Multi-dimensional evaluation of cardiotoxicity in mice following respiratory exposure to polystyrene nanoplastics
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ABSTRACT:
SUBMITTER: Zhang T
PROVIDER: S-EPMC10685678 | biostudies-literature | 2023 Jan
REPOSITORIES: biostudies-literature
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Project description: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.
| S-EPMC11620075 | biostudies-literature
Project description:BackgroundThe toxicity of microplastics (MPs) has attracted wide attention from researchers. Previous studies have indicated that MPs produce toxic effects on a variety of organs in aquatic organisms and mammals. However, the exact neurotoxicity of MPs in mammals is still unclear.ObjectivesWe aimed to confirm the neurotoxicity of chronic exposure to polystyrene MPs (PS-MPs) at environmental pollution concentrations.MethodsIn the present study, mice were provided drinking water containing 100μg/L and 1,000μg/L PS-MPs with diameters of 0.5, 4, and 10μm for 180 consecutive days. After the exposure period, the mice were anesthetized to gain brain tissues. The accumulation of PS-MPs in brain tissues, integrity of the blood-brain barrier, inflammation, and spine density were detected. We evaluated learning and memory ability by the Morris water maze and novel object recognition tests.ResultsWe observed the accumulation of PS-MPs with various particle diameters (0.5, 4, and 10μm) in the brains of exposed mice. Meanwhile, exposed mice also exhibited disruption of the blood-brain barrier, higher level of dendritic spine density, and an inflammatory response in the hippocampus. In addition, exposed mice exhibited cognitive and memory deficits compared with control mice as determined using the Morris water maze and novel object recognition tests, respectively. There was a concentration-dependent trend, but no particle size-dependent differences were seen in the neurotoxicity of MPs.ConclusionsCollectively, our results suggested that PS-MPs exposure can lead to learning and memory dysfunctions and induce neurotoxic effects in mice, findings which have wide-ranging implications for the public regarding the potential risks of MPs. https://doi.org/10.1289/EHP10255.
| S-EPMC9555296 | biostudies-literature
Project description:IntroductionMicroplastics and nanoplastics are prevalent environmental contaminants. Recent reports indicate that polystyrene nanoparticles may adversely impact male reproductive health. This study aims to examine the effects of polystyrene exposure on sperm metabolism and the development of pre-implantation embryos.MethodsIn this study, male C57BL/6 mice were orally gavage-administered polystyrene nanoplastics (60 nm, 20 mg/kg/day) for 35 days to assess their impact on male reproduction and early embryonic development. Experiments included testicular transcriptome analysis, sperm metabolomics, sperm motility and fertilization assays, embryonic ROS detection, and RNA sequencing of 2-cell embryos, revealing the adverse effects of polystyrene exposure on sperm metabolism and embryo development.ResultsThe results revealed that oral gavage of polystyrene to male mice induced a pronounced immune-inflammatory response in testicular tissue, reduced sperm motility, and significantly lowered the fertilization rate. Notably, sperm from treated mice exhibited substantial metabolic disruptions, affecting key pathways, including glycerophospholipid biosynthesis and DNA repair. After fertilization, embryos at the 2-cell stage suffered damage in apoptotic and DNA repair pathways, subsequently impairing early embryo development.DiscussionIn conclusion, this study demonstrated that the oral gavage administration of polystyrene nanoplastics to male mice significantly affects male reproductive function, resulting in abnormalities in early embryonic development and alterations in associated gene expression profiles. These findings offer essential scientific insights for future research into sperm-mediated transgenerational effects and their impact on early embryonic development.
| S-EPMC11906707 | biostudies-literature
Project description: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.
| S-EPMC10909942 | biostudies-literature
Project description:Nanoplastics (NPs) cause serious contamination of drinking water and potential damage to human health. This study aimed to investigate the effects of NPs with different particle sizes and concentrations on the reproductive function of male mice. In this study, free drinking water exposure was used to expose male BALB/C mice to PS-NPs (20 nm, 200 nm, and 1000 nm) at 0.1 mg/L, 1 mg/L, and 5 mg/L for 4 months. The male reproductive function of the mice was assessed after NPs exposure, and fecal and blood samples were collected for macrogenomics and metabolomics. The results showed that PS-NPs resulted in mice with reduced testicular organ coefficients, decreased sperm quality, altered testicular tissue structure, disturbed sex hormone levels, and abnormal levels of inflammatory factors and oxidative stress. Furthermore, this study found that NP exposure affected the alteration of gut communities and metabolic pathways related to male reproduction, such as Clostridium and glutathione metabolism. Importantly, we found an effect of NP particle size on reproductive function. In the future, more attention should be paid to the smaller particle sizes of NPs.
