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Particle and Fibre Toxicology Nov 2023Nanoplastics (NPs) could be released into environment through the degradation of plastic products, and their content in the air cannot be ignored. To date, no studies...
BACKGROUND
Nanoplastics (NPs) could be released into environment through the degradation of plastic products, and their content in the air cannot be ignored. To date, no studies have focused on the cardiac injury effects and underlying mechanisms induced by respiratory exposure to NPs.
RESULTS
Here, we systematically investigated the cardiotoxicity of 40 nm polystyrene nanoplastics (PS-NPs) in mice exposed via inhalation. Four exposure concentrations (0 µg/day, 16 µg/day, 40 µg/day and 100 µg/day) and three exposure durations (1 week, 4 weeks, 12 weeks) were set for more comprehensive information and RNA-seq was performed to reveal the potential mechanisms of cardiotoxicity after acute, subacute and subchronic exposure. PS-NPs induced cardiac injury in a dose-dependent and time-dependent manner. Acute, subacute and subchronic exposure increased the levels of injury biomarkers and inflammation and disturbed the equilibrium between oxidase and antioxidase activity. Subacute and subchronic exposure dampened the cardiac systolic function and contributed to structural and ultrastructural damage in heart. Mechanistically, violent inflammatory and immune responses were evoked after acute exposure. Moreover, disturbed energy metabolism, especially the TCA cycle, in the myocardium caused by mitochondria damage may be the latent mechanism of PS-NPs-induced cardiac injury after subacute and subchronic exposure.
CONCLUSION
The present study evaluated the cardiotoxicity induced by respiratory exposure to PS-NPs from multiple dimensions, including the accumulation of PS-NPs, cardiac functional assessment, histology observation, biomarkers detection and transcriptomic study. PS-NPs resulted in cardiac injury structurally and functionally in a dose-dependent and time-dependent manner, and mitochondria damage of myocardium induced by PS-NPs may be the potential mechanism for its cardiotoxicity.
Topics: Animals; Mice; Cardiotoxicity; Polystyrenes; Microplastics; Myocardium; Biomarkers; Nanoparticles
PubMed: 38031128
DOI: 10.1186/s12989-023-00557-3 -
The Science of the Total Environment Nov 2023The production of plastics worldwide has been instrumental in the progress of modern society, while the increasing accumulation of plastics castoff in oceans, soils and...
The production of plastics worldwide has been instrumental in the progress of modern society, while the increasing accumulation of plastics castoff in oceans, soils and anywhere else has become a major pressure source on environmental sustainability and animal health. Meanwhile, from a biological perspective, our understanding of the toxicological fingerprints of plastics, especially microplastics (MPs), is still poor. Here, we reported a phenomenon of hepatotoxicity dominated by MPs in the form of polystyrene (PS), was observed in mice model systems and cellular assays. Apoptosis and necroptosis related to the size of particles were seen upon PS-MPs introduction, as revealed by transmission electron microscopy, fluorescence microscopy, flow cytometry, and quantitative analysis of signaling pathways in vivo and vitro. Collectively, the current study demonstrated that the levels of liver cell injury caused by PS-MPs were negatively correlated with the particle diameters. Small-sized particles (1-10 μm) induced cell death primarily as necroptosis whereas the large-sized particles (50-100 μm) mainly induced apoptosis, which was directly accomplished by PTEN/PI3K/AKT signaling axis and its targeted autophagy flux. More interestingly, inhibition of autophagy not only alleviated PS-MPs-triggered cell death, but also changed the form of death injury to a certain extent. This uncovered crosstalk relationship opens up a new avenue for investigating the biological and toxicological effects of MPs, and may provide important insights for preventing and limiting of health hazards from MPs.
Topics: Animals; Mice; Microplastics; Polystyrenes; Plastics; Phosphatidylinositol 3-Kinases; Proto-Oncogene Proteins c-akt; Necroptosis; Liver; Apoptosis; Autophagy
PubMed: 37451460
DOI: 10.1016/j.scitotenv.2023.165461 -
Free Radical Biology & Medicine Nov 2023Nanoplastics (NPs) exposure to humans can occur through various routes, including the food chain, drinking water, skin contact, and respiration. NPs are plastics with a...
