As a common fungicide, tebuconazole are ubiquitous in the natural environment and poses many potential risks. In this study, we examined the effects of exposure to tebuconazole on colitis in mice and explored its underlying mechanism. Specifically, exposure to tebuconazole could cause structural damage and inflammatory cell infiltration in colon tissue, activate the expression of inflammation-related genes, disrupt the expression of barrier function-related genes, and induce the colonic inflammation in mice. Similarly, exposure to tebuconazole could also exacerbate DSS-induced colitis in mice. In addition, we found that tebuconazole also could change the composition of the gut microbiota. In particular, tebuconazole significantly increases the relative abundance of Akkermansia of mice. Moreover, tebuconazole resulted in metabolic profiles disorders of the serum, leading to significant changes in the relative contents of metabolites involving glycolipid metabolism and amino acid metabolism. Particularly, the results of the gut microbiota transplantation experiment showed that exposure to tebuconazole could induced colonic inflammation in mice in a gut microbiota–dependent manner. Taken together, these results indicated that tebuconazole could induce colitis in mice via regulating gut microbiota. Our findings strongly support the concept that the gut microbiota is a key trigger of inflammatory bowel disease caused by pesticide intake.

Insufficient evidence exists regarding the visible physiological toxic endpoints of MPs exposures on zebrafish larvae due to their small sizes. Herein, the impacts of micro-polystyrene particles (μ-PS) and 100 nm polystyrene particles (n-PS) on the toxicity of cadmium (Cd) through altering neutrophil expressions were identified and quantified in the transgenic zebrafish (Danio rerio) larvae Tg(lyz:DsRed2), and the effects were size-dependent. When exposed together with μ-PS, the amount of neutrophils in Cd treated zebrafish larvae decreased by 25.56% through reducing Cd content in the larvae. By contrast, although n-PS exposure caused lower Cd content in the larvae, the expression of neutrophils under their combined exposure remained high. The mechanism of immune toxicity was analyzed based on the results of metabonomics. n-PS induced high oxidative stress in the larvae, which promoted taurine metabolism and unsaturated fatty biosynthesis in n-PS + Cd treatment. This observation was accordance with the significant inhibition of the activities of superoxide dismutase and catalase enzymes detected in their combined treatment. Moreover, n-PS promoted the metabolic pathways of catabolic processes, amino acid metabolism, purine metabolism, and steroid hormone biosynthesis in Cd treated zebrafish larvae. Nanoplasctis widely coexist with other pollutants in the environment at relatively low concentrations. We conclude that more bio-markers of immune impact should be explored to identify their toxicological mechanisms and mitigate the effects on the environment.

Steroid hormones are prevalent in the environment and have become emerging pollutants, but little is known about their effects on soil microbial community composition and function. In the present study, three representative soils in China were amended with environmentally relevant concentrations of testosterone and responses of soil bacterial community composition and soil function were assessed using high-throughput sequencing and nontargeted metabolomics. Our results showed that testosterone exposure significantly shifted bacterial community structure and metabolic profiles in soils at Ningbo (NB) and Kunming (KM), which may reflect high bioavailability of the hormone. Abundances of several bacterial taxa associated with nutrient cycling were reduced by testosterone and metabolites related to amino acid metabolism were downregulated. A close connection between bacterial taxa and specific metabolites was observed and confirmed by Procrustes tests and a co-occurrence network. These results provide an insight into the effects of steroid hormones on soil microbial community and highlight that nontargeted metabolomics is an effective tool for investigating the impacts of pollutants.

Excess nitrate has been reported to be associated with many adverse effects in humans and experimental animals. However, there is a paucity of information of the effects of nitrate on intestinal microbial community. In this study, the effects of nitrate on development, intestinal microbial community, and metabolites of Bufo gargarizans tadpoles were investigated. B. gargarizans were exposed to control, 5, 20 and 100 mg/L nitrate-nitrogen (NO₃–N) from eggs to Gosner stage 38. Our data showed that the body size of tadpoles significantly decreased in the 20 and 100 mg/L NO₃–N treatment group when compared to control tadpoles. Exposure to 20 and 100 mg/L NO₃–N also caused indistinct cell boundaries and nuclear pyknosis of mucosal epithelial cells in intestine of tadpoles. In addition, exposure to NO₃–N significantly altered the intestinal microbiota diversity and structure. The facultative anaerobic Proteobacteria occupy the niche of the obligately anaerobic Bacteroidetes and Fusobacteria under the pressure of NO₃–N exposure. According to the results of functional prediction, NO₃–N exposure affected the fatty acid metabolism pathway and amino acid metabolism pathway. The whole-body fatty acid components were found to be changed after exposure to 100 mg/L NO₃–N. Therefore, we concluded that exposure to 20 and 100 mg/L NO₃–N could induce deficient nutrient absorption in intestine, resulting in malnutrition of B. gargarizans tadpoles. High levels of NO₃–N could also change the intestinal microbial communities, causing dysregulation of fatty acid metabolism and amino acid metabolism in B. gargarizans tadpoles.

