Explore the vast range of titles available.

Background Microplastics (MPs), which are smaller in size and difficult to degrade, can be easily ingested by marine life and enter mammals through the food chain. Our previous study demonstrated that following acute exposure to MPs, the serum testosterone content reduced and sperm quality declined, resulting in male reproductive dysfunction in mice. However, the toxic effect of long-term exposure to MPs at environmental exposure levels on the reproductive system of mammals remains unclear. Results In vivo, mice were given drinking water containing 100 μg/L and 1000 μg/L polystyrene MPs (PS-MPs) with particle sizes of 0.5 μm, 4 μm, and 10 μm for 180 consecutive days. We observed alterations in testicular morphology and reductions in testosterone, LH and FSH contents in serum. In addition, the viability of sperm was declined and the rate of sperm abnormality was increased following exposure to PS-MPs. The expression of steroidogenic enzymes and StAR was downregulated in testis tissues. In vitro, we used primary Leydig cells to explore the underlying mechanism of the decrease in testosterone induced by PS-MPs. First, we discovered that PS-MPs attached to and became internalized by Leydig cells. And then we found that the contents of testosterone in the supernatant declined. Meanwhile, LHR, steroidogenic enzymes and StAR were downregulated with concentration-dependent on PS-MPs. We also confirmed that PS-MPs decreased StAR expression by inhibiting activation of the AC/cAMP/PKA pathway. Moreover, the overexpression of LHR alleviated the reduction in StAR and steroidogenic enzymes levels, and finally alleviated the reduction in testosterone induced by PS-MPs. Conclusions PS-MPs exposure resulted in alterations in testicular histology, abnormal spermatogenesis, and interference of serum hormone secretion in mice. PS-MPs induced a reduction in testosterone level through downregulation of the LH-mediated LHR/cAMP/PKA/StAR pathway. In summary, our study showed that chronic exposure to PS-MPs resulted in toxicity of male reproduction under environmental exposure levels, and these potential risks may ring alarm bells of public health. Graphical abstract

Due to the continuous increase in polystyrene microplastics (PS MPs) incorporation in the environment, growing number of adverse effects on living organisms and ecosystem have become a global concern. Therefore, current study was planned to elucidate the impacts of 5 different concentrations control, 2, 20, 200, and 2000 μgL-1 of PS MPs on testicular tissues of rats. PS MPs significantly reduced the activities of antioxidant enzymes (catalase, superoxide dismutase and peroxidase) as well as total protein contents, while elevated the level of lipid peroxidation and reactive oxygen species. Moreover, expressions of steroidogenic enzymes (3β-hydroxysteroid dehydrogenase, 17β-hydroxysteroid dehydrogenase and steroidogenic acute regulatory protein) as well as the levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH) in plasma, intra-testicular testosterone and plasma testosterone were reduced and a significant (P < 0.05) reduction was noticed in the sperm count, motility and viability. Furthermore, PS MPs significantly up-regulated the expressions of Bax and caspase-3, while down-regulated the Bcl-2 expression. The histomorphological assessment revealed significant damages in the testicles as well as decrease in the number of germ cells (spermatogenic, spermatocytes and spermatids). Collectively, PS MPs generated oxidative stress (OS) and caused potential damage to the testicles of rats in a dose-dependent manner.