Nanoplastics (NPs) exposure to humans can occur through various routes, including the food chain, drinking water, skin contact, and respiration. NPs are plastics with a diameter of less than 100 nm and have the potential to accumulate in tissues, leading to toxic effects. This study aimed to investigate the neurotoxicity of polystyrene NPs on neural progenitor cells (NPCs) and hippocampal neurogenesis in a rodent model. Toxicity screening of polystyrene NPs based on their charge revealed that cationic amine-modified polystyrene (PS-NH) exhibited cytotoxicity, while anionic carboxylate-modified polystyrene (PS-COO) and neutral NPs (PS) did not. NPCs treated with PS-NH showed a significant reduction in growth rate due to G1 cell cycle arrest. PS-NH increased the expression of cell cycle arrest markers p21 and p27, while decreasing cyclin D expression in NPCs. Interestingly, PS-NH accumulated in mitochondria, leading to mitochondrial dysfunction and energy depletion, which caused G1 cell cycle arrest. Prolonged exposure to PS-NH in C17.2 NPCs increased the expression of p16 and senescence-associated secretory phenotype factors, indicating cellular senescence. In vivo studies using C57BL/6 mice demonstrated impaired hippocampal neurogenesis and memory retention after 10 days of PS-NH administration. This study suggests that NPs could deplete neural stem cell pools in the brain by mitochondrial dysfunction, thereby adversely affecting hippocampal neurogenesis and neurocognitive functions.
Topics: Humans; Animals; Mice; Polystyrenes; Microplastics; Mice, Inbred C57BL; Neural Stem Cells; Hippocampus; Neurogenesis; Mitochondria; Nanoparticles; Water Pollutants, Chemical
PubMed: 37553025
DOI: 10.1016/j.freeradbiomed.2023.08.010 -
Journal of Hazardous Materials Jul 2023In the era of plastic use, organisms are constantly exposed to polystyrene particles (PS-Ps). PS-Ps accumulated in living organisms exert negative effects on the body,...
In the era of plastic use, organisms are constantly exposed to polystyrene particles (PS-Ps). PS-Ps accumulated in living organisms exert negative effects on the body, although studies evaluating their effects on brain development are scarce. In this study, the effects of PS-Ps on nervous system development were investigated using cultured primary cortical neurons and mice exposed to PS-Ps at different stages of brain development. The gene expression associated with brain development was downregulated in embryonic brains following PS-Ps exposure, and Gabra2 expression decreased in the embryonic and adult mice exposed to PS-Ps. Additionally, offspring of PS-Ps-treated dams exhibited signs of anxiety- and depression-like behavior, and abnormal social behavior. We propose that PS-Ps accumulation in the brain disrupts brain development and behavior in mice. This study provides novel information regarding PS-Ps toxicity and its harmful effects on neural development and behavior in mammals.
Topics: Animals; Mice; Polystyrenes; Depression; Water Pollutants, Chemical; Anxiety; Social Behavior; Nanoparticles; Mammals
PubMed: 37130475
DOI: 10.1016/j.jhazmat.2023.131465 -
Ecotoxicology and Environmental Safety Oct 2023As emerging pollutants in the environment, nanoplastics (NPs) can cross biological barriers and be enriched in organisms, posing a greatest threat to the health of...
As emerging pollutants in the environment, nanoplastics (NPs) can cross biological barriers and be enriched in organisms, posing a greatest threat to the health of livestock and humans. However, the size-dependent toxic effects of NPs in higher mammals remain largely unknown. To determine the size-dependent potential toxicities of NPs, we exposed mouse (AML-12) and human (L02) liver cell lines in vitro, and 6-week-old C57BL/6 mice (well-known preclinical model) in vivo to five different sizes of polystyrene NPs (PS-NPs) (20, 50, 100, 200 and 500 nm). We found that ultra-small NPs (20 nm) induced the highest cytotoxicity in mouse and human liver cell lines, causing oxidative stress and mitochondrial membrane potential loss on AML-12 cells. Unexpectedly in vivo, after long-term oral exposure to PS-NPs (75 mg/kg), medium NPs (200 nm) and large NPs (500 nm) induced significant hepatotoxicity, evidenced by increased oxidative stress, liver dysfunction, and lipid metabolism disorders. Most importantly, medium or large NPs generated local immunotoxic effects via recruiting and activating more numbers of neutrophils and monocytes in the liver or intestine, which potentially resulted in increased proinflammatory cytokine secretion and the tissue damage. The discrepancy in in vitro-in vivo toxic results might be attributed to the different properties of biodistribution and tissue accumulation of different sized NPs in vivo. Our study provides new insights regarding the hepatotoxicity and immunotoxicity of NPs on human and livestock health, warranting us to take immense measures to prevent these NPs-associated health damage.
