addition of PS-NPs within 24 h reduced the acute toxicity of pyriproxyfen to D. magna, resulting in an increase in the 24-h EC50 values of pyriproxyfen on D. magna from 0.24 mg/L to 0.35, 0.51, and 1.26 mg/L, respectively when 1, 5, and 10 mg/L of PS-NPs were added. Compared with PS-NPs, pyriproxyfen significantly disturbed the growth and reproduction of D. magna in the chronic toxicity test at 21 days. The adverse effects caused by pyriproxyfen were alleviated when PS-NPs and pyriproxyfen were co-exposed. In addition, it was observed that the addition of pyriproxyfen resulted in less PS-NPs uptake by D. magna using a time-gated imaging technique. These findings provide new insight into the combined toxic effects of NPs and pyriproxyfen on the reproduction and growth of D. magna, and it is important to understand the effects of complex pollutants on aquatic systems. Moreover, it has provided an important scientific basis for environmental protection and sustainable development. [ABSTRACT FROM AUTHOR]

It is well known that polystyrene nanoplastics (PS‐NaP) and nano‐titanium dioxide (TiO2 NPs) are frequently co‐appeared in daily life and can cause liver injury when they accumulate in the liver. Nonetheless, the combined toxicological impacts and potential molecular mechanisms of PS‐NaP and TiO2 NPs in the hepatic system have not been revealed. Thus, we conducted experiments on C57BL/6 mice exposed to PS‐NaP or/and TiO2 NPs for 4 weeks. The findings suggested that PS‐NaP and TiO2 NPs co‐exposed significantly altered the hepatic function parameters, levels of antioxidant‐related enzymes and genes expression of Keap‐1/Nrf2/ARE signaling pathway, as well as significantly increased the hepatic Ti contents, aggravated hepatic pathological and oxidative stress (OS) damage compared with individual exposure to PS‐NaP or TiO2 NPs. Using N‐Acetyl‐L‐cysteine (NAC), an OS inhibitor, we further demonstrated that OS played a pivotal role in coexposure‐induced liver injury. NAC reduced the levels of OS in mice, which mitigated co‐exposure‐induced liver injury. Taken together, we proposed that PS‐NaP and TiO2 NPs co‐exposed activated the Keap‐1, then inhibited the recognition of Nrf2 and ARE, consequently exacerbated liver injury. These findings shed light on the co‐toxicity and potential mechanism of nanoplastics and nanoparticles, which informed the risk assessment of human exposure to environmental pollutants. [ABSTRACT FROM AUTHOR]

In recent years, there has been a significant rise in the utilization of amino-functionalized polystyrene nanoplastics (PS-NH2). This surge in usage can be attributed to their exceptional characteristics, including a substantial specific surface area, high energy, and strong reactivity. These properties make them highly suitable for a wide range of industrial and medical applications. Nevertheless, there is a growing apprehension regarding their potential toxicity to aquatic organisms, particularly when considering the potential impact of heavy metals like lead (Pb) on the toxicity of PS-NH2. Herein, we examined the toxic effects of sole PS-NH2 (90 nm) at five concentrations (e.g., 0, 0.125, 0.25, 0.5, and 1 mg/L), as well as the simultaneous exposure of PS-NH2 and Pb2+ (using two environmental concentrations, e.g., 20 μg/L for Pb low (PbL) and 80 μg/L for Pb higher (PbH)) to the microalga Chlorella vulgaris. After a 96-h exposure, significant differences in chlorophyll a content and algal growth (biomass) were observed between the control group and other treatments (ANOVA, p < 0.05). The algae exposed to PS-NH2, PS-NH2 + PbL, and PS-NH2 + PbH treatment groups exhibited dose-dependent toxicity responses to chlorophyll a content and biomass. According to the Abbott toxicity model, the combined toxicity of treatment groups of PS-NH2 and PbL,H showed synergistic effects. The largest morphological changes such as C. vulgaris' size reduction and cellular aggregation were evident in the medium treated with elevated concentrations of both PS-NH2 and Pb2+. The toxicity of the treatment groups followed the sequence PS-NH2 < PS-NH2 + PbL < PS-NH2 + PbH. These results contribute novel insights into co-exposure toxicity to PS-NH2 and Pb2+ in algae communities. [ABSTRACT FROM AUTHOR]

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Background: With rapid increase in the global use of various plastics, microplastics (MPs) and nanoplastics (NPs) pollution and their adverse health effects have attracted global attention. MPs have been detected out in human body and both MPs and NPs showed female reproductive toxicological effects in animal models. Miscarriage (abnormal early embryo loss), accounting for 15-25% pregnant women worldwide, greatly harms human reproduction. However, the adverse effects of NPs on miscarriage have never been explored. Results: In this study, we identified that polystyrene (PS) plastics particles were present in women villous tissues. Their levels were higher in villous tissues of unexplained recurrent miscarriage (RM) patients vs. healthy control (HC) group. Furthermore, mouse assays further confirmed that exposure to polystyrene nanoplastics (PS-NPs, 50 nm in diameter, 50 or 100 mg/kg) indeed induced miscarriage. In mechanism, PS-NPs exposure (50, 100, 150, or 200 µg/mL) increased oxidative stress, decreased mitochondrial membrane potential, and increased apoptosis in human trophoblast cells by activating Bcl-2/Cleaved-caspase-2/Cleaved-caspase-3 signaling through mitochondrial pathway. The alteration in this signaling was consistent in placental tissues of PS-NPs-exposed mouse model and in villous tissues of unexplained RM patients. Supplement with Bcl-2 could efficiently suppress apoptosis in PS-NPs-exposed trophoblast cells and reduce apoptosis and alleviate miscarriage in PS-NPs-exposed pregnant mouse model. Conclusions: Exposure to PS-NPs activated Bcl-2/Cleaved-caspase-2/Cleaved-caspase-3, leading to excessive apoptosis in human trophoblast cells and in mice placental tissues, further inducing miscarriage. [ABSTRACT FROM AUTHOR]

