Ecotoxicology and Environmental Safety最新文献

Genetic diversity within plant populations is a key determinant of ecosystem functioning, especially, in shaping plant productivity. However, existing research examining how genetic diversity influences productivity has primarily focused on genotypic richness (number of genotypes), leaving the role of genotypic evenness (relative abundance of genotypes) understudied. Moreover, while microplastics has become a widespread contaminant, it is unknown whether microplastics could influence the impact of genetic diversity on plant growth performance. To address these gaps, we conducted an experiment using the clonal plant Hydrocotyle verticillata, manipulating both genotypic richness (1, 3, 6) and genotypic evenness (low, medium, high), crossing treatments with three types of soil microplastics (polylactic acid (PLA), poly-3-hydroxybutyrate (PHB) and polybutylene succinate (PBS)) and a control group without microplastics. All three microplastics significantly decreased biomass of H. verticillata. Genotypic richness had no effects on biomass, however, its effect on ramet numbers was altered by microplastics. The effect of genotypic evenness on both biomass and ramets were regulated by microplastics. With PBS, H. verticillata with high genotypic evenness produced significantly lower biomass and ramet numbers than those with low or medium evenness. However, this pattern was not observed under the PHB or PLA treatments. The study concludes that microplastics can modulate the effects of genotypic richness and evenness on the population performance of H. verticillata, but the effects vary depending on the type of microplastics. Our findings highlight the role of microplastics in regulating biodiversity-productivity relationships.

Environmental plasticizers are increasingly implicated in asthma susceptibility, yet the mechanisms linking chemical exposure to airway inflammation remain poorly defined. Here we show that the plasticizer di(2-ethylhexyl) phthalate (DEHP) directly drives a neutrophil-dominant asthma phenotype through activation of IL-17-centered immune pathways. Integrative network toxicology identified IL-6 and IL-1β as central inflammatory nodes connecting DEHP exposure with Th17 differentiation and IL-17 signaling. Consistent with these predictions, inhalational DEHP exposure in mice induced airway hyperresponsiveness, mixed granulocytic airway inflammation, mucus hypersecretion, and elevated pulmonary IL-6, IL-1β, and IL-17A expression. Immune profiling revealed expansion of IL-17A-producing lymphocytes, including Th17 cells and type 3 innate lymphoid cells (ILC3s). Genetic ablation of IL-17A markedly attenuated airway hyperresponsiveness and neutrophilic inflammation following DEHP exposure. Together, these findings identify an IL-6/IL-1β-Linked Th17/ILC3 axis as a mechanistic link between environmental plasticizer exposure and non-type 2 asthma, providing a conceptual framework for pollutant-driven airway disease.

Purpose: This study aims to screen and identify potential atherosclerosis (AS) biomarkers associated with common plasticizer exposure, providing a basis for future investigation into targeted therapeutic strategies.

Methods: AS-related datasets (from public databases) and common plasticizers (ATBC, DEP, DMP, DOP) were used. First, plasticizer-related genes (PRGs) and AS-related genes (ASRGs) were ascertained from public databases, respectively. Biomarkers were then determined through differential expression, machine learning, receiver operating characteristic (ROC), and gene expression analyses. To further explore the biological mechanisms underlying AS, functional enrichment, immune infiltration, molecular docking, molecular dynamics (MD) simulations, and single-cell RNA sequencing (scRNA-seq) analyses were conducted.

Principal results: In this study, AR and CCR2 were recognized as biomarkers for AS, with AR showing significantly lower expression in AS samples and CCR2 demonstrating significantly higher expression. These biomarkers were co-enriched in the "cytokine-cytokine receptor interaction" pathway. Additionally, 5 immune cell types with differential infiltration were ascertained, with regulatory T cells showing a strong correlation with both biomarkers. Molecular docking revealed favorable binding between the biomarkers and ATBC, with a particularly moderate binding energy of -7.1 kcal/mol between CCR2 and ATBC. MD simulations confirmed the stability of the CCR2-ATBC complex. Finally, scRNA-seq analysis ascertained vascular smooth muscle cells (VSMCs) and T lymphocytes as key cell types in AS, with dynamic expression patterns of AR and CCR2 observed during their differentiation.

Major conclusion: Our study identifies AR and CCR2 as biomarkers linking plasticizer exposure to AS. These findings elucidate potential molecular mechanisms and offer promising directions for future experimental validation and therapeutic exploration.

