Toxicity Of Nanoplastics Research Articles

Application of spectrochemical analysis with chemometrics to profile biochemical alterations in nanoplastic-exposed HepG2 cells

Humans are routinely exposed to nanoplastics (NPs) in various ways, and this exposure presents a significant health risk. Nevertheless, there remain gaps in our knowledge, particularly in the mechanisms of toxicity of NPs with different surface charges at very low environmental concentrations. Herein, a spectrochemical approach was used to profile the cytotoxicity of NPs with different surface charges in HepG2 cells. It was found that all three NPs can cause some biomolecular alterations in cells, affecting cellular lipids, proteins, amino acids, and genetic material. Of these, PS and PS-COOH led to a non-linear dose-response, which may be related to a biphasic dose-response, whereas PS-NH2 led to a linear dose-response with a gradual increase in toxicity with increasing exposure concentration. In addition, the spectroscopic results showed that surface modifications led to cellular biochemical changes and caused adverse biological effects, with PS-NH2 exhibiting higher toxicity compared to PS or PS-COOH along with an inhibition of cell proliferation. Surprisingly PS-COOH, although considered the least toxic NP, appears to cause DNA damage. Overall, the toxic effects of different surface-modified NPs in cells were detected for the first time by applying spectrochemical techniques, and these findings provide important data towards understanding the emerging widespread environmental pollution of NPs and their effects on humans.

The effects of a polystyrene nanoplastic on the immune response and gut microbiota of Eriocheir sinensis and its post-recovery state

Although there is increasing concern about the toxicity of nanoplastics, the effects of nanoplastic exposure and subsequent recovery on immune responses, as well as antioxidant responses and gut microbiota, in crustaceans are rarely reported. In this study, the nonspecific immunity and antioxidant defense of Eriocheir sinensis were evaluated after acute exposure to various concentrations (0, 2.5, 5, 10 and 20 mg/L) of 75-nm polystyrene nanoplastics (PS-NPs) for 48 h, as well as after 7 days of recovery from the nanoplastic environment. The results showed that, after 48 h of exposure, nanoplastics were observed in the gills, hepatopancreas and gut. However, no nanoplastics were found in the gut after 7 days of recovery. Under nanoplastic-induced stress, Hc, Relish, proPO, and LITAF mRNA levels increased in the gills and hepatopancreas for 48 h. Expression of the myd88, Hc, Relish and proPO genes decreased in the gills during the 7-day recovery period. Exposure to nanoplastics for 48 h and recovery for 7 days significantly decreased the activities of lysozyme (LZM) alkaline phosphatase (AKP), total superoxide dismutase (SOD) and phenoloxidase (POD) and, glutathione peroxidase (GPX) in the hepatopancreas. Meanwhile, the relative abundance of pathogens exposed to 10 mg/L nanoplastics for 48 h increased at the species level, and these pathogens decreased significantly in the 7-day recovery period. These results suggested that exposure to nanoplastics for 48 h affected the activities of immune system enzymes and expression of immune-related genes in Eriocheir sinensis and altered the diversity and composition of their gut microbiota. E. sinensis could not recover from damage to the hepatopancreas within a 7-day recovery period. The results of this study provided insight into the effects of nanoplastics on crustaceans and it filled a gap in research on crustacean recovery after exposure to nanoplastics.

Long-term exposure to polystyrene nanoparticles at environmentally relevant concentration causes suppression in heme homeostasis signal associated with transgenerational toxicity induction in Caenorhabditis elegans