Polystyrene nanoplastics are a novel class of pollutants. They are easily absorbed by living organisms, and their potential toxicity has raised concerns. However, the impact of polystyrene nanoplastics on auditory organs remains unknown. Here, our results showed that polystyrene nanoplastics entered the cochlea of mice, HEI-OC1 cells, and lateral line hair cells of zebrafish, causing cellular injury and increasing apoptosis. Additionally, we found that exposure to polystyrene nanoplastics resulted in a significant elevation in the auditory brainstem response thresholds, a loss of auditory sensory hair cells, stereocilia degeneration and a decrease in expression of Claudin-5 and Occludin proteins at the blood-lymphatic barrier in mice. We also observed a significant decrease in the acoustic alarm response of zebrafish after exposure to polystyrene nanoplastics. Mechanistic analysis revealed that polystyrene nanoplastics induced up-regulation of the Nrf2/HO-1 pathway, increased levels of malondialdehyde, and decreased superoxide dismutase and catalase levels in cochlea and HEI-OC1 cells. Furthermore, we observed that the expression of ferroptosis-related indicators GPX4 and SLC7A11 decreased as well as increased expression of ACLS4 in cochlea and HEI-OC1 cells. This study also revealed that polystyrene nanoplastics exposure led to increased expression of the inflammatory factors TNF-α, IL-1β and COX2 in cochlea and HEI-OC1 cells. Further research found that the cell apoptosis, ferroptosis and inflammatory reactions induced by polystyrene nanoplastics in HEI-OC1 cells was reversed through the pretreatment with N-acetylcysteine, a reactive oxygen species inhibitor. Overall, our study first discovered and systematically revealed the ototoxicity of polystyrene nanoplastics and its underlying mechanism. [ABSTRACT FROM AUTHOR]

Despite the development of polystyrene nanoplastics (PSNPs) in different fields, including nanotechnology, environment, industries, and their possible approach to aquatic ecosystems, a few studies have been conducted on nanoecotoxicology in aquatic animals. Therefore, this study was designed and conducted to measure the effect of toxicity of the PSNPs while transferring from the diet to the body of the fish (food concentrations=0.1, 10, and 100 mg/kg) on juvenile rainbow trout (Oncorhynchus mykiss) in a 28-day chronic treatment and the control group (food concentration = 0 mg/kg) after the 7-day adaptation period, in three repetitions (15 juvenile trout were included in each repetition per concentration). Depending on the target test, fish sampling in the treatment group was taken after 24 h without food. According to the results, the survival rate (SR) (84.44 ± 3.14%) was significantly reduced with the highest dose of PSNPs compared to other treatments (P<0.05). But other growth indices did not show statistically significant difference (P>0.05). From the point of view of tissue pathology of polystyrene nanoplastic in the liver tissue in treatment 3 and 4, injuries such as vacuolation, necrosis, sinusoidal expansion and pyknotic nucleus were observed in rainbow trout. Based on the obtained results, the negative effects of polystyrene nanoplastic release on health and immunity at the cellular level were seen in liver histology in the studied aquatic sample. In general, this study showed that the entry of nanoplastic particles through the digestive tract causes changes in the histological parameters of the liver. However, more comprehensive studies are needed in this field. [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.

Introduction: It has been shown that polystyrene nanoplastic (PS-NP) exposure induces toxicity in the lungs. Objectives: This study aims to provide foundational evidence to corroborate that ferroptosis and abnormal HIF-1α activity are the main factors contributing to pulmonary dysfunction induced by PS-NP exposure. Methods: Fifty male and female C57BL/6 mice were exposed to distilled water or 100 nm or 200 nm PS-NPs via intratracheal instillation for 7 consecutive days. Hematoxylin and eosin (H&E) and Masson trichrome staining were performed to observe the histomorphological changes in the lungs. To clarify the mechanisms of PS-NP-induced lung injury, we used 100 μg/ml, 200 μg/ml and 400 μg/ml 100 or 200 nm PS-NPs to treat the human lung bronchial epithelial cell line BEAS-2B for 24 h. RNA sequencing (RNA-seq) of BEAS-2B cells was performed following exposure. The levels of glutathione, malondialdehyde, ferrous iron (Fe2+), and reactive oxygen species (ROS) were measured. The expression levels of ferroptotic proteins were detected in BEAS-2B cells and lung tissues by Western blotting. Western blotting, immunohistochemistry, and immunofluorescence were used to evaluate the HIF-1α/HO-1 signaling pathway activity. Results: H&E staining revealed substantial perivascular lymphocytic inflammation in a bronchiolocentric pattern, and Masson trichrome staining demonstrated critical collagen deposits in the lungs after PS-NP exposure. RNA-seq revealed that the differentially expressed genes in PS-NP-exposed BEAS-2B cells were enriched in lipid metabolism and iron ion binding processes. After PS-NP exposure, the levels of malondialdehyde, Fe2+, and ROS were increased, but glutathione level was decreased. The expression levels of ferroptotic proteins were altered significantly. These results verified that PS-NP exposure led to pulmonary injury through ferroptosis. Finally, we discovered that the HIF-1α/HO-1 signaling pathway played an important role in regulating ferroptosis in the PS-NP-exposed lung injury. Conclusion: PS-NP exposure caused ferroptosis in bronchial epithelial cells by activating the HIF-1α/HO-1 signaling pathway, and eventually led to lung injury.