The western honey bee (Apis mellifera L.) is increasingly affected by chronic dietary exposure to pesticide-contaminated pollen. This study investigates the long-term effects of Malus domestica, Phacelia tanacetifolia, and Taraxacum sp. pollen collected from orchard and alpine habitats alongside a commercial feed additive (Promotor-L Apis) on honey bee survival, physiology, and gut microbiota. Multiresidue analysis revealed distinct pesticide and heavy metal profiles across pollens, while compositional analyses showed variation in amino acids, flavonoids, and phenolamides. Despite high contamination, Malus pollen with elevated flavonoid content promoted the highest vitellogenin accumulation and did not totally inhibit survival. Phacelia pollen from organic vineyards, though low in pesticides, had high copper levels and showed high mortality. Taraxacum pollen from apple orchards, though moderately contaminated, supported high survival. Unexpectedly, alpine Taraxacum pollen with elevated histidine content caused the highest mortality and microbial disruption, despite no pesticide residues. Promotor-L improved survival but did not increase vitellogenin. Pollen-fed bees generally exhibited higher gut microbiota abundance, while pathogen levels (including Nosema ceranae and Serratia marcescens) were specifically elevated under Taraxacum-based diets. These findings highlight that the impact of pollen nutrition on bee health is multifactorial, governed not only by pesticide exposure but also by botanical origin, nutritional traits, and secondary metabolites.

Intensified disinfectant use since the COVID-19 pandemic has increased the occurrence of disinfection byproducts (DBPs) in aquatic environments, raising concerns about their ecological effects. In this study, we evaluated the acute toxicity of 23 representative DBPs to the marine bacterium Vibrio fischeri (V. fischeri), including quinone DBPs (Q-DBPs), phenolic DBPs (P-DBPs), and haloacetic acids (HAAs). Toxicity followed the order Q-DBPs > P-DBPs > HAAs and was further influenced by halogenation patterns, solubility, and lipophilicity. Excess toxicity analysis indicated that Q-DBPs mainly act through electrophilic and redox reactions, whereas HAAs primarily undergo nucleophilic substitution (SN2). Molecular docking and molecular dynamics simulations suggested that DBPs interact with multiple proteins in V. fischeri, with the quorum-sensing regulator LuxR proposed as a potential target contributing to luminescence inhibition. Based on these mechanistic insights, we developed mechanism-based QSAR models that integrated molecular descriptors with receptor-binding parameters. The models showed strong predictive power (R² = 0.917, Q² = 0.798) and mechanistic interpretability. LuxR binding energy, ionization (pKa), and electronic reactivity (E_HOMO) were key determinants of P-DBP and HAA toxicity. In contrast, Q-DBPs toxicity was mainly associated with electronic reactivity consistent with electrophilic and redox behavior.

Marine aquaculture uses a wide variety of chemicals that go directly out into waterbodies, but little is known about the combined impact of these substances. As much of salmon aquaculture is situated in fjords where early development occurs for fish and other aquatic organisms, we have used zebrafish larvae as a model organism to assess the impacts of the combined exposure of a common antifoulant (ZnPT) and nanoplastics (NPs). Embryos were exposed to a control, 100 nm NPs (50 mg/L), 0.002 μM ZnPT (635.4 ng/L), and their combination. Zebrafish were studied from fertilization to 116 hpf, and developmental processes, early embryonic movement, heart rate, oxygen saturation, and swimming behavior, as well as DNA methylation and RNA transcriptome, were included as endpoints. We observed higher toxicity in larvae exposed to a combined treatment of ZnPT+NPs, with significant decreases in eye size and body length at 72 hpf, significantly increased burst activity at 24 hpf, significantly decreased oxygen saturation, hypomethylation of 5mC%, and 3054 significantly differentially expressed genes. These differentially expressed genes were mainly associated with immunogenic pathways, such as leukocyte (white blood cell) activation and proliferation, interleukin-1 production, neutrophil migration, interleukin-17 (antimicrobial proteins), cytokine and chemokine-mediated pathways, and C-type lectin receptors. At 72 hpf, co-exposure resulted in significantly stronger effects on developmental parameters (body length and eye size) and behavioral responses (burst activity). By 116 hpf, immunotoxic outcomes were substantially more pronounced in the co-exposure group, while impacts on global methylation levels had decreased in the co-exposure. Overall, these findings demonstrate that simultaneous exposure to ZnPT and NPs produce significantly stronger biological impacts than exposure to either compound alone.

