Arsenic (As) is a metalloid element that is ubiquitous in the marine environment and its contamination has received worldwide attention due to its potential toxicity. Arsenic can induce multiple adverse effects, such as lipid metabolism disorder, immune system dysfunction, oxidative stress and carcinogenesis, in animals. Inorganic arsenic includes two chemical forms, arsenite (As (III)) and arsenate (As (V)), in natural environment. As (V) is the dominant form in natural waters. In the present study, metabolomic and proteomic alterations were investigated in juvenile rockfish Sebastes schlegelii exposed to environmentally relevant concentrations of As (V) for 14 d. The analysis of iTRAQ-based proteomics combined with untargeted NMR-based metabolomics indicated apparent toxicological effects induced by As (V) in juvenile rockfish. In details, the metabolites, including lactate, alanine, ATP, inosine and phosphocholine were significantly altered in As-treated groups. Proteomic responses suggested that As (V) could not only affected energy and primary metabolisms and signal transduction, but also influenced cytoskeleton structure in juvenile rockfish. This work suggested that the combined proteomic and metabolomic approach could shed light on the toxicological effects of pollutants in rockfish S. schlegelii.

Dibenzofuran (DBF) derivatives have caused serious environmental problems, especially those produced by paper pulp bleaching and incineration processes. Prominent for its resilient mutagenicity and toxicity, DBF poses a major challenge to human health. In the present study, a new strain of Pseudomonas aeruginosa, FA-HZ1, with high DBF-degrading activity was isolated and identified. The determined optimum conditions for cell growth of strain FA-HZ1 were a temperature of 30 °C, pH 5.0, rotation rate of 200 rpm and 0.1 mM DBF as a carbon source. The biochemical and physiological features as well as usage of different carbon sources by FA-HZ1 were studied. The new strain was positive for arginine double hydrolase, gelatinase and citric acid, while it was negative for urease and lysine decarboxylase. It could utilize citric acid as its sole carbon source, but was negative for indole and H2S production. Intermediates of DBF 1,2-dihydroxy-1,2-dihydrodibenzofuran, 1,2-dihydroxydibenzofuran, 2-hydroxy-4-(3′-oxo-3′H-benzofuran-2′-yliden)but-2-enoic acid, 2,3-dihydroxybenzofuran, 2-oxo-2-(2′-hydrophenyl)lactic acid, and 2-hydroxy-2-(2′-hydroxyphenyl)acetic acid were detected and identified through liquid chromatography-mass analyses. FA-HZ1 metabolizes DBF by both the angular and lateral dioxygenation pathways. The genomic study identified 158 genes that were involved in the catabolism of aromatic compounds. To identify the key genes responsible for DBF degradation, a proteomic study was performed. A total of 1459 proteins were identified in strain FA-HZ1, of which 100 were up-regulated and 104 were down-regulated. A novel enzyme “HZ6359 dioxygenase”, was amplified and expressed in pET-28a in E. coli BL21(DE3). The recombinant plasmid was successfully constructed, and was used for further experiments to verify its function. In addition, the strain FA-HZ1 can also degrade halogenated analogues such as 2, 8-dibromo dibenzofuran and 4-(4-bromophenyl) dibenzofuran. Undoubtedly, the isolation and characterization of new strain and the designed pathways is significant, as it could lead to the development of cost-effective and alternative remediation strategies. The degradation pathway of DBF by P. aeruginosa FA-HZ1 is a promising tool of biotechnological and environmental significance.

The bioremediation potential of an aquifer contaminated with tetrachloroethene (PCE) was assessed by combining hydrogeochemical data of the site, microcosm studies, metabolites concentrations, compound specific-stable carbon isotope analysis and the identification of selected reductive dechlorination biomarker genes. The characterization of the site through 10 monitoring wells evidenced that leaked PCE was transformed to TCE and cis-DCE via hydrogenolysis. Carbon isotopic mass balance of chlorinated ethenes pointed to two distinct sources of contamination and discarded relevant alternate degradation pathways in the aquifer. Application of specific-genus primers targeting Dehalococcoides mccartyi species and the vinyl chloride-to-ethene reductive dehalogenase vcrA indicated the presence of autochthonous bacteria capable of the complete dechlorination of PCE. The observed cis-DCE stall was consistent with the aquifer geochemistry (positive redox potentials; presence of dissolved oxygen, nitrate, and sulphate; absence of ferrous iron), which was thermodynamically favourable to dechlorinate highly chlorinated ethenes but required lower redox potentials to evolve beyond cis-DCE to the innocuous end product ethene. Accordingly, the addition of lactate or a mixture of ethanol plus methanol as electron donor sources in parallel field-derived anoxic microcosms accelerated dechlorination of PCE and passed cis-DCE up to ethene, unlike the controls (without amendments, representative of field natural attenuation). Lactate fermentation produced acetate at near-stoichiometric amounts. The array of techniques used in this study provided complementary lines of evidence to suggest that enhanced anaerobic bioremediation using lactate as electron donor source is a feasible strategy to successfully decontaminate this site.