Contamination of the environment with nano- and microplastic particles exerts a threatening impact on the aquatic ecosystems and sustainable catfish aquaculture. The presence of nanoplastics has been found to have a detrimental impact on both aquatic and terrestrial ecosystems. The present study examines the effect of polystyrene nanoplastics (PS NPs) on the DNA, erythrocytes, oxidative status and renal histology of catfish, in addition to the potential protective effects of Chlorella vulgaris bioremediation and selenium to hinder this effect. Six equal groups of fish were used as follows: Group 1 served as a control group and received water free from PS NPs; Group 2 was exposed to PS NPs at a concentration of 5 mg/L; Group 3 was exposed to PS NPs (5 mg/L) + selenium (1 mg/kg diet); Group 4 was exposed to PS NPs (5 mg/L) + C. vulgaris (25 g/kg diet); Group 5 was supplemented with C. vulgaris (25 g/kg diet); and Group 6 was supplemented with selenium (1 mg/kg diet). The exposure period was 30 days. The results indicated that PS NPs induced oxidative stress by significantly elevating malondialdehyde activities and slightly reducing antioxidant biomarkers, resulting in DNA damage, increased frequency of micronuclei, erythrocyte alterations, and numerous histopathological alterations in kidney tissue. Selenium and C. vulgaris significantly ameliorated the oxidative/antioxidant status, reducing DNA damage, micronucleus frequency, erythrocyte alterations, and improving the morphology of kidney tissue. Nevertheless, further research is needed for a profound understanding of the mechanism behind the toxicity of nano-microplatics in aquatic systems. [ABSTRACT FROM AUTHOR]

[Display omitted] • The specific mechanisms of PS-NP-induced pulmonary injury are unclear. • A mouse model of lung injury is created based on the real-world NP exposure in human. • PS-NP exposure induces ferroptosis in lung tissues and bronchial epithelial cells. • HIF-1α inhibition rescues PS-NP-induced ferroptosis in bronchial epithelial cells. • PS-NP exposure induces ferroptosis via the HIF-1α/HO-1 signaling pathway in lungs. It has been shown that polystyrene nanoplastic (PS-NP) exposure induces toxicity in the lungs. This study aims to provide foundational evidence to corroborate that ferroptosis and abnormal HIF-1α activity are the main factors contributing to pulmonary dysfunction induced by PS-NP exposure. Fifty male and female C57BL/6 mice were exposed to distilled water or 100 nm or 200 nm PS-NPs via intratracheal instillation for 7 consecutive days. Hematoxylin and eosin (H&E) and Masson trichrome staining were performed to observe the histomorphological changes in the lungs. To clarify the mechanisms of PS-NP-induced lung injury, we used 100 μg/ml, 200 μg/ml and 400 μg/ml 100 or 200 nm PS-NPs to treat the human lung bronchial epithelial cell line BEAS-2B for 24 h. RNA sequencing (RNA-seq) of BEAS-2B cells was performed following exposure. The levels of glutathione, malondialdehyde, ferrous iron (Fe2+), and reactive oxygen species (ROS) were measured. The expression levels of ferroptotic proteins were detected in BEAS-2B cells and lung tissues by Western blotting. Western blotting, immunohistochemistry, and immunofluorescence were used to evaluate the HIF-1α/HO-1 signaling pathway activity. H&E staining revealed substantial perivascular lymphocytic inflammation in a bronchiolocentric pattern, and Masson trichrome staining demonstrated critical collagen deposits in the lungs after PS-NP exposure. RNA-seq revealed that the differentially expressed genes in PS-NP-exposed BEAS-2B cells were enriched in lipid metabolism and iron ion binding processes. After PS-NP exposure, the levels of malondialdehyde, Fe2+, and ROS were increased, but glutathione level was decreased. The expression levels of ferroptotic proteins were altered significantly. These results verified that PS-NP exposure led to pulmonary injury through ferroptosis. Finally, we discovered that the HIF-1α/HO-1 signaling pathway played an important role in regulating ferroptosis in the PS-NP-exposed lung injury. PS-NP exposure caused ferroptosis in bronchial epithelial cells by activating the HIF-1α/HO-1 signaling pathway, and eventually led to lung injury. [ABSTRACT FROM AUTHOR]