| S-EPMC11360567 | biostudies-literature
Project description:The release of plastics into the environment has been identified as an important issue for some time. Recent publications have suggested that the degradation of plastic materials will result in the release of nano-sized plastic particles to the environment. Nanoparticle tracking analysis was applied to characterise the formation of nanoplastics during the degradation of a polystyrene (PS) disposable coffee cup lid. The results clearly show an increase in the formation of nanoplastics over time. After 56 days' exposure the concentration of nanoplastics in the PS sample was 1.26 × 10(8) particles/ml (average particles size 224 nm) compared to 0.41 × 10(8) particles/ml in the control.
| S-EPMC5250697 | biostudies-literature
Project description:Despite the growing concern over nanoplastics' (NPls) environmental impacts, their long-term effects on terrestrial organisms remain poorly understood. The main aim of this study was to assess how NPls exposure impacts both the parental (F1) and subsequent generations (F2 and F3) of the soil-dwelling species Folsomia candida. After a standard exposure (28 days), we conducted a multigenerational study along three generations (84 days), applying polystyrene nanoparticles (PS NPs; diameter of 44 nm) as representatives of NPls. Endpoints from biochemical to individual levels were assessed. The standard test: PS NPs (0.015 to 900 mg/kg) had no effect in F. candida survival or reproduction. The multigenerational test: PS NPs (1.5 and 300 mg/kg) induced no effects on F. candida survival and reproduction along the three generations (F1 to F3). PS NPs induced no effects in catalase, glutathione reductase, glutathione S-transferases, and acetylcholinesterase activities for the juveniles of the F1 to F3. Oxidative damage through lipid peroxidation was detected in the offspring of F1 but not in the juveniles of F2 and F3. Our findings underscore the importance of evaluating multigenerational effects to gain comprehensive insights into the contaminants long-term impact, particularly when organisms are continuously exposed, as is the case with NPls.
| S-EPMC10610651 | biostudies-literature
Project description: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.
| S-EPMC11312894 | biostudies-literature
Project description:BackgroundMany 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.ResultsTransmission 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.ConclusionVitamin 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.
| S-EPMC10680193 | biostudies-literature
Project description:Single-use plastic production is higher now than ever before. Much of this plastic is released into aquatic environments, where it is eventually weathered into smaller nanoscale plastics. In addition to potential direct biological effects, nanoplastics may also modulate the biological effects of hydrophobic persistent organic legacy contaminants (POPs) that absorb to their surfaces. In this study, we test the hypothesis that developmental exposure (0-7 dpf) of zebrafish to the emerging contaminant polystyrene (PS) nanoplastics (⌀100 nm; 2.5 or 25 ppb), or to environmental levels of the legacy contaminant and flame retardant 2,2',4,4'-Tetrabromodiphenyl ether (BDE-47; 10 ppt), disrupt organismal energy metabolism. We also test the hypothesis that co-exposure leads to increased metabolic disruption. The uptake of nanoplastics in developing zebrafish was validated using fluorescence microscopy. To address metabolic consequences at the organismal and molecular level, metabolic phenotyping assays and metabolic gene expression analysis were used. Both PS and BDE-47 affected organismal metabolism alone and in combination. Individually, PS and BDE-47 exposure increased feeding and oxygen consumption rates. PS exposure also elicited complex effects on locomotor behaviour with increased long-distance and decreased short-distance movements. Co-exposure of PS and BDE-47 significantly increased feeding and oxygen consumption rates compared to control and individual compounds alone, suggesting additive or synergistic effects on energy balance, which was further supported by reduced neutral lipid reserves. Conversely, molecular gene expression data pointed to a negative interaction, as co-exposure of high PS generally abolished the induction of gene expression in response to BDE-47. Our results demonstrate that co-exposure to emerging nanoplastic contaminants and legacy contaminants results in cumulative metabolic disruption in early development in a fish model relevant to eco- and human toxicology.
| S-EPMC8888882 | biostudies-literature