Ecotoxicology and Environmental Safety最新文献

Aniline is a widely distributed environmental pollutant, but its impact on gut health and underlying mechanisms remain poorly understood. This study investigated the effects of aniline on intestinal epithelial cell apoptosis and intestinal inflammation, and explored the role of the ATF2 signaling pathway using in vitro and in vivo models. IEC-6 rat intestinal crypt epithelial cells were treated with different concentrations of aniline (0, 2.5, 5, 10, 20, 40 mM). Cell viability, apoptosis, reactive oxygen species (ROS) production, and signaling pathway activation were assessed by CCK-8 assay, flow cytometry, and Western blotting. In vivo, eight-week-old male C57BL/6 mice without pre-existing intestinal disease were exposed to aniline by daily oral gavage (10, 20, 40 mg/kg) for 14 days. Ileal tissues were analyzed by histopathology, immunohistochemistry, and Western blotting. Aniline exposure significantly reduced IEC-6 cell viability (≥ 5 mM), induced apoptosis and ROS generation, and activated the p38 MAPK pathway, accompanied by upregulation of pro-apoptotic proteins Bax and Cleaved-caspase-3 and downregulation of tight junction proteins ZO-1, occludin, and claudin-1. In mice, aniline exposure led to shortened small intestine length, inhibition of weight gain, crypt architectural damage, and inflammatory cell infiltration, together with increased expression of TNF-α, IL-17, and CD68 and decreased tight junction proteins. These changes indicate intestinal inflammation and disruption of the intestinal barrier with morphological and molecular features that resemble experimental inflammatory bowel disease (IBD). Mechanistically, aniline exposure markedly activated the ATF2 signaling pathway in ileal tissues. Silencing ATF2 in IEC-6 cells significantly attenuated aniline-induced apoptosis, ROS production, and the expression of inflammation-related proteins. Collectively, our findings demonstrate that aniline promotes intestinal epithelial cell apoptosis and disrupts the mucosal barrier via activation of the ATF2 pathway, thereby inducing intestinal inflammation with IBD-like pathological features. This work provides mechanistic insight into how environmental pollutants such as aniline may contribute to intestinal inflammatory diseases and identifies ATF2 as a potential molecular target for mitigating pollutant-related gut injury. However, because classic clinical indicators of IBD (e.g., diarrhea, hematochezia, disease activity index) were not assessed, our model should be interpreted as chemically induced intestinal inflammation rather than a complete IBD model.

Cadmium (Cd) and lead (Pb) contamination in soils pose a serious environmental challenge requiring urgent remediation. This study aimed to evaluate the efficiency of Serratia marcescens 2G5 and Amorpha fruticosa L. in the synergistic remediation of heavy metal-contamination in soil, and to investigate the effect of 2G5 inoculation on the bioaccumulation and translocation of Pb and Cd in A. fruticosa L. and the rhizosphere soil microbiomes. The results showed that 2G5 inoculation mitigated the negative impacts of Cd and Pb stress on A. fruticosa L., increasing total plant biomass by 22.19 % and enhancing the phytoextraction efficiency of Cd and Pb by 64.18-102.87 %. The positive effects of 2G5 inoculation on the growth and soil remediation of A. fruticosa L. were probably attributed to the significant improvements in soil enzyme activities (urease, acid phosphatase, catalase, and sucrase) and soil nutrient contents [Total phosphorus (TP), available phosphorus (AP) and hydrolyzed nitrogen (AN)]. Principal co-ordinate analysis revealed that both heavy metal contamination and 2G5 inoculation significantly influenced the bacterial community structure in the rhizosphere soil, with the influence of heavy metals being greater than that of the inoculation. Patescibacteria (27.02 %-30.12 %) have replaced Proteobacteria (22.38-24.02 %) as the dominant phyla in contaminated soil. The Mantel test results indicated that soil heavy metals, along with AP and urease, were the primary environmental factors influencing the bacterial community at the phylum level under heavy metal contamination. Furthermore, linear discriminant analysis effect size (LEfSe) identified Ellin6067 (Nitrosomonadaceae) and Dongia (Rhodospirillaceae) as the key bioindicators of heavy metal contamination and Sphingomonas and Micropepsis as the key bioindicators of 2G5 inoculation. In conclusion, the findings of this study revealed the potential and feasibility of combining S. marcescens 2G5 and A. fruticosa L. for the remediation of soil heavy metal- contamination, offering a viable strategy for microbial agents and plants to cooperate in mitigating heavy metal contamination in soil.