Nanoplastics, as a hot topic of novel contaminants, lack extensive concern in higher plants; especially the potential impact and mechanism of nanoplastics on legume crops remains elusive. In this study, the toxicity of polystyrene nanoplastics (PS-NPs, 200 nm) with diverse doses (control, 10, 50, 100, 200, 500 mg/L) to soybean and mung bean plants grown hydroponically for 7 d was investigated at both the macroscopic and molecular levels. The results demonstrated that the root length of both plants was markedly suppressed to varying degrees. Similarly, mineral elements (Fe, Zn) were notably decreased in soybean roots, consistent with Cu alteration in mung bean. Moreover, PS-NPs considerably elevated malondialdehyde (MDA) levels only in soybean roots. Enzyme activity data indicated mung bean exhibited significant damage only at higher doses of PS-NPs stress than soybean, implying mung bean is more resilient. Transcriptome analysis showed that PS-NPs stimulated the expression of genes associated with the antioxidant system in plant roots. Furthermore, starch and sucrose metabolism might play a key role in coping with PS-NPs to enhance soybean resistance, but the MAPK pathway was enriched in mung bean. Our findings provide valuable perspectives for an in-depth understanding of the performance of plants growing in waters contaminated by nanoplastics. [ABSTRACT FROM AUTHOR]

Abstract Background Many studies have investigated how nanoplastics (NPs) exposure mediates nerve and intestinal toxicity through a dysregulated brain-gut axis interaction, but there are few studies aimed at alleviating those effects. To determine whether and how vitamin D can impact that toxicity, fish were supplemented with a vitamin D-low diet and vitamin D-high diet. Results Transmission electron microscopy (TEM) showed that polystyrene nanoplastics (PS-NPs) accumulated in zebrafish brain and intestine, resulting in brain blood–brain barrier basement membrane damage and the vacuolization of intestinal goblet cells and mitochondria. A high concentration of vitamin D reduced the accumulation of PS-NPs in zebrafish brain tissues by 20% and intestinal tissues by 58.8% and 52.2%, respectively, and alleviated the pathological damage induced by PS-NPs. Adequate vitamin D significantly increased the content of serotonin (5-HT) and reduced the anxiety-like behavior of zebrafish caused by PS-NPs exposure. Virus metagenome showed that PS-NPs exposure affected the composition and abundance of zebrafish intestinal viruses. Differentially expressed viruses in the vitamin D-low and vitamin D-high group affected the secretion of brain neurotransmitters in zebrafish. Virus AF191073 was negatively correlated with neurotransmitter 5-HT, whereas KT319643 was positively correlated with malondialdehyde (MDA) content and the expression of cytochrome 1a1 (cyp1a1) and cytochrome 1b1 (cyp1b1) in the intestine. This suggests that AF191073 and KT319643 may be key viruses that mediate the vitamin D reduction in neurotoxicity and immunotoxicity induced by PS-NPs. Conclusion Vitamin D can alleviate neurotoxicity and immunotoxicity induced by PS-NPs exposure by directionally altering the gut virome. These findings highlight the potential of vitamin D to alleviate the brain-gut-virome disorder caused by PS-NPs exposure and suggest potential therapeutic strategies to reduce the risk of NPs toxicity in aquaculture, that is, adding adequate vitamin D to diet. Video Abstract

Nanoplastics, as emerging environmental pollutants, can transport contaminants across marine environments, polluting pristine ecosystems and being ingested by marine organisms. This transfer poses a severe threat to global aquatic ecosystems and potentially impacts human health through the food chain. Neurobehavioral and reproductive toxicity are critical areas of concern because they directly affect the survival, health, and population dynamics of aquatic species, which can have cascading effects on the entire ecosystem. Using zebrafish as a model organism, we investigated the toxic effects of environmental concentrations of polystyrene nanoplastics (PS-NPs). Behavioral assessments, including the novel tank test and open field test, demonstrated significant neurobehavioral changes, indicating increased anxiety and depressive behaviors. A pathological analysis of brain and gonadal tissues, along with evaluations of neurobehavioral and reproductive toxicity biomarkers, revealed that exposure to PS-NPs leads to brain tissue lesions, inflammatory responses, oxidative stress activation, hormone level disruptions, and gonadal damage. Real-time quantitative PCR studies of reproductive gene expression further showed that PS-NPs disrupt the endocrine regulation pathways of the brain-pituitary-gonadal (BPG) axis, causing reproductive toxicity with sex-specific differences. These findings provide crucial insights into the impacts of nanoplastics on aquatic organisms and their ecological risks, offering theoretical support for future environmental protection and pollutant management efforts.

Polystyrene nanoplastics (PS-NPs) are widely used in industry, pharmaceutical and consumer packaging materials, and medical products. The biological health impacts of PS-NPs are receiving increasing attention. Therefore, it is necessary to conduct a literature review of in vitro and in vivo experimental studies from a biological mechanism perspective. Based on the latest research results at home and abroad, this review introduced the characteristics and cell internalization of PS-NPs in cytotoxicity experiments, and summarized the effects of PS-NPs on cytotoxic targets such as mitochondria, lysosomes, proteins, and DNA. In addition, the influencing factors of the health effects of PS-NPs were analyzed from the aspects of physical and chemical properties and cell types. Finally, by discussing the current research hotspots of cytotoxicity mechanism and biological effects, it was anticipated to provide a reference for the health risk management and biological safety assessment of PS-NPs.