Heme homeostasis related signaling participates in inducing a protective response when controlling nanopolystyrene toxic effects in parental generation. However, whether the heme homeostasis signal is involved in regulation of transgenerational toxicity of nanopolystyrene toxicity is still unclear. Herein, with the model organism of Caenorhabditis elegans, 0.1–10 μg/L nanopolystyrene particles (PS-NPs) at 20-nm treatment downregulated glb-18, and the decrease was also discovered in the offspring following PS-NPs exposure. Germline glb-18 RNAi induced susceptive property to transgenerational PS-NPs toxicity, suggesting that a decreased GLB-18 level mediated induction of transgenerational toxicity. Importantly, germline GLB-18 transgenerationally activated the function of intestinal HRG-4 in controlling transgenerational PS-NPs toxicity. In transgenerational toxicity control, HRG-1/ATFS-1/HSP-6 was recognized to be the downstream pathway of HRG-4. Briefly, germline GLB-18 in P0 generation can transgenerationally activate the downstream intestinal HRG-4/HRG-1/ATFS-1/HSP-6 pathway among offspring for controlling the transgenerational toxicity of PS-NPs. Findings in the present work strengthens the possible association of heme homeostasis signal changes with transgenerational nanoplastic toxicity within the organisms.

Examining the impact of nanoplastics and PFAS exposure on immune functions through inhibition of secretory immunoglobin A in human breast milk

Emerging contaminants such as nanoplastics (NPs) and per- and polyfluoroalkyl substances (PFAS), have been detected in the environment and breast milk, thus exposing infants to potentially harmful chemicals during breastfeeding. Breast milk contains secretory immunoglobulin A (SIgA), an antibody that plays a vital role in disease protection and the development of the infant's immune system. This study employed molecular simulation and fractional factorial designs to assess the toxicity of NPs and PFAS on breast milk and their influence on infant immunity by inhibiting SIgA. The research found that NPs and PFAS have higher binding affinities to SIgA compared to the control compound. Polycarbonate (−10.7 kcal/mol) had the highest binding affinity among plastics, while Perfluorodecanoic acid (PFDA, - 8.0 kcal/mol) had the highest binding affinity among PFAS. The relative toxic index was higher for PFAS (2.4) than for plastics (1.9), suggesting that PFAS may pose a higher overall toxicity burden on the protein. The presence of specific combinations of NPs and PFAS in breast milk may potentially harm breastfeeding infants, although additional experimental studies are required to validate these findings. These results underscore the potential risks associated with these emerging contaminants in breast milk and their impact on infant immunity.

Interaction of polystyrene nanoplastics and hemoglobin is determined by both particle curvature and available surface area

Understanding nanoplastic (NP, or nanoparticle in general) toxicity requires establishing the causal relationships between the physical properties of the nanoparticles and their biological impact. We use spectroscopic, zeta-potential, and dynamic light scattering (DLS) techniques to investigate the formation, structure, and catalytic properties of hemoglobin corona complexes with polystyrene NPs (0–10 mg/mL) of various diameters (20, 50, 100, 500, and 5000 nm). Resonance light scattering, zeta-potential analysis, and DLS demonstrated that hemoglobin corona complexes formed different forms of aggregates with NPs in terms of diameter. Medium-sized (100 nm) NPs induced the most significant conformational alterations in the protein corona compared to smaller and larger ones, which was revealed by spectroscopic assays. However, the catalase-like activity of hemoglobin was promoted in the presence of 100 nm NPs by as high as 35.2 %. NP curvature and surface area are antagonistic factors that govern the conformation of proteins together. This also suggests that 100 nm NPs are more likely to disrupt protein-dependent physiological processes at a given mass concentration than small or large NPs.

Microcystins-Loaded Aged Nanoplastics Provoke a Metabolic Shift in Human Liver Cells.

Studies concerning the toxicity of pollutant-loaded nanoplastics (NPs) toward humans are still in their infancy. Here, we evaluated the adsorption of microcystins (MCs) by pristine and aged polystyrene nanoplastics (PSNPs), prepared MCs-loaded aged PSNPS (1, 5, 10, 15, and 19 μg/mg), and systematically mapped the key molecular changes induced by aged and MCs-loaded PSNPs to human hepatoblastoma (HepG2) cells. According to the results, MC-LR adsorption is increased 2.64-fold by aging, and PSNP accumulation is detected in HepG2 cells. The cytotoxicity of the MC-LR-loaded aged PSNPs showed a positive relationship with the MC-LR amount, as the cell viability in the 19 μg/mg loading treatment (aPS-MC19) was 10.84% lower than aged PSNPs; meanwhile, more severe oxidative damage was observed. Primary approaches involved stressing the endoplasmic reticulum and reducing protein synthesis that the aged PSNPs posed for HepG2 cells, while the aggravated cytotoxicity in aPS-MC19 treatment was a combined result of the metabolic energy disorder, oxidative damage, endoplasmic reticulum stress, and downregulation of the MC-LR target protein. Our results confirm that the aged PSNPs could bring more MC-LR into the HepG2 cells, significantly interfere with biological processes, and provide new insight into deciphering the risk of NPs to humans.