Cadmium (Cd) contamination modifies both soil processes and plant physiology, but the relationship between photosynthetic carbon allocation and Cd uptake in C3 and C4 accumulator plants remains unclear. Here, the C3 accumulator Solanum photeinocarpum (SP) and the C4 accumulator Pennisetum americanum × P. purpureum (PA) were studied using a ¹³C pulse-labeling technique. Results showed that fixed carbon was mainly transferred to soil as labile organic carbon (LOC) and light fraction organic carbon (LFOC). In SP, Cd pollution promoted Cd accumulation in shoots and roots, increased soil available Cd and pH, and enhanced carbon transfer to soil, leading to greater remediation efficiency. In PA, Cd pollution decreased soil pH and microbial biomass carbon, but increased available Cd and soil organic carbon, with shoot-fixed carbon positively correlated with Cd uptake. These findings demonstrate that Cd pollution differentially regulates carbon allocation in C3 and C4 accumulators through different mechanisms, supporting both phytoremediation efficiency and carbon sequestration.

The large-scale production and widespread use of the triazole fungicide prothioconazole (PTC) have led to its frequent detection in environmental samples. However, the effects of PTC and its metabolite prothioconazole-desthio (dPTC) on the aquatic organism intestinal metabolic activities remain insufficiently studied. In this study, adult male and female zebrafish were exposed to PTC and dPTC at environmental-related doses (0.5 and 10 μg/L) for 30 days to investigate their sex-specific effects on intestinal injury. PTC and dPTC induced intestinal mucosal injury, with more severe effects in females. Compared to the control group, female zebrafish treated with PTC or dPTC exhibited a significant decrease in intestinal goblet cells (0.67-, 0.64-fold), damage to intestinal villi, and an increase in macrophages (2.21-, 2.79-fold). 16S rRNA sequencing, targeted metabolomics, and molecular docking analysis showed that significant reductions in bacterial metabolites, including betaine, choline, and methylthioadenosine, caused abnormal methyl transfer in one-carbon metabolism, mediating gut microbiota dysbiosis. The fundamental causes of this difference are rooted in three interconnected biological mechanisms, which together amplify toxicity in females while conferring relative resistance in males. Changes in DNA methylation-related transcription levels further confirmed that the interaction between intestinal metabolic activity and epigenetic regulation had a cascade effect on intestinal injury. PTC and dPTC have sex-specific effects on zebrafish intestinal health through one-carbon metabolism via the betaine-homocysteine methyltransferase -mediated pathway, emphasizing the importance of considering microbiota and sex dependence in ecological risk assessment.

Karst water serves as a crucial water source in global karst regions. However, acid mine drainage (AMD) produced by coal mining, characterized by low pH and elevated concentrations of trace elements (TEs), threatens karst water quality. Thus, identifying priority control elements is key to controlling TEs pollution in karst water. In this study, a typical karst river basin affected by abandoned coal mines in Southwest China was taken as the research object to comprehensively analyze the spatiotemporal distribution of TEs, quantitatively identify pollution sources and associated human health risks, and determine the priority factors for health risk management. Spatiotemporal analysis revealed that elevated TEs were near abandoned coal mines, indicating their distribution was closely associated with AMD discharge, and TEs showed higher concentrations in the wet season. Furthermore, Fe, Mn, Ni, and As exceeded World Health Organization (WHO) guidelines to varying degrees in both seasons, while Cd only exceeded these guidelines in the wet season. Positive Matrix Factorization (PMF) identified four primary sources of TEs: abandoned coal mine drainage source, natural geological weathering source, water-rock reaction and agricultural activity superimposed source, and sewage-agricultural activity composite sources. Health Risk Assessment (HRA) based on Monte Carlo simulation indicated that non-carcinogenic risks and total carcinogenic risks for children exceeded safety thresholds during the wet season, with As posing cautionary risk. The relationship between TEs, pollution sources, and health risks indicated that abandoned coal mine drainage, Fe, and As were identified as priority control factors. These findings could offer critical guidance for safe health risk control in karst basins globally affected by similar mining activities.