Polystyrene nanoplastics (PS-NPs) are environmental pollutants that induce oxidative stress (OS) in multiple organs particularly, liver. Sinensetin (SNS) is a naturally present flavones that shows diverse pharmaceutical properties i.e., anti-oxidant, anti-inflammatory and anti-apoptotic. Therefore, the present study was designed to evaluate the therapeutic role of SNS against PS-NPs induced hepatotoxicity. 48 rats were distributed into 4 groups i.e., control, PS-NPs (50 µgkg−1) treated, PS-NPs + SNS (50 µgkg−1 + 20 mgkg−1) co-treated and only SNS (20 mgkg−1) treated group. PS-NPs intoxication reduced the activities of catalase (CAT), glutathione-S-transferase (GST), superoxide dismutase (SOD), glutathione peroxidases (GPx) glutathione reductase (GSR) and glutathione (GSH) level, whereas increased the levels of ROS and MDA. Additionally, PS-NPs increased the levels of liver serum marker enzymes i.e., alanine transaminase (ALT), alkaline phosphatase (ALP) and aspartate aminotransferase (AST). Moreover, the level of inflammatory makers such as nuclear factor-kappa B (NF-κB), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), interleukin-1 beta (IL-1β) and cyclooxygenase-2 (COX-2) activity were increased following the PS-NPS exposure. The intoxication of PS-NPs elevated Caspase-3, Bax and Caspase-9 levels, while reducing the Bcl-2 level. Furthermore, the exposure of PS-NPs induced significant histopathological damages in hepatic tissue of rats. However, the supplementation of SNS considerably improved the PS-NPs induced damages as well as histological changes due to its hepatoprotective, anti-inflammatory, anti-apoptotic and anti-oxidant nature.

Polystyrene nanoplastics (PS-NPs) are ubiquitous environmental pollutants that can cause oxidative stress in various organs, including the liver. Didymin is a dietary flavanone that displays multiple pharmacological activities. Therefore, the present study evaluated the palliative role of didymin against PS-NPs-induced hepatic damage in rats. Albino rats (n=48) were randomly distributed into 4 groups: control, PS-NPs treated group, PS-NPs + didymin co-administered group, and didymin supplemented group. After 30 days, PS-NPs intoxication lowered the expression of Nrf-2 and anti-oxidant genes [catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GSR), glutathione-S-transferase (GST), and heme oxygenase-1 (HO-1)], whereas the expression of KEAP1 kelch like ECH associated protein 1 (Keap-1) was increased. PS-NPs exposure also reduced the activities of anti-oxidants enzymes (CAT, SOD, GPx, GSR, GST, GSH, and OH-1), while malondialdehyde (MDA) and reactive oxygen species (ROS) levels were increased. The levels of alanine transaminase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) were increased in PS-NPs-exposed rats. Moreover, inflammatory indices [interleukin-1β (IL-1β), tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), nuclear factor-kappa B (NF-κB), and cyclooxygenase-2 (COX-2)] were increased in PS-NPs-exposed rats. Furthermore, PS-NPs intoxication increased the expressions of apoptotic markers including Bax and Caspase-3, as well as reducing Bcl-2 expression. The histopathological analysis showed significant damage in PS-NPs-treated rats. However, didymin supplementation ameliorated all the PS-NPs-induced damage in the liver of rats. Therefore, it was concluded that didymin can act as a remedy against PS-NPs-induced liver toxicity due to its anti-apoptotic, anti-oxidant, and anti-inflammatory activities.

Micro(nano)plastics are prevalent in the environment, and prolonged exposure to them represents a threat to human health. The goal of this study is to assess the health risk of long-term exposure to nanoplastics (NPs) at environmental concentrations on the intestinal mechanical and immune barrier in mice. In this study, mice were provided drinking water containing polystyrene NPs (PS-NPs; 0.1, 1, and 10 mg·L−1) for 32 consecutive weeks. The levels of endocytosis proteins caveolin and clathrin and of tight junctional proteins claudin-1, occludin, and ZO-1, and morphological changes, proportion of lymphocytes B in MLNs and lymphocytes T in IELs and LPLs were determined by immunohistochemistry, hematoxylin–eosin, and flow cytometry assays in the intestinal tissues of mice at 28 weeks. The activities or concentrations of ROS, SOD, MDA, and GSH-Px and inflammatory factors (IL-1β, IL-6, and TNF-α) in the intestinal tissues of mice were measured by ELISA at 12, 16, 20, 24, and 32 weeks. Compared with the control group, oral ingested PS-NPs entered the intestinal tissues of mice and upregulated expression levels of the clathrin and caveolin. The intestinal tissue structure of mice in the PS-NPs (1 and 10 mg·L−1) exposure groups showed significant abnormalities, such as villus erosion, decreased of crypts numbers and large infiltration of inflammatory cells. Exposure to 0.1 mg·L−1 PS-NPs decreased occludin protein levels, but not claudin-1 and ZO-1 levels. The levels of these three tight junction proteins decreased significantly in the 1 and 10 mg·L−1 PS-NPs exposed groups. Exposure to PS-NPs led to a significant time- and dose-dependent increase in ROS and MDA levels, and concurrently decreased GSH-Px and SOD contents. Exposure to PS-NPs increased the proportion of B cells in MLNs, and decreased the proportion of CD8+ T cells in IELs and LPLs. The levels of pro-inflammatory cytokines IL-6, TNF-α and IL-1β were markedly elevated after PS-NPs exposure. Long-term PS-NPs exposure impaired intestinal mechanical and immune barrier, and indicate a potentially significant threat to human health.