Nanoplastics are widely used in modern life, for example, in cosmetics and daily use products, and are attracting concern due to their potential toxic effects on environments. In this study, the uptake of nanopolystyrene particles by Caenorhabditis elegans (C. elegans) and their toxic effects were evaluated. Nanopolystyrene particles with sizes of 50 and 200 nm were prepared, and the L4 stage of C. elegans was exposed to these particles for 24 h. Their uptake was monitored by confocal microscopy, and various phenotypic alterations of the exposed nematode such as locomotion, reproduction and oxidative stress were measured. In addition, a metabolomics study was performed to determine the significantly affected metabolites in the exposed C. elegans group. Exposure to nanopolystyrene particles caused the perturbation of metabolites related to energy metabolism, such as TCA cycle intermediates, glucose and lactic acid. Nanopolystyrene also resulted in toxic effect including induction of oxidative stress and reduction of locomotion and reproduction. Collectively, these findings provide new insights into the toxic effects of nanopolystyrene particles.

Hypoxia is as an endocrine disruptor, and, in crustaceans, the energy metabolic consequences of hypoxia in the brain tissue are still poorly understood. We combined gas chromatography-mass spectrometry (GC-MS)-based metabolomic analysis and high-throughput RNA sequencing to evaluate the metabolic effects and subjacent regulatory pathways in the brain tissue of the male Oriental river prawn (Macrobrachium nipponense) in response to hypoxia and reoxygenation. We recorded LC₅₀ and heartbeats per minute of male M. nipponense juveniles. Hypoxia resulted in the generation of reactive oxygen species in the brain cells and alterations in gene expression and metabolite concentrations in the prawn brain tissue in a time-dependent manner. The transcriptomic analyses revealed specific changes in the expression of genes associated with metabolism pathways, which was consistent with the changes in energy metabolism indicated by the GC-MS metabolomic analysis. Quantitative real-time polymerase chain reaction and western blot confirmed the transcriptional induction of these genes because of hypoxia. The lactate levels increased significantly during hypoxia and decreased to normal after reoxygenation; this is consistent with a shift towards anaerobic metabolism, which may cause metabolic abnormalities in the brain tissue of M. nipponense. Overall, these results are consistent with metabolic disruption in the brain of M. nipponense exposed to hypoxia and will help in understanding how crustacean brain tissue adapts and responds to hypoxia and reoxygenation.

Earthworms improve the soil fertility and they are also sensitive to soil contaminants. Earthworms (Eisenia fetida), standard reference species, were usually chosen to culture and handle for toxicity tests. Metabolic responses in earthworms exposed to 2, 2′, 4, 4′-tetrabromodiphenyl ether (BDE-47) and decabromodiphenyl ether (BDE-209) were inhibitory and interfered with basal metabolism. In this study, 1H-NMR based metabolomics was used to identify sensitive biomarkers and explore metabolic responses of earthworms under sub-lethal BDE-47 and BDE-209 concentrations for 14 days. The results revealed that lactate was accumulated in earthworms exposed to BDE-47 and BDE-209. Glutamate increased significantly when the concentration of BDE-47 and BDE-209 reached 10 mg/kg. The BDE-47 exposure above 50 mg/kg concentration decreased the content of fumarate significantly, which was noticed different from that of BDE-209. Whereas, the BDE-207 or BDE-209 exposure increased the protein degradation into amino acids in vivo. The increased betaine content indicated that earthworms may maintain the cell osmotic pressure and protected enzyme activity by metabolic regulation. Moreover, the BDE-47 and BDE-209 exposure at 10 mg/kg changed most of the metabolites significantly, indicating that the metabolic responses were more sensitive than growth inhibition and gene expression. The metabolomics results revealed the toxic modes of BDE-47 and BDE-209 act on the osmoregulation, energy metabolism, nerve activities, tricarboxylic acid cycle and amino acids metabolism. Furthermore, our results highlighted that the 1H-NMR based metabolomics is a strong tool for identifying sensitive biomarkers and eco-toxicological assessment.

Uranium (U) contamination often occurs in the topsoil (arable layer), and is a serious threat to crop growth. However, conventional microbial reduction methods are sensitive to oxygen and cannot be used to treat aerobic topsoils. In this study, phosphate-solubilizing microorganisms (PSM) were isolated from U-contaminated topsoil and used for soil remediation. Microbial metabolites and products were analyzed, and the pathways and mechanisms of PSM immobilization were revealed. The results showed that strain PSM8 had the highest phosphate-solubilizing capacity (dissolved P was 208 ± 5 mg/L) and the highest U removal rate (97.3 ± 0.1%). Multi-technical analyses indicated that bacterial surface functional groups adsorbed (UO₂)²⁺ ions on the cell surface, glycolysis produced 3–10 mg/L of lactic acid (pH 4.7–6.0), and lactic acid solubilized Ca₃(PO₄)₂ to form stable chernikovite (a type of uranyl phosphate) on the cell surface. The coupled application of Ca₃(PO₄)₂ and strain PSM8 significantly reduced the bioavailability of soil U (62 ± 11%), converting U from the exchangeable to the residual phase and P from the steady to the available form. In addition, pot experiments showed that soil remediation promoted crop growth and significantly reduced U uptake and toxicity to photosynthetic systems. These findings demonstrate that PSM and Ca₃(PO₄)₂ are good coupled fertilizers for U-contaminated agricultural soil.

