The decay of algal biomass and aquatic plants in freshwater lakes leads to the overproduction of autochthonous organic matter (OM) and the exhaustion of dissolved oxygen, impacting the microbial community and subsequent biodegradation of emerging contaminants in sediment. This study explored how the microbial processing of aquatic plant- and algal-derived OM (POM and AOM) mediates 17α-ethinylestradiol (EE2) biodegradation in the anoxic sediments of Lake Taihu in China. In four months of microcosm incubations, the increased concentrations of protein-like substances in AOM and POM exhibited temporary activation on microbial metabolic enzyme activity (fluorescein diacetate hydrolase and dehydrogenase) and significantly promoted the carbon mineralization with iron reduction (P < 0.001). These in turn increased the EE2 biodegradation efficiency to 77–90 ng g⁻¹ in the anoxic sediment. However, a higher EE2 biodegradation of 109 ng g⁻¹ was achieved with the humic acid augmentation containing more quinone-like compounds, showing a weaker substrate-priming effect but accelerated redox cycling of iron and organic substrates in the later period of incubation. The microbial analysis further revealed that the quinone-like compounds in OM were more closely associated with microbial electron transfer and strengthened their interspecies syntrophic cooperation favorable to contaminant biodegradation, even though the connective members exposed to protein-like components upregulated more functional genes related to organic carbon and xenobiotics metabolism and biodegradation. Our findings will help predict the fate of estrogens in various sedimentary environments under increasing eutrophication and further climate change scenarios.

Plant-derived saponins are bioactive surfactant compounds that can solubilize organic pollutants in environmental matrices, thereby facilitating pollutant remediation. Externally applied saponin has potential to enhance total petroleum hydrocarbon (TPH) biodegradation in the root zone (rhizosphere) of wild plants, but the associated mechanisms are not well understood. For the first time, this study evaluated a triterpenoid saponin (from red ash leaves, Alphitonia excelsa) in comparison to a synthetic surfactant (Triton X-100) for their effects on plant growth and biodegradation of TPH in the rhizosphere of two native wild species (a grass, Chloris truncata, and a shrub, Hakea prostrata). The addition of Triton X-100 at the highest level (1000 mg/kg) in the polluted soil significantly hindered the plant growth (reduced plant biomass and photosynthesis) and associated rhizosphere microbial activity in both the studied plants. Therefore, TPH removal in the rhizosphere of both plant species treated with the synthetic surfactant was not enhanced (at the lower level, 500 mg/kg soil) and even slightly decreased (at the highest level) compared to that in the surfactant-free (control) treatment. By contrast, TPH removal was significantly increased with saponin application (up to 60% in C. truncata at 1000 mg/kg due to enhanced plant growth and associated rhizosphere microbial activity). No significant difference was observed between the two saponin application levels. Dehydrogenase activity positively correlated with TPH removal (p < 0.001) and thus this parameter could be used as an indicator to predict the rhizoremediation efficiency. This work indicates that saponin-amended rhizoremediation could be an environmentally friendly and effective biological approach to remediate TPH-polluted soils. It was clear that the enhanced plant growth and rhizosphere microbial activity played a crucial role in TPH rhizoremediation efficiency. The saponin-induced molecular processes that promoted plant growth and soil microbial activity in the rhizosphere warrant further studies.

Nowadays, microplastics represent emergent pollutants in terrestrial ecosystems that exert impacts on soil properties, affecting key soil ecological functions. In agroecosystems, plastic mulching is one of the main sources of plastic residues in soils. The present research aimed to evaluate the effects of two types of plastic sheets (un-biodegradable and biodegradable) on soil abiotic (pH, water content, concentrations of organic and total carbon, and total nitrogen) and biotic (respiration, and activities of hydrolase, dehydrogenase, β-glucosidase and urease) properties, and on phytotoxicity (germination index of Sorghum saccharatum L. and Lepidium sativum L.). Results revealed that soil properties were mostly affected by exposure time to plastics rather than the kind (un-biodegradable and biodegradable) of plastics. After six months since mesocosm setting up, the presence of un-biodegradable plastic sheets significantly decreased soil pH, respiration and dehydrogenase activity and increased total and organic carbon concentrations, and toxicity highlighted by S. saccharatum L. Instead, the presence of biodegradable plastic sheets significantly decreased dehydrogenase activity and increased organic carbon concentrations. An overall temporal improvement of the investigated properties in soils covered by biodegradable plastic sheets occurred.