Background: Many studies have investigated how nanoplastics (NPs) exposure mediates nerve and intestinal toxicity through a dysregulated brain-gut axis interaction, but there are few studies aimed at alleviating those effects. To determine whether and how vitamin D can impact that toxicity, fish were supplemented with a vitamin D-low diet and vitamin D-high diet. Results: Transmission electron microscopy (TEM) showed that polystyrene nanoplastics (PS-NPs) accumulated in zebrafish brain and intestine, resulting in brain blood–brain barrier basement membrane damage and the vacuolization of intestinal goblet cells and mitochondria. A high concentration of vitamin D reduced the accumulation of PS-NPs in zebrafish brain tissues by 20% and intestinal tissues by 58.8% and 52.2%, respectively, and alleviated the pathological damage induced by PS-NPs. Adequate vitamin D significantly increased the content of serotonin (5-HT) and reduced the anxiety-like behavior of zebrafish caused by PS-NPs exposure. Virus metagenome showed that PS-NPs exposure affected the composition and abundance of zebrafish intestinal viruses. Differentially expressed viruses in the vitamin D-low and vitamin D-high group affected the secretion of brain neurotransmitters in zebrafish. Virus AF191073 was negatively correlated with neurotransmitter 5-HT, whereas KT319643 was positively correlated with malondialdehyde (MDA) content and the expression of cytochrome 1a1 (cyp1a1) and cytochrome 1b1 (cyp1b1) in the intestine. This suggests that AF191073 and KT319643 may be key viruses that mediate the vitamin D reduction in neurotoxicity and immunotoxicity induced by PS-NPs. Conclusion: Vitamin D can alleviate neurotoxicity and immunotoxicity induced by PS-NPs exposure by directionally altering the gut virome. These findings highlight the potential of vitamin D to alleviate the brain-gut-virome disorder caused by PS-NPs exposure and suggest potential therapeutic strategies to reduce the risk of NPs toxicity in aquaculture, that is, adding adequate vitamin D to diet. A5myG_s1qHAhSjY9k6V2Q1 Video Abstract [ABSTRACT FROM AUTHOR]

Polystyrene nanoplastics (PS-NPs) have recently been found to be present in human blood and kidney. However, the renal toxicity of PS-NPs and the underlying mechanisms have not been fully elucidated. Here, we found that exposure of PS-NPs induced apoptosis of human renal proximal tubular epithelial cells (HK-2) in a size- and dose-dependent manner as revealed by AnnexinV-FITC assay. In addition, PS-NPs promoted ROS production and caused structure changes of mitochondrial and endoplasmic reticulum. Mechanistically, transcriptional sequencing indicated the involvement of MAPK pathway in apoptosis, which was further confirmed by the upregulation of p-p38, p-ERK, CHOP, BAX, cytochrome C, and caspase 3 expression. This study clarified the molecular mechanism underlying PS-NP-induced apoptosis in HK-2 cells and contributed to our risk estimation of PS-NPs in human kidney. [ABSTRACT FROM AUTHOR]

The occurrence of nanoplastics in agricultural land is a potential threat to human health and food security, yet the fate of nanoplastics is soil–root systems is poorly known. Here we investigated the aggregation behavior of polystyrene nanoplastics bearing different charges in cucumber root exudates and soil leachate, and in the presence of common environmental Ca2+ ions. Results show an increase in the aggregation size of positively charged amino-modified polystyrene nanoplastics, whereas negatively charged nanoplastics did not aggregate and showed no significant changes in particle size. This is possibly due to the adsorption of organic acids from soil leachates and root exudates onto the surfaces of nanoparticles. We observed that the critical condensation concentrations of Ca2+ for negatively charged nanoplastics increased by more than 1.4 times in root exudates and soil leachates compared with that in deionized water. Our findings suggest that root exudates and soil leachates can reduce the aggregation of negatively charged nanoplastics in Ca2+ solutions. [ABSTRACT FROM AUTHOR]

Nanoplastics (NPs) has become a worrying serious environmental problem. However, the toxicological effects and mechanisms of NPs on hematopoiesis are still unknown. To this end, male C57BL/6J mice were directly exposed to the serial concentration gradient of polystyrene NPs (PSNPs, 0, 30, 60, and 120 μg d), respectively, for 42 days by intragastric administration. Results show that PSNPs were clearly visible in bone tissues, meanwhile, induced the count of major blood indicators (WBC, RBC, and LYM) decreased. H&E staining displayed that exposed to PSNPs can cause hematopoietic damage of BM and extramedullary hematopoiesis in spleen. Flow cytometry result show that the proportion of LSK represented a dose‐dependent significantly decreased after PSNPs exposure. Further research found that PSNPs can cause the systemic oxidative stress occurs manifested as MDA accumulated. In addition, as the dose of PSNPs increased, the fluorescence intensity of Keap1 and p53 in femur sections gradually increased, meanwhile, the expression of cell oxeiptosis signal pathway Keap1/PGAM5/AIFM1 and the cell senescence signal pathway p53/p21 was all increased, markedly. Overall, our study demonstrated that PSNPs exposure caused oxidative stress, potentially resulting in cell oxeiptosis and senescence to develop haematotoxicity in C57BL/6J mice. [ABSTRACT FROM AUTHOR]

