Environmental Pollution最新文献

Chronic UVB exposure poses a significant threat to both skin and visceral health. In recent years, the adverse role of chronic UVB exposure in liver health has been suggested but not fully elucidated. This study aims to comprehensively investigate the effects of chronic UVB exposure on liver health in male SKH-1 hairless mice and clarify potential mechanisms through multi-omics approaches. The findings suggested that 10-week chronic skin exposure to UVB not only triggers hepatic inflammation and oxidative stress but also, more importantly, results in lipid metabolism abnormalities in the liver. Hepatic transcriptomic analysis revealed significant alterations in various signaling pathways and physiological processes associated with inflammation, oxidative stress, and lipid metabolism. Further lipidomic analysis illustrated significant changes in the metabolism of glycerolipids, sphingolipids, and glycerophospholipids in the liver following chronic UVB exposure. The 16S rRNA sequencing analysis indicated that chronic UVB exposure disrupts the structure and function of the microbiota. In search of potential mechanisms used by the microbiome to regulate the hepatic disease morphology, we filtered mouse fecal supernatants and cultured the supernatants with HepG2 cells. Fecal supernatant from UVB-exposed mice induced increased secretion of the inflammatory cytokine IL-8, accumulation of MDA, reduced SOD activity, and decreased lipid content in normal hepatic cells. In summary, skin chronic exposure to UVB induces multiple liver injuries and gut microbiota dysbiosis in mice and gut microbiota metabolites may be one of the contributing factors to hepatic injury caused by chronic UVB exposure. These discoveries deepen the comprehension of the health risks associated with chronic UVB exposure.

Modern agriculture relies heavily on pesticide use to meet the demands of food quality and quantity. Therefore, pesticides are often applied in mixtures, leading to a diverse cocktail of chemicals and their metabolites in soils, which can affect non-target organisms such as soil microorganisms. Pesticides are tested for their single effects, but studies on their interactive effects are scarce. This study aimed to determine the effects of up to three simultaneously applied pesticides on the soil microbial community and on their special function in pesticide degradation. Agricultural soil without previous pesticide application was exposed to different mixtures of the herbicide glyphosate (GLP), the phenoxy herbicide MCPA (2-methyl-4-chlorophenoxyacetic acid) and the fungicide difenoconazole (DFC) for up to 56 days. Isotopic and molecular methods were used to investigate effects of the mixtures on the microbial community and to follow the mineralization and utilization of GLP. An initial increase in the metabolic quotient by up to 35 % in the presence of MCPA indicated a stress reaction of the microbial community. The presence of multiple pesticides reduced both gram positive bacterial fatty acid methyl esters (FAMEs) by 13 % and the abundance of microorganisms with the genetic potential for GLP degradation via the AMPA (aminomethylphosphonic acid) pathway. Both the number of pesticides and the identities of individual pesticides played major roles. Surprisingly, an increase in ¹³C-labelled GLP mineralization of up to 40 % was observed while carbon use efficiency (CUE) decreased. Interactions between multiple pesticides might alter the behavior of individual pesticides and be reflected in the microbial community. Our results highlight the importance of investigating not only single pesticides, but also pesticide mixtures and their interactions.

Second-generation anticoagulant rodenticides (SGARs) are commonly used for rodent control, affecting various non-target wildlife species. Here, blood samples from common kestrels (Falco tinnunculus, n = 70 chicks) and barn owls (Tyto alba, n = 54 chicks and 12 adults) from Southeastern Spain were analysed using HPLC-TQ. SGAR prevalence was 68.6% in kestrel chicks, 50% in barn owl chicks and 100% in adult barn owls, with multiple SGARs in both species. Prothrombin time analysis in barn owls revealed a positive correlation with blood ΣSGARs, suggesting a potential adverse effect on coagulation. Analysis of variables potentially influencing SGAR prevalence indicated that, for kestrels, it was only related to the extent of artificial surface, showing no differences across study sites. In owlets, the highest prevalence occurred in the most urbanized study site, with human population density being a key factor. This study highlights species-specific differences in SGAR exposure, likely influenced by ecological traits. Barn owls probably encounter contaminated prey near anthropized areas, with widespread SGAR use and higher presence of target rodents. Conversely, kestrels, hunting a variety of prey often near human settlements, face consistently elevated exposure from multiple sources. Understanding these variations is crucial for effective conservation and minimizing SGAR impact on non-target wildlife.