Topics: Humans; Animals; Mice; Mice, Inbred C57BL; Microplastics; Polystyrenes; Tissue Distribution; Antineoplastic Agents; Livestock; Chemical and Drug Induced Liver Injury; Leukemia, Myeloid, Acute; Nanoparticles; Water Pollutants, Chemical; Mammals
PubMed: 37690176
DOI: 10.1016/j.ecoenv.2023.115447 -
Food and Chemical Toxicology : An... Nov 2023Microplastics (MPs) are plastic pollutants with a diameter of less than 5 mm and microcystins (MCs) are natural toxins produced by cyanobacteria. In recent years, the...
Microplastics (MPs) are plastic pollutants with a diameter of less than 5 mm and microcystins (MCs) are natural toxins produced by cyanobacteria. In recent years, the pollution of MPs and MCs attracted widespread attention. However, our understanding about the toxic effects of co-exposure of MPs and MCs on male reproduction is limited. Mice were continuously exposed to 0.04mg/(kg*bw) microcystin-leucine-arginine (MC-LR) or 45 mg/(kg*bw) polystyrene microplastics (PS-MPs) or a mixed solution of 0.04mg/(kg*bw) MC-LR and 45 mg/(kg*bw) PS-MPs by gavage for 28 days in this study. The results showed that PS-MPs could absorb MC-LR in ddHO and MC-LR content in testis was increased in the group with combined exposure when compared to the group only exposed to MC-LR. Exposure to PS-MPs or MC-LR individually could destroy testis structure, increase the level of tissue apoptosis and decrease the quality of sperm, while the co-exposure enhanced the toxic effects. Furthermore, PS-MPs could carry MC-LR into testis Leydig cells, reduce testosterone levels and mRNA expression levels of key molecules involved in testosterone synthesis (StAR, P450scc, P450c17,3β-HSD and 17β-HSD). Among them, the combined effect of PS-MPs-MC-LR was the most severe. In summary, this study provides new insights into the toxicity of MPs and MCs in mammals.
Topics: Mice; Male; Animals; Microcystins; Microplastics; Plastics; Polystyrenes; Semen; Reproduction; Testosterone; Mammals
PubMed: 37848122
DOI: 10.1016/j.fct.2023.114104 -
The Science of the Total Environment Sep 2023The widespread consumption of nanoplastics (NPs) and bisphenol A (BPA) affected the aquatic ecosystem and imposed risks to the safety of aquatic organisms. This study...
Combined exposure to polystyrene nanoplastics and bisphenol A induces hepato- and intestinal-toxicity and disturbs gut microbiota in channel catfish (Ictalurus punctatus).
The widespread consumption of nanoplastics (NPs) and bisphenol A (BPA) affected the aquatic ecosystem and imposed risks to the safety of aquatic organisms. This study was aimed at assessing the ecotoxicological effects of single and combined exposure to BPA and polystyrene nanoplastics (PSNPs) on the channel catfish (Ictalurus punctatus). A total of 120 channel catfish were separated into four groups with triplicate (each contains 10 fish) and exposed to chlorinated tap water (control group), PSNP single exposure (0.3 mg/L), BPA single exposure (500 μg/L) and PSNPs (0.3 mg/L) + BPA (500 μg/L) co-exposure for 7 days. Our results showed a relatively higher intestinal accumulation of PSNPs in co-exposure group, compared to PSNP single exposure group. Histopathological analysis showed that single exposure to PSNPs and BPA caused breakage of intestinal villi and swelling of hepatocytes in channel catfish, while the co-exposure exacerbated the histopathological damage. In addition, co-exposure significantly increased SOD, CAT activities and MDA contents in the intestine and liver, inducing oxidative stress. In terms of immune function, the activities of ACP and AKP were significantly decreased. The expressions of immune-related genes such as IL-1β, TLR3, TLR5, hepcidin and β-defensin were significantly up-regulated, and the expression of IL-10 was down-regulated. Additionally, the co-exposure significantly altered the composition of the intestinal microbiota, leading to an increase in the Shannon index and a decrease in the Simpson index. In summary, this study revealed that mixture exposure to PSNPs and BPA exacerbated toxic effects on histopathology, oxidative stress, immune function and intestinal microbiota in channel catfish. It emphasized the threat of NPs and BPA to the health of aquatic organisms and human food safety, with a call for effective ways to regulate the consumption of these anthropogenic chemicals.