Background: The effects of polystyrene nanoplastic (PS-NP) on the human body is a matter of global concern, as they are mainly absorbed through the food chain after release into the water ecosystem. In this study, mucin (Mu) was extracted from Aurelia aurita and its effect to reduce the toxicity of PS-NP present in water was verified. However, the effect of Mu on genotoxicity was not verified. Objective: Zebrafish embryos were exposed to PS-NP, Mu, and Mu + PS-NP to verify their effects on genotoxicity. Based on the subsequent phenotypic anomalies in the juvenile fish, mRNA sequencing (mRNA-seq) was employed to determine the changes in the levels of gene transcription induced by PS-NP. Results: Compared with the control group, the experimental group exposed to Mu or PS-NP + Mu showed no specific variations in phenotypic anomalies. In contrast, the experimental group exposed to PS-NP alone showed effects, such as pericardial edema, yolk-sac edema, thicker yolk, tail deformity, and spinal curvature. Analyses of differentially expressed genes (DEGs) indicated that changes in gene expression occurred in 340, 16, and 17 genes in the PS-NP, Mu, and PS-NP + Mu groups, respectively. Conclusion: Our results showed that PS-NP induced changes in mRNA expression and had toxic effects that caused phenotypic anomalies in the zebrafish embryos. However, further studies are necessary to investigate the effects of different types of plastic and properties on genotoxicity and phenotypic anomalies in aquatic organisms. A trend of reduction was found in genotoxicity and phenotypic anomalies when the embryos were exposed to PS-NP together with Mu, suggesting that Mu extracted from Aurelia aurita could reduce the genotoxicity of PS-NP. [ABSTRACT FROM AUTHOR]

Copyright of Asian Journals of Ecotoxicology is the property of Gai Kan Bian Wei Hui and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The ubiquitous nature of plastics, particularly nanoplastics, raises concern about their potential effects on primary producer microalgae. Currently, the impacts and potential mechanisms of nanoplastics on microalgae are not fully understood. In this study, the effects of two plain commercial polystyrene nanoplastics (PS-NPs) with different sizes (50 nm and 70 nm) on C. vulgaris were assessed in a concentration range of 0–50 mg/L during 72 h exposure periods. Results revealed that both PS-NPs have dose-dependent toxicity effects on C. vulgaris, as confirmed by the decrease of growth rates, chlorophyll a and esterase activities, and the increase of ROS, MDA, and membrane damage. The membrane damage was caused by the agglomeration of PS-NPs on microalgae and may be the key reason for the toxicity. Compared with 70 nm PS-NPs (72 h EC50 >50 mg/L), 50 nm PS-NPs posed greater adverse effects on algae, with an EC50–72h of 19.89 mg/L. FTIR results also proved the stronger variation of macromolecules in the 50 nm PS-NPs treatment group. This phenomenon might be related to the properties of PS-NPs in exposure medium. The lower absolute zeta potential value of 50 nm PS-NPs induced the stronger interaction between PS-NPs and algae as compared to 70 nm PS-NPs, leading to severe membrane damage and the loss of esterase activity as well as settlement. These findings emphasized the importance of considering the impacts of commercial PS-NPs properties in toxicity evaluation. [ABSTRACT FROM AUTHOR]

The continuous release of nanoparticles and nanoplastics into the marine environment necessitates the examination of their combined effects in marine organisms. Natural Organic Matter (NOM) can significantly influence the behavior of nanomaterials in the marine environment. The present study explores the effects of algal Extracellular Polymeric Substances (EPS) in reducing the combined toxic effects of three different polystyrene nanoplastics (PSNPs)— aminated (NH2-PSNPs), carboxylated (COOH-PSNPs), and plain PSNPs — and P25 titanium dioxide nanoparticles (Nano-TiO2) towards the marine alga, Chlorella sp. Two doses (0.25 and 2.5 mg/L) of nano-TiO2 mixed with the PSNPs (1 mg/L) were employed. The COOH-PSNPs with 2.5 mg/L nano-TiO2 exhibited higher growth inhibition toward algal cells. Addition of algal EPS to the mixture of NMs decreased the negative effect significantly. The mean hydrodynamic diameter increased significantly from 666 to 797 nm and 1248 to 3589 nm at concentrations 0.25 and 2.5 mg/L, respectively when the mixtures of nano-TiO2 and COOH-PSNPs were incubated with the algal EPS. In comparison to the pristine NMs, the EPS-NMs were found to significantly reduce the superoxide and hydroxyl radical production. The results were further validated with the estimation of lipid peroxidation (LPO), esterase activity, photosynthetic efficiency, and membrane permeability in the cells. The major outcomes from this study highlight the role of algal EPS in significantly reducing the toxic impact of binary mixture of NMs in marine organisms. [ABSTRACT FROM AUTHOR]