As an important part of extracellular secondary metabolites, extracellular polymeric substances (EPS) can play a significant role in protecting cells from the threat of exogenous substances, including nanoparticles (NPs). However, the regulation mechanisms of EPS secretion under NPs exposure remain largely unknown. This study investigated the signaling pathways and molecular responses related to EPS secretion of algae (Chlorella pyrenoidosa) upon the exposures to anatase and rutile TiO₂ NPs (nTiO₂-A and nTiO₂-R, respectively) at two similar toxic (20% and 50% of algal growth inhibition) concentrations. The results showed that EPS responded to nTiO₂ stress via excess secretion and compositional variation, and nTiO₂-A induced more EPS secretion than nTiO₂-R at similar toxicity concentrations. The up-regulation of the Ca²⁺ signaling pathway might play a greater role in promoting EPS secretion under nTiO₂-R exposure compared with nTiO₂-A exposure, while the significantly increased intracellular ROS could mainly account for the increased EPS secretion under nTiO₂-A exposure. The up-regulated genes related to biological synthesis and protein metabolism and the enhanced biosynthetic metabolism might be the direct causes of the increased EPS secretion. The increased ROS could have a greater effect on the amino acid metabolism and related genes upon the exposure to nTiO₂-A than nTiO₂-R to induce more EPS secretion. More serious membrane damage caused by nTiO₂-R than nTiO₂-A would affect the intracellular inositol phospholipid metabolism more severely, while the inositol phospholipid pathway and Ca²⁺ signaling pathway might agree and communicate with each other inherently to regulate EPS secretion upon nTiO₂-R exposure. The findings address the regulation mechanisms of algal EPS secretion under nTiO₂ exposure and provide new insights into algal bio-responses to nTiO₂ exposure.

Natural environments are receiving an increasing number of contaminants. Therefore, the evaluation and identification of early responses to pollution in these complex habitats is an urgent and challenging task. Doñana National Park (DNP, SW Spain) has been widely used as a model area for environmental studies because, despite its strictly protected core, it is surrounded by numerous threat sources from agricultural, mining and industrial activities. Since many pollutants often induce oxidative stress, redox proteomics was used to detect redox-based variations within the proteome of Mus spretus mice captured in DNP and the surrounding areas. Functional analysis showed that most differentially oxidized proteins are involved in the maintenance of homeostasis, by eliciting mechanisms to respond to toxic substances and oxidative stress, such as antioxidant and biotransformation processes, immune and inflammatory responses, and blood coagulation. Furthermore, changes in the overall protein abundance were also analysed by label-free quantitative proteomics. The upregulation of phase I and II biotransformation enzymes in mice from Lucio del Palacio may be an alert for organic pollution in the area located at the heart of DNP. Metabolic processes involved in protein turnover (proteolysis, amino acid catabolism, new protein biosynthesis and folding) were activated in response to oxidative damage to these biomolecules. Consequently, aerobic respiratory metabolism increased to address the greater ATP demands. Alterations of cholesterol metabolism that could cause hepatic steatosis were also detected. The proteomic detection of globally altered metabolic and physiological processes offers a complete view of the main biological changes caused by environmental pollution in complex habitats.

Concerns regarding microplastic contamination have spread from aquatic environments to terrestrial systems with a growing number of studies have been reported. Notwithstanding, the potential effects on soil ecosystems remain largely unexplored. In this study, the effects of polyethylene microplastics on soil enzymatic activities and the bacterial community were evaluated, and the microbiota colonizing on microplastics were also investigated. Microplastic amendment (2000 fragments per kg soil) significantly increased the urease and catalase activities in soil after 15 days, and no discernible alteration of invertase activities was detected. Results from high-throughput sequencing of 16S rRNA revealed that the alpha diversities (richness, evenness, and diversity) of the microbiota in soil were not obviously changed by the PE amendment, whereas the diversity indexes of microbiota on plastic fragments were significantly lower than those in the control and amended soils. Different taxonomic composition was observed in between the control and amended soils after 90 days of incubation. Bacterial assemblages with distinct community structure colonized the PE microplastics. Additionally, several taxa including plastic-degrading bacteria and pathogens were more abundant on microplastics. Simultaneously, the predicted functional profiles showed that the pathways of amino acid metabolism and xenobiotics biodegradation and metabolism were higher on the microplastics. These results indicated that microplastics in soil, compared with those in aquatic environments, can also act as a distinct microbial habitat, potentially altering the ecological functions of soil ecosystems.