A new bacterium, Rhodococcus sp. S2-17, which could completely degrade an emerging organic pollutant, benzophenone-3 (BP-3), was isolated from contaminated sediment through an enrichment procedure, and its BP-3 catabolic pathway and genes were identified through metabolic intermediate and transcriptomic analyses and biochemical and genetic studies. Metabolic intermediate analysis suggested that strain S2-17 may degrade BP-3 using a catabolic pathway progressing via the intermediates BP-1, 2,4,5-trihydroxy-benzophenone, 3-hydroxy-4-benzoyl-2,4-hexadienedioic acid, 4-benzoyl-3-oxoadipic acid, 3-oxoadipic acid, and benzoic acid. A putative BP-3 catabolic gene cluster including cytochrome P450, flavin-dependent oxidoreductase, hydroxyquinol 1,2-dioxygenase, maleylacetate reductase, and α/β hydrolase genes was identified through genomic and transcriptomic analyses. Genes encoding the cytochrome P450 complex that demethylates BP-3 to BP-1 were functionally verified through protein expression, and the functions of the other genes were also verified through knockout mutant construction and intermediate analysis. This study suggested that strain S2-17 might have acquired the ability to catabolize BP-3 by recruiting the cytochrome P450 complex and α/β hydrolase, which hydrolyzes 4-benzoyl-3-oxoadipic acid to benzoic acid and 3-oxoadipic acid, genes, providing insights into the recruitment of genes of for the catabolism of emerging organic pollutants.

This experiment was conducted to evaluate the ecotoxicity of typical explosives and their mechanisms in the soil microenvironment. Here, TNT (trinitrotoluene), RDX (cyclotrimethylene trinitramine), and HMX (cyclotetramethylene tetranitramine) were used to simulate the soil pollution of single explosives and their combination. The changes in soil enzyme activity and microbial community structure and function were analyzed in soil, and the effects of explosives exposure on the soil metabolic spectrum were revealed by non-targeted metabonomics. TNT, RDX, and HMX exposure significantly inhibited soil microbial respiration and urease and dehydrogenase activities. Explosives treatment reduced the diversity and richness of the soil microbial community structure, and the microorganisms able to degrade explosives began to occupy the soil niche, with the Sphingomonadaceae, Actinobacteria, and Gammaproteobacteria showing significantly increased relative abundances. Non-targeted metabonomics analysis showed that the main soil differential metabolites under explosives stress were lipids and lipid-like molecules, organic acids and derivatives, with the phosphotransferase system (PTS) pathway the most enriched pathway. The metabolic pathways for carbohydrates, lipids, and amino acids in soil were specifically inhibited. Therefore, residues of TNT, RDX, and HMX in the soil could inhibit soil metabolic processes and change the structure of the soil microbial community.

Microbial denitrification is a main source of nitrous oxide (N₂O) emissions which have strong greenhouse effect and destroy stratospheric ozone. Though the importance of sulfide driven chemoautotrophic denitrification has been recognized, its contribution to N₂O emissions in nature remains elusive. We built up long-term sulfide-added microcosms with sediments from two freshwater lakes. Chemistry analysis confirmed sulfide could drive nitrate respiration in long term. N₂O accumulated to over 1.5% of nitrate load in both microcosms after long-term sulfide addition, which was up to 12.9 times higher than N₂O accumulation without sulfide addition. Metagenomes were extracted and sequenced during microcosm incubations. 16 S rRNA genes of Thiobacillus and Defluviimonas were gradually enriched. The nitric oxide reductase with c-type cytochromes as electron donors (cNorB) increased in abundance, while the nitric oxide reductase receiving electrons from quinols (qNorB) decreased in abundance. cnorB genes similar to Thiobacillus were enriched in both microcosms. In parallel, enrichment was observed for enzymes involved in sulfur oxidation, which supplied electrons to nitrate respiration, and enzymes involved in Calvin Cycle, which sustained autotrophic cell growth, implying the coupling relationship between carbon, nitrogen and sulfur cycling processes. Our results suggested sulfur pollution considerably increased N₂O emissions in natural environments.