Nanoplastics (NPs), regarded as the emerging contaminants, can enter and be mostly accumulated in the digest tract, which pose the potential threat to intestinal health. In this study, mice were orally exposed to polystyrene (PS), PS-COOH and PS-NH2 NPs with the size of ∼100 nm at a human equivalent dose for 28 consecutive days. All three kinds of PS-NPs triggered Crohn’s ileitis-like features, such as ileum structure impairment, increased proinflammatory cytokines and intestinal epithelial cell (IEC) necroptosis, and PS-COOH/PS-NH2 NPs exhibited higher adverse effects on ileum tissues. Furthermore, we found PS-NPs induced necroptosis rather than apoptosis via activating RIPK3/MLKL pathway in IECs. Mechanistically, we found that PS-NPs accumulated in the mitochondria and subsequently caused mitochondrial stress, which initiated PINK1/Parkin-mediated mitophagy. However, mitophagic flux was blocked due to lysosomal deacidification caused by PS-NPs, and thus led to IEC necroptosis. We further found that mitophagic flux recovery by rapamycin can alleviate NP-induced IEC necroptosis. Our findings revealed the underlying mechanisms concerning NP-triggered Crohn’s ileitis-like features and might provide new insights for the further safety assessment of NPs.

Nanoplastics, as a hot topic of novel contaminants, lack extensive concern in higher plants; especially the potential impact and mechanism of nanoplastics on legume crops remains elusive. In this study, the toxicity of polystyrene nanoplastics (PS-NPs, 200 nm) with diverse doses (control, 10, 50, 100, 200, 500 mg/L) to soybean and mung bean plants grown hydroponically for 7 d was investigated at both the macroscopic and molecular levels. The results demonstrated that the root length of both plants was markedly suppressed to varying degrees. Similarly, mineral elements (Fe, Zn) were notably decreased in soybean roots, consistent with Cu alteration in mung bean. Moreover, PS-NPs considerably elevated malondialdehyde (MDA) levels only in soybean roots. Enzyme activity data indicated mung bean exhibited significant damage only at higher doses of PS-NPs stress than soybean, implying mung bean is more resilient. Transcriptome analysis showed that PS-NPs stimulated the expression of genes associated with the antioxidant system in plant roots. Furthermore, starch and sucrose metabolism might play a key role in coping with PS-NPs to enhance soybean resistance, but the MAPK pathway was enriched in mung bean. Our findings provide valuable perspectives for an in-depth understanding of the performance of plants growing in waters contaminated by nanoplastics.

Contamination of the environment with nano- and microplastic particles exerts a threatening impact on the aquatic ecosystems and sustainable catfish aquaculture. The presence of nanoplastics has been found to have a detrimental impact on both aquatic and terrestrial ecosystems. The present study examines the effect of polystyrene nanoplastics (PS NPs) on the DNA, erythrocytes, oxidative status and renal histology of catfish, in addition to the potential protective effects of Chlorella vulgaris bioremediation and selenium to hinder this effect. Six equal groups of fish were used as follows: Group 1 served as a control group and received water free from PS NPs; Group 2 was exposed to PS NPs at a concentration of 5 mg/L; Group 3 was exposed to PS NPs (5 mg/L) + selenium (1 mg/kg diet); Group 4 was exposed to PS NPs (5 mg/L) + C. vulgaris (25 g/kg diet); Group 5 was supplemented with C. vulgaris (25 g/kg diet); and Group 6 was supplemented with selenium (1 mg/kg diet). The exposure period was 30 days. The results indicated that PS NPs induced oxidative stress by significantly elevating malondialdehyde activities and slightly reducing antioxidant biomarkers, resulting in DNA damage, increased frequency of micronuclei, erythrocyte alterations, and numerous histopathological alterations in kidney tissue. Selenium and C. vulgaris significantly ameliorated the oxidative/antioxidant status, reducing DNA damage, micronucleus frequency, erythrocyte alterations, and improving the morphology of kidney tissue. Nevertheless, further research is needed for a profound understanding of the mechanism behind the toxicity of nano-microplatics in aquatic systems.

Both of nanoplastics (NPs) and Tetrabromobisphenol A (TBBPA) are organic pollutants widely detected in the environment and organisms. The large specific surface area of NPs makes them ideal vectors for carrying various toxicants, such as organic pollutants, metals, or other nanomaterials, posing potential threats to human health. This study used Caenorhabditis elegans (C. elegans) to investigate the neurodevelopmental toxicity induced by combined exposure of TBBPA and polystyrene NPs. Our results showed that combined exposure caused synergistic inhibitory effects on the survival rate, body length/width, and locomotor ability. Furthermore, the overproduction of reactive oxygen species (ROS), lipofuscin accumulation, and dopaminergic neuronal loss suggested that oxidative stress was involved in induction of neurodevelopmental toxicity in C. elegans. The expressions of Parkinson's disease related gene (pink-1) and Alzheimer's disease related gene (hop-1) were significantly increased after combined exposure of TBBPA and polystyrene NPs. Knock out of pink-1 and hop-1 genes alleviated the adverse effects such as growth retardation, locomotion deficits, dopaminergic loss, and oxidative stress induction, indicating that pink-1 and hop-1 genes play an important role in neurodevelopmental toxicity induced by TBBPA and polystyrene NPs. In conclusion, TBBPA and polystyrene NPs had synergistic effect on oxidative stress induction and neurodevelopmental toxicity in C. elegans, which was mediated through increased expressions of pink-1 and hop-1. [ABSTRACT FROM AUTHOR]