Zinc oxide nanoparticles (ZnO-NPs) are nanomaterials mainly produced and used worldwide. They translocate to circulatory systems from various exposure routes. While blood and endothelial cells are persistently exposed to circulating ZnO-NPs, the potential risks posed by ZnO-NPs to the cardiovascular system are largely unknown. Our study identified the potential risk of thrombosis and disturbance of the blood-brain barrier (BBB) by coagulant activity on red blood cells (RBCs) caused by ZnO-NPs. ZnO-NPs promoted the externalization of phosphatidylserine and the generation of microvesicles through an imbalance of intracellular mechanisms regulating procoagulant activity in human RBCs. The coagulation cascade leading to thrombin generation was promoted in ZnO-NPs-treated human RBCs. Combined with human RBCs, ZnO-NPs caused coagulant activity on isolated rat RBCs and rat venous thrombosis models. We identified the erythrophagocytosis of RBCs into brain endothelial cells via increased PS exposure induced by ZnO-NPs. Excessive erythrophagocytosis contributes to disrupting the BBB function of endothelial cells. ZnO-NPs increased the procoagulant activity of RBCs, causing venous thrombosis. Excessive erythrophagocytosis through ZnO-NPs-treated RBCs resulted in the dysfunction of BBB. Our study will help elucidate the potential risk ZnO-NPs exert on the cardiovascular system.

Tire microplastics (TMPs) and antibiotics are emerging pollutants that widely exist in water environments. The coexistence of these pollutants poses severe threats to aquatic organisms. However, the toxicity characteristics and key molecular factors of the combined exposure to TMPs in aquatic organisms remain unknown. Therefore, the joint toxicity of styrene–butadiene rubber TMPs (SBR-TMPs) and 32 antibiotics (macrolides, fluoroquinolones, β-lactams, sulfonamides, tetracyclines, nitroimidazoles, highly toxic antibiotics, high-content antibiotics, and common antibiotics) in zebrafish was investigated using a full factorial design, molecular docking, and molecular dynamics simulation. Sixty-four combinations of antibiotics were designed to investigate the hepatotoxicity of the coexistence of SBR-TMPs additives and antibiotics in zebrafish. Results indicated that low-order effects of antibiotics (e.g., enoxacin–lomefloxacin and ofloxacin–enoxacin–lomefloxacin) had relatively notable toxicity. The van der Waals interaction between additives and zebrafish cytochrome P450 enzymes primarily affected zebrafish hepatotoxicity. Zebrafish hepatotoxicity was also affected by the ability of SBR-TMPs to adsorb antibiotics, the relation between antibiotics, the affinity of antibiotics docking to zebrafish cytochrome P450 enzymes, electronegativity, atomic mass, and the hydrophobicity of the antibiotic molecules. This study aimed to eliminate the joint toxicity of TMPs and antibiotics and provide more environmentally friendly instructions for using different chemicals.

This study investigated the efficacy of incorporating nitric oxide (NO; 10 μM) and ascorbic acid (Asc; 10 μM) into the culture medium to confer cadmium (Cd; 5 μM) tolerance in thyme (Zataria multiflora). The phytotoxicity of Cd resulted in a decrease in shoot biomass, which NO or Asc mitigated. Adding Asc and NO to the culture medium was associated with substantial DNA hypomethylation. The NO + Cd and Asc + Cd treatments were accompanied by an increase in the unmethylation percentages, about 3-fold higher than the control. The hemi-methylation percentages in the Asc-supplemented seedlings also displayed an upward trend. The transcriptional upregulation in the γ-terpinene synthase (TPS) gene resulted from the applied elicitors, especially NO. In response to the NO and Asc treatments, the transcription of two cytochrome P450 monooxygenase genes (CYP71D178 and CYP71D180) went up. Incorporating Asc or NO into the culture medium enhanced the concentrations of proline, carvacrol, and thymol metabolites. Employing NO or Asc mitigated the 43% decrease in protein content due to the Cd cytotoxicity. The NO and Asc applications improved the activity of the phenylalanine ammonia-lyase (PAL) enzyme. NO and Asc utilization increased the accumulation of flavonoids. NO and Asc also up-regulated the activities of two enzymatic antioxidants (catalase and peroxidase). Collectively, this study provided novel insight into how Asc or NO confers Cd tolerance by epigenetically remodeling DNA methylation, transcriptionally up-regulating terpenoid and phenylpropanoid metabolism, increasing proline concentration, and improving antioxidants.