Enhanced hepatic metabolic perturbation of polystyrene nanoplastics by UV irradiation-induced hydroxyl radical generation

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.

The reproductive and transgenerational toxicity of microplastics and nanoplastics: A threat to mammalian fertility in both sexes.

Microplastics (MPs) and nanoplastics (NPs) are extensively distributed in the environment. However, a comprehensive review and in-depth discussion on the effects of MPs and NPs to reproductive capacity and transgenerational toxicity on mammals, especially on humans, is lacked. It is suggested that microplastics and nanoplastics could accumulate in mammalian reproductive organs and exert toxic effects on the reproductive system for both sexes. For males, the damage of microplastics consists of abnormal testicular and sperm structure, decreased sperm vitality, and endocrine disruption, which were caused by oxidative stress, inflammation, apoptosis of testicular cells, autophagy, abnormal cytoskeleton, and abnormal hypothalamic-pituitary-testicular axis. For females, the damage of microplastics includes abnormal ovary and uterus structure and endocrine disruption, which were caused by oxidative stress, inflammation, granulosa cell apoptosis, hypothalamic-pituitary-ovary axis abnormalities, and tissue fibrosis. For transgenerational toxicity, premature mortality existed in the rodent offspring after maternal exposure to microplastics. Among the surviving offspring, metabolic disorders, reproductive dysfunction, immune, neurodevelopmental, and cognitive disorders were detected, and these events directly correlated with transgenerational translocation of MPs and NPs. Studies on human-derived cells or organoids demonstrated that transgenerational toxicity studies for both sexes are yet in the phase of exploring suitable experimental models, and more detailed research on the threat of MPs and NPs to human fertility is still urgently needed. Further studies will help assess the MPs and NPs threat to public fertility and reproductive health risks.

Sentinel supervised lung-on-a-chip: A new environmental toxicology platform for nanoplastic-induced lung injury

Nanoplastics are prevalent in the air and can be easily inhaled, posing a threat to respiratory health. However, there have been few studies investigating the impact of nanoplastics on lung injury, especially chronic obstructive pulmonary disease (COPD). Furthermore, cell and animal models cannot deeply understand the pollutant-induced COPD. Existing lung-on-a-chip models also lack interactions among immune cells, which are crucial in monitoring complex responses. In the study, we built the lung-on-a-chip to accurately recapitulate the structural features and key functions of the alveolar-blood barrier while integrating multiple immune cells. The stability and reliability of the lung-on-a-chip model were demonstrated by toxicological application of various environmental pollutants. We Further focused on exploring the association between COPD and polystyrene nanoplastics (PS-NPs). As a result, the cell viability significantly decreased as the concentration of PS-NPs increased, while TEER levels decreased and permeability increased. Additionally, PS-NPs could induce oxidative stress and inflammatory responses at the organ level, and crossed the alveolar-blood barrier to enter the bloodstream. The expression of α1-antitrypsin (AAT) was significantly reduced, which could be served as early COPD checkpoint on the lung-chips. Overall, the lung-on-a-chip provides a new platform for investigating the pulmonary toxicity of nanoplastics, demonstrating that PS-NPs can harm the alveolar-blood barrier, cause oxidative damage and inflammation, and increase the risk of COPD.