Lanthanide-doped up-converting nanoparticles (UCNPs) are promising structures for researchers due to their unique properties and luminescence capabilities under near-infrared (NIR) excitation. They have found applications in various industries and scientific fields, including biology, medicine, and chemistry. In this study, we investigated the biodistribution and accumulation of SrF₂:Yb³⁺,Er³⁺ UCNPs (bare UCNPs) and SrF₂:Yb³⁺,Er³⁺@polyethylene glycol UCNPs (PEG-modified UCNPs) in tissues and organs of Tenebrio molitor larvae and analysed their impact on larval development, lifespan and metabolic status. We successfully visualised the presence of bare and PEG-modified UCNPs in T. molitor larvae and determined their distribution across different organs and tissues. An elemental analysis revealed no differences in the levels of either UCNP type in whole-body invertebrate samples. However, the imaging method revealed that PEG-modified UCNPs penetrate mealworms more effectively than bare UCNPs do at lower concentrations. These outcomes suggest that the distribution of PEG-modified UCNPs is greater than that of bare UCNPs in insects. Toxicity assays revealed that neither of the tested UCNPs had adverse effects on the lifespan or development of T. molitor at the tested concentrations. However, some of the experimental treatments altered lipid and carbohydrate levels. Specifically, bare UCNPs led to increased glycerol levels in the haemolymph after 3 h of incubation (at 100 µg/mL) and decreased triglyceride (TAG) levels in the fat body 24 h after injection (at 500 µg/mL). PEG-modified UCNPs increased glycogen levels in the fat body after 3 h of incubation (at 100 µg/mL). There were no changes in the other parameters. Overall, our findings revealed the accumulation of UCNPs in specific tissues and highlighted the influence of PEG modification on these processes. The studied UCNPs exhibited low toxicity and demonstrated the potential for effective bioimaging within insect organisms (especially those with PEG surface modifications). Moreover, the results showed that investigating the effects on metabolism is important, even if the impacts on lifespan and development are not observed.

The abundance of songbirds has declined across North America over the last 50 years. Thus, it is crucial to understand drivers of population losses, including environmental contaminants, such as mercury. The effects of mercury on songbird health are still not fully understood. We studied the effect of mercury on the corticosterone-mediated stress response in captive zebra finches (Taeniopygia guttata). Birds were subjected to 45 days of sublethal (approximately 1 mg/kg) dietary mercury alone or in combination with another stressor, 25 consecutive days of unpredictable food availability, beginning 17 days into dietary mercury exposure. Mercury alone or in combination with unpredictable food resulted in elevated baseline corticosterone. As expected, birds sampled later within a three-minute capture-and-sampling window had higher circulating corticosterone, reflecting the beginning of an acute stress response due to handling. However, in birds that experienced both mercury exposure and unpredictable food availability, longer sampling latency was not associated with increased corticosterone, suggesting a different or delayed stress response. We also found that birds that lost weight over the study period had higher corticosterone levels, but only if they received mercury exposure alone, suggesting a complex relationship between mercury exposure, stress, and body condition. Our study demonstrates experimentally that exposure to an environmentally relevant concentration of mercury elevates baseline corticosterone in an adult songbird, and that the physiological response to mercury may be impacted differently dependent on whether it is combined with another stressor.

16S rRNA amplicon sequencing and redundancy analysis to reveal the depth-stratified patterns of microbial communities driving methane cycling and mercury methylation in sediments of East Dongting Lake across a water depth gradient (deep: 25-35 m, middle: 15-25 m, shallow: 5-15 m). Methanogens,including Methanosaeta, were most abundant in the organic-rich middle layer (TOC: 11.56 ± 2.25 mg g⁻¹). Methylmercury concentrations were significantly higher in the middle (0.1966 ± 0.0868 μg kg⁻¹) and deep layers (0.1944 ± 0.0676 μg kg⁻¹) than in the shallow layer, even though the deep layer contained the lowest total mercury (THg: 47.90 ± 4.07 μg kg⁻¹). Mercury-methylating Bacillus was most abundant in the deep layer. Redundancy analysis revealed THg and sulfide were strongly associated with microbial community stratification across sediment depths. These results demonstrate that sediment depth couples methanogenesis and mercury methylation via redox and sulfur gradients, offering new insights into the co-regulation of greenhouse gas emissions and metal toxicity in freshwater ecosystems.