Polystyrene microplastics (PS‐MPs) are increasingly associated with carcinogenesis. However, their specific role in clear cell renal cell carcinoma (ccRCC) remains unclear. In this study, the microplastics in ccRCC tissues and normal adjacent tissues (NAT) are detected utilizing Py‐GC/MS, LDIR, and SEM. Tumor functional assays are conducted to assess the effects of PS‐MPs on ccRCC cellular behaviors. Transcriptomic alterations induced by PS‐MPs are characterized via RNA‐sequencing (RNA‐seq) analysis. Key signaling pathways are investigated through immunoblotting, immunocytochemistry, and ELISA. PDO and CDX models are employed to evaluate the effects of PS‐MPs on ccRCC progression and intervention strategies. The results demonstrate that PS‐MPs are markedly abundant in ccRCC tissues compared to NAT. Cytoplasmic accumulation of PS‐MPs promotes malignant phenotypes in ccRCC cells. RNA‐seq analysis demonstrates significant enrichment of oncogenic pathways following PS‐MPs exposure. Mechanistic validation confirms PS‐MPs exposure activates the NF‐κB and TGF‐β pathways in ccRCC. In preclinical models, PS‐MPs accelerate ccRCC growth, which is attenuated by treatment with the pathway inhibitors. In conclusion, this study provides the first comprehensive evidence that PS‐MPs exacerbate ccRCC progression through activating the NF‐κB and TGF‐β pathways. These findings establish PS‐MPs as an environmental risk factor for ccRCC and identify potential therapeutic targets to counteract PS‐MPs‐mediated oncogenic effects. This research provides the first comprehensive evidence that PS‐MPs exacerbate ccRCC progression by activating the NF‐κB and TGF‐β pathways. These findings establish PS‐MPs as an environmental risk factor for ccRCC progression and identify the NF‐κB and TGF‐β signaling as potential therapeutic targets to mitigate the adverse effects of ‐PS‐MPs exposure.

In recent years, the environmental health issue of microplastics has aroused an increasingly significant concern. Some studies suggested that exposure to polystyrene microplastics (PS-MPs) may lead to renal inflammation and oxidative stress in animals. However, little is known about the essential effects of PS-MPs with high-fat diet (HFD) on renal development and microenvironment. In this study, we provided the single-cell transcriptomic landscape of the kidney microenvironment induced by PS-MPs and HFD in mouse models by unbiased single-cell RNA sequencing (scRNA-seq). The kidney injury cell atlases in mice were evaluated after continued PS-MPs exposure, or HFD treated for 35 days. Results showed that PS-MPs plus HFD treatment aggravated the kidney injury and profibrotic microenvironment, reshaping mouse kidney cellular components. First, we found that PS-MPs plus HFD treatment acted on extracellular matrix organization of renal epithelial cells, specifically the proximal and distal convoluted tubule cells, to inhibit renal development and induce ROS-driven carcinogenesis. Second, PS-MPs plus HFD treatment induced activated PI3K-Akt, MAPK, and IL-17 signaling pathways in endothelial cells. Besides, PS-MPs plus HFD treatment markedly increased the proportions of CD8 + effector T cells and proliferating T cells. Notably, mononuclear phagocytes exhibited substantial remodeling and enriched in oxidative phosphorylation and chemical carcinogenesis pathways after PS-MPs plus HFD treatment, typified by alterations tissue-resident M2-like PF4 + macrophages. Multispectral immunofluorescence and immunohistochemistry identified PF4 + macrophages in clear cell renal cell carcinoma (ccRCC) and adjacent normal tissues, indicating that activate PF4 + macrophages might regulate the profibrotic and pro-tumorigenic microenvironment after renal injury. In conclusion, this study first systematically revealed molecular variation of renal cells and immune cells in mice kidney microenvironment induced by PS-MPs and HFD with the scRNA-seq approach, which provided a molecular basis for decoding the effects of PS-MPs on genitourinary injury and understanding their potential profibrotic and carcinogenesis in mammals. Graphical Abstract

Plastic is a polymer extremely resistant to degradation that can remain for up to hundreds or thousands of years, leading to the accumulation of massive amounts of plastic waste throughout the planet’s ecosystems. Due to exposure to various environmental factors, plastic breaks down into smaller particles named microplastics (1–5000 μm) and nanoplastics (<1 μm). Microplastics (MPs) are ubiquitous pollutants but, still, little is known about their effects on human and animal health. Herein, our aim is to investigate cytotoxicity, oxidative stress, inflammation and correlated gene modulation following exposure to polystyrene microplastics (PS-MPs) in HRT-18 and CMT-93 epithelial cell lines. After 6, 24 and 48 h PS-MPs treatment, cell viability (MTT) and oxidative stress (SOD) assays were performed; subsequently, expression changes and cytokines release were investigated by Real-Time PCR and Magnetic-beads panel Multiplex Assay, respectively. For each exposure time, a significantly increased cytotoxicity was observed in both cell lines, whereas SOD activity increased only in CMT-93 cells. Furthermore, Magnetic-beads Multiplex Assay revealed an increased release of IL-8 in HRT-18 cells’ medium, also confirmed by gene expression analysis. Results obtained suggest the presence of a pro-inflammatory pattern induced by PS-MPs treatment that could be related to the observed increase in cytotoxicity.