Evaluation of the pulmonary toxicity of PSNPs using a Transwell-based normal human bronchial epithelial cell culture system

To reduce the nanoplastics (NPs) toxicity assessment error, we established a Transwell-based bronchial epithelial cell exposure system to assess the pulmonary toxicity of polystyrene NPs (PSNPs). Transwell exposure system was more sensitive than submerged culture for toxicity detection of PSNPs. PSNPs adhered to the BEAS-2B cell surface, were ingested by the cell, and accumulated in the cytoplasm. PSNPs induced oxidative stress and inhibited cell growth through apoptosis and autophagy. A noncytotoxic dose of PSNPs (1 ng/cm2) increased the expression levels of inflammatory factors (ROCK-1, NF-κB, NLRP3, ICAM-1, etc) in BEAS-2B cells, whereas a cytotoxic dose (1000 ng/cm2) induced apoptosis and autophagy, which might inhibit the activation of ROCK-1 and contribute to reducing inflammation. In addition, the noncytotoxic dose increased the expression levels of zonula occludens-2 (ZO-2) and α1-antitrypsin (α-AT) proteins in BEAS-2B cells. Therefore, in response to PSNP exposure, a compensatory increase in the activities of inflammatory factors, ZO-2, and α-AT may be triggered at low doses as a mechanism to preserve the survival of BEAS-2B cells. In contrast, exposure to a high dose of PSNPs elicits a noncompensatory response in BEAS-2B cells. Overall, these findings suggest that PSNPs may be harmful to human pulmonary health even at an ultralow concentration.

Effects of selenite on the responses of lettuce (Lactuca sativa L.) to polystyrene nano-plastic stress

Nowadays, nano-plastics are widespread in agricultural soils and could be uptaken by crops to cause an increased risk for food safety. As a beneficial element for plants, selenium (Se) can alleviate oxidative damages under various environmental stresses (eg. heavy metals, heat, cold). This study investigated the single and co-applications of nano-size polystyrene (PS) (80 nm and 200 nm) and selenite (0.8 ppm and 5 ppm) in lettuce (Lactuca sativa L.). Results showed nano-PS significantly decreased the root-shoot fresh biomass ratios, inhibited physiological functions in roots and leaves (e.g. root length, chlorophyll content and net photosynthetic rate), as well as stimulated the activities of the antioxidant enzymes in roots and shoots with greater toxicity at the smaller particle size (80 nm). However, both exogenous selenite applications significantly alleviated the above toxic effects of nano-PS in lettuces, especially at a high Se level of 5 ppm. Regression Path Analysis (RPA) revealed that regulation of chlorophyll levels by Se might be a key mechanism for counteracting PS stress in lettuces, which led to the increase in indigenous defense capacity. The present findings provide a novel but safer and cleaner agricultural strategy to alleviate or minimize nano-plastics toxicity in agricultural soils for staple crops and vegetables via application of Se.

Are Microplastics Toxic? A Review from Eco-Toxicity to Effects on the Gut Microbiota.

Emerging studies have presented an initial picture of the toxic effects of exposure to environmental micro- and nanoplastics. They have indicated that micro- and nanoplastics may induce toxicity by leading to oxidative stress, energy metabolism disorders, gene damage, and so forth in environmental organisms, marine invertebrates and vertebrates, and laboratory mouse models. In recent years, micro- and nanoplastics have been discovered in human fecal samples, placentas, lung tissue, and even blood; thus, micro- and nanoplastics pose an alarming and ever-increasing threat to global public health. However, current research on the health effects of micro- and nanoplastics and the possible adverse outcomes in humans has only presented the tip of the iceberg. More robust clinical data and basic experiments are still warranted to elucidate the specific relationships and mechanisms. In this paper, we review studies on micro- and nanoplastic toxicity from the perspectives of eco-toxicity, the adverse effects on invertebrates and vertebrates, and the impact of micro- and nanoplastics on the gut microbiota and its metabolites. In addition, we evaluate the toxicological role of micro- and nanoplastic exposure and its potential implications in respect to human health. We also summarize studies regarding preventive strategies. Overall, this review provides insights on micro- and nanoplastic toxicity and its underlying mechanisms, opening up scientific avenues for future in-depth studies.

