As a novel pollutant, microplastic pollution has become a global environmental concern. Melatonin (MT) has a protective effect on the damage caused by pollutants. However, there is still a lack of research on the transgenerational toxicity of microplastics and the alleviation of microplastics toxicity by MT. In this study, the adult zebrafish was exposed to (0, 0.1 and 1 mg/L) polystyrene nanoplastics (PSNP) with or without (1 μM) MT for 14 days, and embryos (F1) were used for experiments. Our study found that long-term exposure of parents to 1 mg/L PSNP reduced fertilization rate and survival rate of offspring, increased the deformity rate and induced embryos to hatch in advance. The growth inhibition of offspring was related to the gene transcription of the growth hormone/insulin-like growth factor axis. Moreover, PSNP caused oxidative stress in offspring, damaged immune system, reduced antioxidant capacity and induced apoptosis. MT supplementation could effectively alleviate the developmental toxicity and oxidative damage of offspring, but the negative effects brought by PSNP could not be completely eliminated. Our research provided a new reference for the protective effect of MT on transgenerational toxicity induced by PSNP.

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.

Nanoplastics (NPs), which belong to emerging environmental pollutants, threaten environmental sustainability and human health. Despite recent studies have reported that NPs damage the gastrointestinal tract and immune homeostasis, the underlying mechanisms remain unclear. Polyphenols have been found to promote NPs excretion by interacting with intestinal flora (IF). However, the potential mechanisms and action targets of this are still poorly understood. To address these knowledge gaps, we investigated the impact of quercetin and three concentrations of polystyrene nanoplastics (PS-NPs) in mice using an integrated phenotypic and multi-omics analysis. Our findings demonstrated that PS-NPs accumulate within the intestine, resulting in impairments to intestinal tissue and barrier function, as well as disturbing the expression of immune-response small intestinal genes and composition of IF. Exposure to PS-NPs significantly elevate the level of intestinal IgG and CD20+ B cells, while inhibiting T cells activation. Furthermore, PS-NPs could induce systemic immune and serum insulin level disorders. Quercetin might mitigate PS-NPs-induced intestinal damage and immune disorders though reversing IF disorders, gene expression changes, and their interaction.

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.

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.

Novel pollutants nanoplastics (NPs) are widely distributed in aquatic environments and may pose a health threat to aquatic organisms. Notably, the contribution of NPs to the occurrence of viral diseases in aquatic animals remains largely uncertain. In this study, the effects of polystyrene nanoplastics (PS-NPs) on Largemouth bass ranavirus (LMBV)-infected MsF cells were investigated. MsF cells took up PS-NPs in a time- and dose-dependent manner and significantly affect cell viability at an exposure concentration of 500 μg/mL. Western blot and qPCR assays indicated that exposure to PS-NPs accelerated LMBV replication in MsF cells. PS-NPs act synergistically with LMBV to disrupt the cellular antioxidant system, as evidenced by increased ROS production and decreased mRNA levels of antioxidant-associated genes. Furthermore, PS-NPs was found to exacerbate LMBV-induced inflammatory responses, as demonstrated by disturbed expression of inflammation-related factors. In addition, our results suggest that PS-NPs reduce IFN production by inhibiting the expression of molecules related to the cGAS-STING signaling pathway, thereby promoting viral replication. Collectively, our findings suggest the potential threat of NPs to infectious diseases caused by freshwater fish viruses and provide new insights for fish disease prevention and control.

Nanoplastics represent a global environmental concern due to their ubiquitous presence and potential adverse impacts on public and environmental health. There is a growing need to advance the mechanistic understanding of their reactivity as they interact with biological and environmental systems. Herein, for the first time, we report that polystyrene nanoplastics (PSNPs) have intrinsic peroxidase-like activity and are able to mediate oxidative stress. The peroxidase-like activity is dependent on temperature and pH, with a maximum at pH 4.5 and 40 °C. The catalytic activity exhibits saturation kinetics, as described by the Michaelis-Menten model. The peroxidase-like activity of PSNPs is attributed to their ability to mediate electron transfer from peroxidase substrates to H2O2. Ozone-induced PSNP aging can introduce oxygen-containing groups and disrupt aromatic structures on the nanoplastic surface. While ozonation initially enhances peroxidase-like activity by increasing oxygen-containing groups without degrading many aromatic structures, extended ozonation destroys aromatic structures, significantly reducing this activity. The peroxidase-like activity of PSNPs can mediate oxidative stress, which is generally positively correlated with their aromatic structures, as suggested by the ascorbic acid assay. These results help explain the reported oxidative stress exerted by nanoplastics and provide novel insights into their environmental and public health implications.

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.

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.

Plastic nanoparticles are extensively used in various products, leading to inevitable pollution in soil. Understanding their transport in soils where various organic substances exist is crucial. This study examined the impact of low-molecular-weight organic acids (LMWOAs) on the transport of polystyrene nanoplastics (PS-NPs) through saturated quartz sand. The experiments involved three dibasic acids-malonic acid (MA1), malic acid (MA2) and tartaric acid (TA) - and four monobasic acids- formic acid (FA), acetic acid (AA), propanoic acid (PA) and glycolic acid (GA) -under different pH levels (4.0, 5.5, 7.0) and in the presence of cations (Na+, Ca2+). The results demonstrated that in the presence of Na+, dibasic acids significantly enhanced PS-NPs transport, with TA being the most effective, followed by MA2 and MA1. This enhancement is attributed to the adsorption of LMWOAs onto the nanoparticles and sand, creating a more negative ζ-potential, which increases the electrostatic repulsion and decreases the PS-NPs deposition, thereby facilitating the transport. Applying the Derjaguin-Landau-Verwey-Overbeek theory, higher pH levels increased the energy barrier and secondary energy minimum, decreasing PS-NPs deposition. Moreover, dibasic acids significantly enhanced the hydrophilicity of PS-NPs. Conversely, monobasic acids, except for GA, slightly reduced the hydrophilicity of PS-NPs, as indicated by a small increase in the water contact angle, hereby minimally affecting PS-NPs transport. As for GA, although it is a monobasic acid, the additional -OH group in its molecular structure promoted PS-NPs transport, similar to dibasic acids. For example, GA also significantly enhanced the hydrophilicity of PS-NPs. In the presence of Ca2+, the enhancement of PS-NPs transport by LMWOAs was comparable to that with Na+, primarily due to the complex-forming and bridging effects of Ca2+ with the organic acids and PS-NPs. These findings provide important insights into predicting and analyzing the transport behaviors of PS-NPs.