The impact of polystyrene microplastics (PS-MPs) on the nervous system has been documented in the literature. Numerous studies have demonstrated that the activation of the epidermal growth factor receptor 4 (ErbB4) is crucial in neuronal injury and regeneration processes. This study investigated the role of targeted activation of ErbB4 receptor through a small molecule agonist, 4-bromo-1-hydroxy-2-naphthoic acid (C11H7BrO3, E4A), in mitigating PS-MPs-induced neuronal injury. The findings revealed that targeted activation of ErbB4 receptor significantly ameliorated cognitive behavioral deficits in mice exposed to PS-MPs. Furthermore, E4A treatment upregulated the expression of dedicator of cytokinesis 3 (DOCK3) and Sirtuin 3 (SIRT3) and mitigated mitochondrial and synaptic dysfunction within the hippocampus of PS-MPs-exposed mice. E4A also diminished the activation of the TLR4-NF-κB-NLRP3 signaling pathway, consequently reducing neuroinflammation. In vitro experiments demonstrated that E4A partially alleviated PS-MPs-induced hippocampal neuronal injury and its effects on microglial inflammation. In conclusion, the findings of this study indicate that targeted activation of ErbB4 receptor may mitigate neuronal damage and subsequent neuroinflammation, thereby alleviating hippocampal neuronal injury induced by PS-MPs exposure and ameliorating cognitive dysfunction. These results offer valuable insights for the development of potential therapeutic strategies.

In recent years, the environmental pollution caused by microplastics (MPs) has attracted extensive attention. Numerous studies have shown that MPs could cause liver damage in aquatic animals. However, there is a limited range of technical approaches available to mitigate and minimize the detrimental impact of MPs on both wild fish populations and aquaculture operations. Thus, this study aimed to investigate the impact of dietary chitosan supplementation on the prevention and treatment of liver damage induced by exposure to polystyrene microplastics (PS-MPs) in Nile tilapia (Oreochromisniloticus). The results indicated that after two weeks of exposure, the liver of tilapia showed oxidative stress, inflammatory response and fibrosis. Meanwhile, after the chitosan addition, the oxidative stress, inflammatory response and fibrosis of tilapia liver were reversed, the pyroptosis and ferroptosis in tilapia liver were inhibited, the combination of mitochondria with PS-MPs in tilapia liver cells was inhibited, and the mitochondrial damage was reversed. In summary, the study confirmed the potential prophylaxis and treatment effect of dietary chitosan supplementation on PS-MPs exposure-induced liver damage in tilapia, and provided basic data for further studies on prophylaxis and treatment of the toxic effects of MPs. This study also presented efficacious strategies for alleviating the deleterious impacts of MPs on fish farming, thereby fostering sustainable and eco-friendly approaches in aquaculture.

Polystyrene microplastics (PS-MPs) are microplastic particles produced during plastic manufacturing and environmental degradation, accumulating over time and entering ecosystems through various pathways, ultimately affecting organisms and inducing toxic effects. Current research on the impact of PS-MPs on mammalian oocyte quality, along with potential preventive mechanisms and strategies to mitigate toxicity, remains limited. This study investigates the effects of antioxidant melatonin on oocyte quality in the presence of PS-MPs, focusing on their influence on oocyte meiotic maturation and embryonic developmental potential. PS-MPs at a concentration of 30 μg/mL significantly impaired first polar body extrusion and reduced the success rate of parthenogenetic activation of mature oocytes in vitro. Furthermore, exposure to PS-MPs exacerbated oxidative stress, mitochondrial dysfunction, apoptosis, and autophagy impairment. Additionally, PS-MPs exposure led to a reduction in antioxidant gene expression and an increase in apoptosis-related gene expression in porcine oocytes. Immunofluorescence assays revealed that PS-MPs may induce oxidative stress, mitochondrial damage, and inflammation through the NF-KB/Nrf2/JNK MAPK signaling pathway crosstalk. Further investigation demonstrated that melatonin supplementation alleviated the toxic effects of PS-MPs exposure, offering potential as a therapeutic approach for mitigating PS-MP-induced reproductive toxicity and preserving oocyte quality.