Bisphenol A decreases the developmental toxicity and histopathological alterations caused by polystyrene nanoplastics in developing marine medaka Oryzias melastigma

Nanoplastics (NPs) are emerging pollutants posing risks to marine biota and human health due to their small size and high bioavailability. However, there are still knowledge gaps regarding effects of co-existing pollutants on NPs toxicity to marine organisms at their respective environmentally relevant concentrations. Herein we investigated developmental toxicity and histopathological alterations caused by co-exposure of polystyrene nanoplastics (PS-NPs) and bisphenol A (BPA) to marine medaka, Oryzias melastigma. Embryos at 6 h post-fertilization were exposed to 50-nm PS-NPs (55 μg/L) or BPA (100 μg/L) or co-exposed to a combination of both. Results showed that PS-NPs exhibited decreased embryonic heart rate, larval body length, and embryonic survival as well as larval deformities such as hemorrhaging and craniofacial abnormality. When co-exposed, BPA mitigated all the adverse developmental effects caused by PS-NPs. PS-NPs also led to an increase in histopathological condition index of liver with early inflammatory responses, while co-exposure of BPA with PS-NPs did not. Our data suggest that the toxicity reduction of PS-NPs in the presence of BPA might result from the decreased bioaccumulation of PS-NPs caused by the interaction between BPA and PS-NPs. This study unveiled the impact of BPA on the toxicity of nanoplastics in marine fish during early developmental stages and highlight the need of more research on the long-term effects of complex mixtures in the marine environment by applying omics approaches to better understand the toxicity mechanism.

Toxicity and mechanism of nanoplastics to phytoplankton in high-latitude aquatic ecosystems of Canadian prairie: Effects of multiple environmental factors

The potential ecological risks of nanoplastics (NPs) may be inaccurately assessed in some studies as they fail to consider the impact of environmental factors and their interactive effects. Here, the effects of six representative environmental factors (N, P, salinity, DOM (dissolved organic matter), pH and hardness) on NPs' toxicity and mechanism to microalgae are investigated based on the surface water quality data in Saskatchewan watershed, Canada. Our 10 sets of 26–1 factorial analysis reveal the significant factors and their interactive complexity towards 10 toxic endpoints from cellular and molecular levels. This is the first time to study the toxicity of NPs to microalgae under interacting environmental factors in high-latitude aquatic ecosystems of Canadian prairie. We find that microalgae become more resistant to NPs in N-rich or higher pH environments. Surprisingly, with the increase of N concentration or pH, the inhibitory effect of NPs on microalgae growth even became a promotion effect with the decreased inhibition rate from 10.5 % to −7.1 % or from 4.3 % to −0.9 %, respectively. Synchrotron-based Fourier transform infrared spectromicroscopy analysis reveals that NPs can induce alterations in the content and structure of lipids and proteins. DOM, N*P, pH, N*pH and pH*hardness have a statistically significant effect on NPs' toxicity to biomolecular. The toxicity levels of NPs across Saskatchewan watersheds are evaluated and we find that NPs could have the greatest inhibition on microalgae growth in Souris River. Our findings indicate that multiple environmental factors should be considered during the ecological risk assessment of emerging pollutants.

Global warming and nanoplastic toxicity; small temperature increases can make gill and liver toxicity more dramatic, which affects fillet quality caused by polystyrene nanoplastics in the adult zebrafish model

Increasing nanoplastics (NPs) pollution may lead to unknown environmental risks when considered together with climate change, which has the potential to become an increasingly important environmental issue in the coming decades. In this context, the present study aimed to evaluate the stressor modelling of polystyrene nanoplastic (PS-NPs) combined with temperature increase in zebrafish. For this purpose, changes in gill, liver and muscle tissues of zebrafish exposed to PS-NPs (25 ppm) and/or different temperatures (28, 29 and 30 °C) for 96 h under static conditions were evaluated. The results obtained emphasize that exposure to PS-NPs stressors under controlled conditions with temperature increase induces DNA damage through stress-induced responses accompanied by degeneration, necrosis and hyperaemia in zebrafish liver and adhesion of lamellae, desquamation and inflammation in lamellar epithelium in gills. Metabolomic analyses also supported changes indicating protein and lipid oxidation, especially PS-NPs-mediated. These findings will contribute to the literature as key data on the effects of PS-NPs presence on protein/lipid oxidation and fillet quality in muscle tissues.