Topics: Animals; Humans; Polystyrenes; Ictaluridae; Gastrointestinal Microbiome; Microplastics; Ecosystem; Intestines
PubMed: 37236480
DOI: 10.1016/j.scitotenv.2023.164319 -
Proceedings of the National Academy of... Sep 2023To minimize the incorrect use of antibiotics, there is a great need for rapid and inexpensive tests to identify the pathogens that cause an infection. The gold standard...
To minimize the incorrect use of antibiotics, there is a great need for rapid and inexpensive tests to identify the pathogens that cause an infection. The gold standard of pathogen identification is based on the recognition of DNA sequences that are unique for a given pathogen. Here, we propose and test a strategy to develop simple, fast, and highly sensitive biosensors that make use of multivalency. Our approach uses DNA-functionalized polystyrene colloids that distinguish pathogens on the basis of the frequency of selected short DNA sequences in their genome. Importantly, our method uses entire genomes and does not require nucleic acid amplification. Polystyrene colloids grafted with specially designed surface DNA probes can bind cooperatively to frequently repeated sequences along the entire genome of the target bacteria, resulting in the formation of large and easily detectable colloidal aggregates. Our detection strategy allows "mix and read" detection of the target analyte; it is robust and highly sensitive over a wide concentration range covering, in the case of our test target genome bl21-de3, 10 orders of magnitude from [Formula: see text] to [Formula: see text] copies/mL. The sensitivity compares well with state-of-the-art sensing techniques and has excellent specificity against nontarget bacteria. When applied to real samples, the proposed technique shows an excellent recovery rate. Our detection strategy opens the way to developing a robust platform for pathogen detection in the fields of food safety, disease control, and environmental monitoring.
Topics: Polystyrenes; DNA; Anti-Bacterial Agents; Colloids; Environmental Monitoring; Escherichia coli
PubMed: 37669392
DOI: 10.1073/pnas.2305995120 -
Journal of Hazardous Materials Sep 2023Nanoplastics 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 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.
Topics: Animals; Lung Injury; Microplastics; Ecotoxicology; Reproducibility of Results; Lung; Pulmonary Disease, Chronic Obstructive; Polystyrenes; Environmental Pollutants; Lab-On-A-Chip Devices; Nanoparticles
PubMed: 37406524
DOI: 10.1016/j.jhazmat.2023.131962 -
The Science of the Total Environment Feb 2024It has been shown that exposure to nanoplastics (MNPs) through inhalation can induce pulmonary toxicity, but the toxicological mechanism of MNPs on the respiratory...
It has been shown that exposure to nanoplastics (MNPs) through inhalation can induce pulmonary toxicity, but the toxicological mechanism of MNPs on the respiratory system remains unclear. Therefore, we explored the toxicological mechanism of exposure to polystyrene nanoplastics (PS-NPs) (0.05, 0.15, 0.2 mg/mL) on BEAS-2B cells. Results revealed that PS-NPs induce oxidative stress, increased apoptosis rate measured by flow cytometry, the key ferroptosis protein (GPX4 and FTH1) reduction, increased iron content, mitochondrial alterations, and increased malondialdehyde (MDA) level. Besides, consistent results were observed in mice exposed to PS-NPs (5 mg/kg/2d, 10 mg/kg/2d). Thus, we proved that PS-NPs induced cell death and lung damage through apoptosis and ferroptosis. In terms of mechanism, the elevation of the endoplasmic reticulum (ER) stress protein expression (IRE1α, PERK, XBP1S, and CHOP) revealed that PS-NPs induce lung damage by activating the two main ER stress pathways. Furthermore, the toxicological effects of PS-NPs observed in this study are attenuated by the ROS inhibitor N-acetylcysteine (NAC). Collectively, NPs-induced apoptosis and ferroptosis are attenuated by NAC via inhibiting the ROS-dependent ER stress in vitro and in vivo. This improves our understanding of the mechanism by which PS-NPs exposure leads to pulmonary injury and the potential protective effects of NAC.
Topics: Mice; Animals; Reactive Oxygen Species; Microplastics; Polystyrenes; Endoplasmic Reticulum Chaperone BiP; Endoribonucleases; Ferroptosis; Protein Serine-Threonine Kinases; Lung; Acetylcysteine; Apoptosis; Endoplasmic Reticulum Stress
PubMed: 38086481
DOI: 10.1016/j.scitotenv.2023.169260