The top-selling strobilurin, azoxystrobin (AZ), is a broad-spectrum fungicide that protects against many kinds of pathogenic fungi by preventing their ATP production. The extensive use of AZ can have negative consequences on non-target species and its effects and toxic mechanisms on algae are still poorly understood. In this work, Chlorella pyrenoidosa that had been grown in BG-11 medium was exposed to AZ (0.5–10 mg L⁻¹) for 10 d. The physiological and molecular responses of the algae to AZ treatment, including photosynthetic efficiency, lipid peroxidation level, antioxidant enzyme activities, as well as transcriptome-based analysis of gene expression, were examined to investigate the potential toxic mechanism. Results shows that the photosynthetic pigment (per cell) increased slightly after AZ treatments, indicating that the photosystem of C. pyrenoidosa may have been strengthened. Glutathione and ascorbate contents were increased, and antioxidant enzyme activities were induced to relieve oxidative damage (e.g., from lipid peroxidation) in algae after AZ treatment. Transcriptome-based analysis of gene expression combined with physiological verification suggested that the 5 mg L⁻¹ AZ treatment did not inhibit ATP generation in C. pyrenoidosa, but did significantly alter amino acid metabolism, especially in aspartate- and glutamine-related reactions. Moreover, perturbation of ascorbate synthesis, fat acid metabolism, and RNA translation was also observed, suggesting that AZ inhibits algal cell growth through multiple pathways. The identification of AZ-responsive genes in the eukaryotic alga C. pyrenoidosa provides new insight into AZ stress responses in a non-target organism.

Industrial phosphate rock (PR) treatment has introduced lead (Pb) contamination into phosphate mining wasteland, causing serious contamination. Although bioremediation is considered an effective method and studies have investigated the bioimmobilization of Pb contamination in phosphate mining wasteland by phosphate-solubilizing bacteria (PSB), the bioimmobilization mechanism remains unclear. In this study, a strain Citrobacter farmeri CFI-01 with phosphate-solubilizing and Pb-tolerant abilities was isolated from a phosphate mining wasteland. Liquid culture experiments showed that the maximum content of soluble phosphate and the percentage amount of Pb immobilized after 14 days were 351.5 mg/L and 98.18%, respectively, with a decrease in pH. Soil experiments showed that CFI-01 had reasonable bioimmobilization ability, and the percentage amount of Pb immobilized was increased by 7.790% and 22.18% in the groups inoculated with CFI-01, respectively, compared with that of the groups not inoculated with CFI-01. Fourier transform infrared (FTIR) spectroscopy, X-ray diffraction (XRD), and scanning electron microscopy (SEM) analyses showed that the immobilization of Pb was also ascribed to changes in the functional groups (e.g., hydroxyl and carboxyl groups) and the formation of lead phosphate sediments. Finally, the results of the metagenomic analysis indicated that changes in the microbial community structure, enrichment of related functional abundances (e.g., metal metabolism, carbohydrate metabolism, and amino acid metabolism functions), and activation of functional genes (e.g., zntA, smtB, cadC, ATOX1, smtA, and ATX1) could help immobilize soil Pb contamination and explore the mechanism of bacterial bioimmobilization in Pb-contaminated soil. This study provides insights for exploring the immobilization mechanism of Pb contamination in phosphate mining wasteland using PSB, which has significance for further research.

Owing to environmental health concerns, a number of per- and polyfluoroalkyl substances (PFAS) have been phased-out, and increasingly replaced by various chemical analogs. Most prominent among these replacements are numerous perfluoroether carboxylic acids (PFECA). Toxicity, and environmental health concerns associated with these next-generation PFAS, however, remains largely unstudied. The zebrafish embryo was employed, in the present study, as a toxicological model system to investigate toxicity of a representative sample of PFECA, alongside perfluorooctanoic acid (PFOA) as one of the most widely used, and best studied, of the “legacy” PFAS. In addition, high-resolution magic angle spin (HRMAS) NMR was utilized for metabolic profiling of intact zebrafish embryos in order to characterize metabolic pathways associated with toxicity of PFAS. Acute embryotoxicity (i.e., lethality), along with impaired development, and variable effects on locomotory behavior, were observed for all PFAS in the zebrafish model. Median lethal concentration (LC₅₀) was significantly correlated with alkyl chain-length, and toxic concentrations were quantitatively similar to those reported previously for PFAS. Metabolic profiling of zebrafish embryos exposed to selected PFAS, specifically including PFOA and two representative PFECA (i.e., GenX and PFO3TDA), enabled elaboration of an integrated model of the metabolic pathways associated with toxicity of these representative PFAS. Alterations of metabolic profiles suggested targeting of hepatocytes (i.e., hepatotoxicity), as well as apparent modulation of neural metabolites, and moreover, were consistent with a previously proposed role of mitochondrial disruption and peroxisome proliferator-activated receptor (PPAR) activation as reflected by dysfunctions of carbohydrate, lipid and amino acid metabolism, and consistent with a previously proposed contribution of PFAS to metabolic syndrome. Taken together, it was generally concluded that toxicity of PFECA is quantitatively and qualitatively similar to PFOA, and these analogs, likewise, represent potential concerns as environmental toxicants.