Systemic effects of nanoplastics on multi-organ at the environmentally relevant dose: The insights in physiological, histological, and oxidative damages

Nanoplastics (NPs) are ubiquitous contaminants that have adverse effects on human health. Previous research has explored the toxicity of NPs on specific organs at high doses, but this is insufficient for accurate health risk assessments. In the present study, a systematic study of NPs toxicity in the liver, kidney, and intestine was performed on mice at an equivalent dose of potential human exposure and toxic dose for four weeks. The results revealed that NPs penetrated the intestinal barrier and accumulated in various organs including liver, kidney, and intestine via the clathrin-mediated endocytosis, phagocytosis, and paracellular pathways. At the toxic dose, damage scores on physiology, morphology, and redox balance were more than twice that at the environmentally relevant dose, which was dose-depended. The jejunum experienced the most severe damage compared to the liver and kidney. In addition, a significant correlation between biomarkers was found, such as TNF-α and cholinesterase levels, indicating a close connection between the intestine and liver. Remarkably, the NPs exposed mice had an approximate double reactive oxygen species content compared to the control. This study promotes comprehensive understanding of health risks caused by NPs throughout the body and informs future policies and regulations to mitigate NPs-related health concerns.

Sulfonate-Modified Polystyrene Nanoparticle at Precited Environmental Concentrations Induces Transgenerational Toxicity Associated with Increase in Germline Notch Signal of Caenorhabditis elegans.

Recently, the transgenerational toxicity of nanoplastics has received increasing attention. Caenorhabditis elegans is a useful model to assess the transgenerational toxicity of different pollutants. In nematodes, the possibility of early-life exposure to sulfonate-modified polystyrene nanoparticle (PS-S NP) causing transgenerational toxicity and its underlying mechanisms were investigated. After exposure at the L1-larval stage, transgenerational inhibition in both locomotion behavior (body bend and head thrash) and reproductive capacity (number of offspring and fertilized egg number in uterus) was induced by 1-100 μg/L PS-S NP. Meanwhile, after exposure to 1-100 μg/L PS-S NP, the expression of germline lag-2 encoding Notch ligand was increased not only at the parental generation (P0-G) but also in the offspring, and the transgenerational toxicity was inhibited by the germline RNA interference (RNAi) of lag-2. During the transgenerational toxicity formation, the parental LAG-2 activated the corresponding Notch receptor GLP-1 in the offspring, and transgenerational toxicity was also suppressed by glp-1 RNAi. GLP-1 functioned in the germline and the neurons to mediate the PS-S NP toxicity. In PS-S NP-exposed nematodes, germline GLP-1 activated the insulin peptides of INS-39, INS-3, and DAF-28, and neuronal GLP-1 inhibited the DAF-7, DBL-1, and GLB-10. Therefore, the exposure risk in inducing transgenerational toxicity through PS-S NP was suggested, and this transgenerational toxicity was mediated by the activation of germline Notch signal in organisms.

Nanoplastic uptake temporarily affects the pulsing behavior in ephyrae of the moon jellyfish Aurelia sp.

The aim of this study is to investigate for the first time the uptake and ecotoxicological effects of nanoplastics (NPs) in a marine cnidarian. Ephyrae of the moon jellyfish Aurelia sp. of different ages (0 and 7 days old) were exposed to negatively charged polystyrene NPs for 24 h; then, the uptake was assessed through traditional and novel techniques, namely microscopy and three-dimensional (3D) holotomography. Immobility and behavioral responses (frequency of pulsations) of ephyrae were also investigated to clarify if NP toxicity differed along the first life stages. NP uptake was observed in ephyrae thanks to the 3D technique. Such internalization did not affect survival, but it temporarily impaired the pulsation mode only in 0 day old ephyrae. This may be ascribed to the negative charged NPs, contributing to jellyfish behavioral alteration. These findings promote 3D holotomography as a suitable tool to detect NPs in marine organisms. Moreover, this study recommends the use of cnidarians of different ages to better assess NP ecotoxicological effects in these organisms, key components of the marine food web.