Nitrate (NO₃⁻) is one of the common inorganic nitrogen compound pollutants in natural ecosystems, which may have serious risks for aquatic organisms. However, its toxicological mechanism remains unclear. In the current study, juvenile turbot (Scophthalmus maximus) were exposed to different concentrations of NO₃⁻ (CK− 3.57 ± 0.16, LN − 60.80 ± 1.21, MN − 203.13 ± 10.97 and HN − 414.16 ± 15.22 mg/L NO₃–N) for 60 d. The blood biochemical assays results revealed that elevated NO₃⁻ exposure significantly increased the concentrations of plasma NO₃⁻, NO₂⁻, MetHb, K⁺, cortisol, glucose, triglyceride, lactate, while significantly decreased the concentrations of plasma Hb, Na⁺ and Cl⁻, which meant that NO₃⁻ caused hypoxic stress and further affected the osmoregulation and metabolism in fish. Besides, exposure to MN and HN induced a significant decrease in the level of antioxidants, including SOD (Point: 60th day, MN, HN v.s. CK: 258.36, 203.73 v.s. 326.95 U/mL), CAT (1.97, 1.17 v.s. 2.37 U/mL), GSH (25.38, 20.74 v.s. 37.00 μmol/L), and GPx (85.32, 71.46 v.s. 129.36 U/mL), and a significant increase of MDA (7.54, 9.73 v.s. 5.27 nmol/L), suggesting that NO₃⁻ exposure leading to a disruption of the redox status in fish. Also, further research revealed that NO₃⁻ exposure altered the mRNA levels of p53 (HN: up to 4.28 folds) and p53-regulated downstream genes such as Bcl-2 (inferior to 0.44 folds), caspase-3 (up to 2.90 folds) and caspase-7 (up to 3.49 folds), indicating that NO₃⁻ exposure induced abnormal apoptosis in the fish gills. Moreover, IBRv2 analysis showed that the toxicity of NO₃⁻ exposure to turbot was dose-dependent, and the toxicity peaked on the 15th day. In short, NO₃⁻ is an environmental toxicological factor that cannot be ignored, because its toxic effects are long-term and could cause irreversible damage to fish. These results would be beneficial to improve our understanding of the toxicity mechanism of NO₃⁻ to fish, which provides baseline evidence for the risk assessment of environmental NO₃⁻ in aquatic ecosystems.

Exposure to ambient fine particular matter (PM2.5) are linked to an increased risk of metabolic disorders, leading to enhanced rate of many diseases, such as inflammatory bowel disease (IBD), cardiovascular diseases, and pulmonary diseases; nevertheless, the underlying mechanisms remain poorly understood. In this study, BALB/c mice were exposed to filtered air (FA) or concentrated ambient PM2.5 (CPM) for 2 months using a versatile aerosol concentration enrichment system(VACES). We found subchronic CPM exposure caused significant lung and intestinal damage, as well as systemic inflammatory reactions. In addition, serum and BALFs (bronchoalveolar lavage fluids) metabolites involved in many metabolic pathways in the CPM exposed mice were markedly disrupted upon PM2.5 exposure. Five metabolites (glutamate, glutamine, formate, pyruvate and lactate) with excellent discriminatory power (AUC = 1, p < 0.001) were identified to predict PM2.5 exposure related toxicities. Furthermore, subchronic exposure to CPM not only significantly decreased the richness and composition of the gut microbiota, but also the lung microbiota. Strong associations were found between several gut and lung bacterial flora changes and systemic metabolic abnormalities. Our study showed exposure to ambient PM2.5 not only caused dysbiosis in the gut and lung, but also significant systemic and local metabolic alterations. Alterations in gut and lung microbiota were strongly correlated with metabolic abnormalities. Our study suggests potential roles of gut and lung microbiota in PM2.5 caused metabolic disorders.

Converting biowaste into value-added products has raised the researchers’ interests. In this study, bioconversion was applied to produce chain acids from food waste by anaerobic fermentation. To improve the caproic acid production, different pretreatments (i.e., ultrasonic, hydrothermal, and alkaline-thermal) were used for investigating their effects on the acidogenic production and microbial communities. The results showed that ultrasonic and hydrothermal pretreatments (207.8 and 210.1 mg COD/g VS, respectively) were very efficient for enhancing the caproic acid production, compared to the alkaline-thermal pretreated samples and control samples (72.6 and 97.5 mg COD/g VS, respectively). The ultrasonic pretreatment was beneficial for reducing volatile fatty acids (VFAs) during the caproic acid production, resulting in converting more lactic acid to caproic acid by adding the hydrothermal pretreatment. The microbial community analysis showed that the acidogenic bacteria Caproiciproducens dominated the fermentation in this bioconversion process of food waste into chain acids. The Caproiciproducens mainly degraded the proteins and carbohydrates from the saccharified residues of food waste to produce caproic acids through chain elongation procedure. The investigation and optimized method may help develop the bioconversion technology for producing VFAs products from food wastes.