Background: Studies have focused on the effects of toxic metals and trace elements on child behavioral problems. Findings are inconsistent, and the effects of mixtures of elements remain unclear.

Methods: We measured manganese (Mn), cadmium (Cd), thallium (Tl), molybdenum (Mo), and selenium (Se) concentrations in the first, second, and third trimesters and cord blood among 2514 mother-child dyads from the Ma'anshan Birth Cohort. To assess children's behavioral development, we used the Child Behavior Checklist for Ages 1.5-5. Generalized linear models, Bayesian kernel machine regression, and Quantile g-computation were applied to analyze individual and mixed associations between metals and trace elements and preschoolers' internalizing and externalizing symptoms.

Results: Maternal serum Cd, Tl, and Mo concentrations in the second trimester were positively associated with internalizing symptoms scores, externalizing symptoms scores and total problems scores (P < 0.05). Se was negatively associated with internalizing symptom s scores, externalizing symptoms scores and total problems scores (β_{internalizing = -}6.91, 95 %CI: -11.95, -1.87; β_{externalizing} = -7.23, 95 %CI: -11.25, -3.21; β_total = -8.00, 95 %CI: -12.12, -3.89). The association between Cd and internalizing and externalizing was more pronounced in boys. Exposure to metal mixtures in cord blood was negatively associated with total problems scores.

Conclusions: Prenatal exposure to Cd, Tl, and Mo was associated with an increased risk of behavioral problems in children, with the associations exhibiting sex differences. Conversely, Se may confer a protective effect against childhood behavioral problems. Further studies are warranted to support the findings and explore the mechanism of sex -specific disparity.

Renal fibrosis, characterized by excessive extracellular matrix (ECM) deposition in the interstitium, is a hallmark of chronic kidney disease (CKD). Matrix metalloproteinases (MMPs), including MMP2 and MMP9, are zinc-dependent endopeptidases involved in ECM degradation and have been implicated in renal fibrosis. Exposure to metals and metalloids (collectively referred to as "metals") has been associated with CKD and may influence the expression of MMP2 and MMP9. Additionally, genetic polymorphisms in MMP2 and MMP9 may affect MMP expression. This study aimed to investigate the associations of plasma MMP2 and MMP9 concentrations and polymorphisms in MMP2 and MMP9 with CKD, as well as their interactions with metal exposure. A total of 215 patients with clinically diagnosed CKD and 389 age- and sex-matched controls were recruited. Plasma concentrations of MMP2 and MMP9 were measured using enzyme-linked immunosorbent assays. Plasma selenium, blood cadmium and lead, and total urinary arsenic concentrations were quantified. Common polymorphisms in MMP2 and MMP9 were genotyped. Logistic regression models were used to estimate odds ratios (ORs) and 95 % confidence intervals (CIs) for the associations between these factors and CKD, adjusting for potential confounders. Elevated plasma concentrations of MMP2 and MMP9 were significantly associated with CKD, with ORs (95 % CIs) of 12.45 (6.04-25.66) and 3.77 (2.14-6.66), respectively. No associations were observed between the MMP2 or MMP9 genotypes and CKD. Significant additive interactions were identified between high plasma MMP2 levels and elevated total urinary arsenic, blood cadmium, blood lead, or plasma MMP9, as well as low plasma selenium levels, further increasing the association with CKD. Additionally, a significant multiplicative interaction was observed between high plasma MMP2 and elevated blood lead levels on CKD. To the best of our knowledge, this study is the first to identify the interactions between plasma MMP2 concentrations and metals on increasing the association of CKD.