Elevated temperature decreases cardiovascular toxicity of nanoplastics but adds to their lethality: A case study during zebrafish (Danio rerio) development

To highlight the key role of global warming on the toxicity of contaminants, the cardiovascular toxicity of nanoparticles (NPs) was estimated in developing zebrafish (Danio rerio) at different exposure temperatures, and the toxicity mechanisms were explored via multi-omic analyses. Polystyrene NPs (50 nm) at 0.1 mg·L−1 entered zebrafish embryos at 24 h post-fertilization and caused cardiovascular toxicity in the developing zebrafish at 27 ℃. This was explained by the down-regulation of the branched-chain amino acid and insulin signaling pathways owing to induced oxidative stress. Elevated exposure temperatures promoted the accumulation of NPs in developing zebrafish, increased the levels of oxidative stress and enhanced the oxidative phosphorylation rate in mitochondria, thus resulting in an additive effect on the mortality of zebrafish larvae. Notably, elevated exposure temperatures reduced the cardiovascular toxicity of NPs, as the effective concentration of NPs for inhibiting embryonic heartbeat rate increased from 0.1 mg·L−1 at 27 ℃ to 1.0 mg·L−1 at 30 ℃. Experiments of transgenic zebrafish Tg(myl7:GFP) and multi-omic analyses revealed that elevated temperatures enhanced the myocardial contractility of larvae, thus reducing the cardiovascular toxicity of NPs. However, the health risks of enhanced myocardial contraction caused by NP exposure at elevated temperatures requires further consideration.

Single-cell transcriptomic analysis reveals heterogeneity of the patterns of responsive genes and cell communications in liver cell populations of zebrafish exposed to polystyrene nanoplastics

Nanoplastics (NPs) are a group of emerging environmental pollutants with potential toxicity and health risk on biosystem and ecosystem. Great efforts have been devoted to describing the uptake, distribution, accumulation, and toxicity of NPs at various aquatic organisms; however, the heterogeneous response patterns in zebrafish (Danio rerio) liver cell populations caused by NP exposure have not yet been clarified. Investigation of the heterogeneous response patterns in zebrafish liver cell populations after NPs exposure provides us significances to explore the NP cytotoxicity. In this article, the heterogeneous response patterns in zebrafish liver cell populations after polystyrene (PS)-NPs exposure were studied. Significantly increased content of malondialdehyde and decreased levels of catalase and glutathione were observed, indicating the oxidative damage of zebrafish liver induced by PS-NPs exposure. Afterwards, the liver tissues were enzymatically dissociated and used for single-cell transcriptomic (scRNA-seq) analysis. Nine cell types were identified based on unsupervised cell cluster analysis followed by their marker genes. Hepatocytes were the cell type most impacted by PS-NP exposure, and heterogeneous response patterns of male and female hepatocytes were observed. The PPAR signaling pathway was up-regulated in hepatocytes from both male and female zebrafish. Lipid metabolism-related functions were altered more notably in male-derived hepatocytes, while female-derived hepatocytes were more sensitive to estrogen stimulus and mitochondria. Macrophages and lymphocytes were also highly responsive cell types, with specific immune pathways activated to suggest immune disruption after exposure. Oxidation-reduction process and immune response were significantly altered in macrophages, and oxidation-reduction process, ATP synthesis, and DNA binding were most altered in lymphocytes. Our study not only integrates scRNA-seq with toxicology effects to identify highly sensitive and specific populations of responding cells, revealing highly specialized interactions between parenchymal and non-parenchymal cells and expanding our current understanding of PS-NPs toxicity, but also highlights the importance of cellular heterogeneity in environmental toxicology.