Microplastics (MPs) represent a significant environmental pollutant and have raised considerable concern due to their tendency to accumulate in animals, plants, and humans, thereby posing potential health risks. In this study, female mice were exposed to different doses of polystyrene microplastics (PS-MPs) (0, 0.3, 3, and 30 mg/kg) via intragastric administration for 35 days to investigate their effects on female reproductive health. The results showed a significant reduction in first polar body extrusion (PBE) and glutathione (GSH) levels, accompanied by increased reactive oxygen species (ROS) levels in germinal vesicle (GV) stage oocytes in the 30 mg/kg group. Based on these findings, the 30 mg/kg dose was selected for subsequent reproductive toxicity assessments. Compared with the control group, oocytes from the PS-MPs treated group exhibited a significant increase in spindle abnormalities and lipid droplet accumulation. RNA sequencing and experimental validation in mouse oocytes demonstrated that PS-MPs exposure led to upregulation of SIRT4 protein expression and downregulation of genes associated with fatty acid oxidation. Treatment with BEC2, a CPT1A activator, partially reversed the inhibitory effects of PS-MPs on fatty acid oxidation and improved oocyte maturation. Further analyses revealed that PS-MPs exposure reduced HSPA1A protein expression, potentially contributing to the activation of endoplasmic reticulum (ER) stress in ovarian cells. In addition, PS-MP exposure significantly altered the expression of genes related to ovarian fibrosis, angiogenesis, and aging. Knockdown of Hspa1a in the mouse granulosa cell line KK1 reduced cell proliferation and viability, induced G2/M cell cycle arrest, and triggered ER stress. Collectively, these findings suggest that PS-MPs exposure may accelerate ovarian aging by disrupting protein homeostasis and impair oocyte maturation in mice by disrupting fatty acid oxidation.

The widespread presence of polystyrene microplastics (PS-MPs) and agricultural pollutants such as avermectin (AVM) in aquatic environments poses a significant threat to aquatic organisms. However, the combined toxic effect of PS-MPs and AVM on cardiac development remains poorly understood. This study aimed to investigate the cardiac toxicity of AVM co-exposed with two sizes of MPs (large MPs, LMPs, 20 µm; small MPs, SMPs, 80 nm) in both larval and adult zebrafish. Firstly, under the co-exposure conditions of MPs and AVM, we observed significant cardiac developmental toxicity, including decreased survival rate, body length, and hatching rate, as well as a significant reduction in the number of myocardial cells. Secondly, the number of neutrophils and antioxidant enzyme activities such as CAT and SOD were greatly decreased, while inflammatory cytokines such as TNF-α and IL8 were significantly increased after co-exposure in larval zebrafish. Thirdly, there was severe disorganization of cardiomyocytes and interstitial edema in adult zebrafish hearts under the co-exposure by histopathological examination. Our results suggest that cardiomyocyte proliferation was suppressed, but heart apoptosis level and anti-apoptotic genes were significantly increased in the AVM+MPs co-exposure. Additionally, transcriptome sequencing and bioinformatics analysis revealed that significant changes in differentially expressed genes in the AVM+SMPs co-exposure group, particularly in the processes related to oxidation–reduction, inflammatory response, and the MAPK signaling pathway in the adult zebrafish heart. Furthermore, our pharmacological experiments demonstrated that inhibiting ROS and blocking the MAPK signaling pathway could partially rescue the heart injury induced by AVM and MPs co-exposure in both larval and adult zebrafish. In summary, this study suggested that co-exposure to AVM and MPs could induce heart toxicity mainly via the ROS-mediated MAPK signaling pathway in zebrafish. The information provided important insights into the potential environmental risk of microplastic and pesticide co-exposure on aquatic ecosystems.