Soil microbes influence the uptake of toxic metals (TMs) by changing soil characteristics, bioavailability and translocation of TMs, and soil health indicators in polluted environment. The potential effect of Streptomyces pactum (Act12) and Bacillus consortium (B. subtilis and B. licheniformis; 1:1) on soil enzymes and bacterial abundance, bioavailability and translocation of Zn and Cd by Symphytum officinale, and physiological indicators in soil acquired from Fengxian (FX) mining site. Act12 and Bacillus consortium were applied at 0 (CK), 0.50 (T1), 1.50 (T2), and 2.50 (T3) g kg⁻¹ in a split plot design and three times harvested (H). Results showed that soil pH significantly dropped, whereas, electrical conductivity increased at higher Act12 and Bacillus doses. The extractable Zn lowered and Cd increased at each harvest compared to their controls. Soil β-glucosidase, alkaline phosphatase, urease and sucrase improved, whereas, dehydrogenase reduced in harvest 2 and 3 (H2 and H3) as compared to harvest 1 (H1) after Act12 and Bacillus treatments. The main soil phyla individually contributed ∼5–55.6%. Soil bacterial communities’ distribution was also altered by Act12 and Bacillus amendments. Proteobacteria, Acidobacteria, and Bacteroidetes increased, whereas, the Actinobacteria, Chloroflexi, and Gemmatimonadetes decreased during the one-year trial. The Zn and Cd concentration significantly decreased in shoots at each harvest, whereas, the roots concentration was far higher than the shoots, implicating the rhizoremediation by S. officinale. Accumulation factor (AF) and bioconcentration ratio (BCR) of Zn and Cd in shoots were lower and remained higher in case of roots than the standard level (≥1). BCR values of roots indicated that S. officinale can be used for rhizoremediation of TMs in smelter/mines-polluted soils. Thus, field trials in smelter/mines contaminated soils and the potential role of saponin and tannin exudation in metal translocation by plant will broaden our understanding about the mechanism of rhizoremediation of TMs by S. officinale.

The effects of biological activated carbon treatment using Fe₂O₃ modified coconut shell-based activated carbon (Fe/CAC) were investigated on the occurrence of opportunistic pathogens (OPs) and formation of disinfection by-products (DBPs) in simulated drinking water distribution systems (DWDSs) with unmodified CAC as a reference. In the effluent of annular reactor (AR) with Fe/CAC, the OPs growth and DBPs formation were inhibited greatly. Based on the differential pulse voltammetry and dehydrogenase activity tests, it was verified that extracellular electron transfer was enhanced in the attached biofilms of Fe/CAC, hence improving the microbial metabolic activity and biological removal of organic matter especially DBPs precursors. Meanwhile, the extracellular polymeric substances (EPS) on the surface of Fe/CAC exhibited stronger viscosity, higher flocculating efficiency and better mechanical stability, avoiding bacteria or small-scale biofilms falling off into the water. Consequently, the microbial biomass and EPS substances amount decreased markedly in the effluent of Fe/CAC filter. More importantly, Fe/CAC did significantly enhance the shaping role on microbial community of downstream DWDSs, continuously excluding OPs advantage and inhibiting EPS production. The weakening of EPS in DWDSs resulted in decrease of microbial chlorine-resistance ability and EPS-derived DBPs precursors supply. Therefore, the deterioration of water quality in DWDSs was inhibited greatly, sustainably maintaining the safety of tap water. Our findings indicated that optimizing biological activated carbon treatment by interface modification is a promising method for improving water quality in DWDSs.

Hexafluoropropylene oxide dimer acid (HFPO-DA) is a perfluorooctanoic acid (PFOA) substitute. In the current study, potential developmental cardiotoxicity and hepatotoxicity following HFPO-DA exposure in chicken embryo has been investigated, focusing on the roles of peroxisome proliferator activated receptor alpha (PPARα), the major molecular target in PFOA-induced toxicities. HFPO-DA was exposed to fertile chicken eggs via air cell injection, morphology and function of the target organs (heart and liver) in hatchlings were investigated with histopathology and electrocardiography, and the serum levels of HFPO-DA had been measured with quadrupole-time of flight liquid chromatograph-mass spectrometer (Q-TOF LC/MS). Additionally, lentivirus-mediated in ovo PPARα silencing was used to assess the roles of PPARα in HFPO-DA induced developmental toxicities. The results indicated that developmental exposure to HFPO-DA induced developmental cardiotoxicity, including thinned right ventricular wall and elevated heart rates, similar to those observed with PFOA exposure, as well as developmental hepatotoxicity in the form of steatosis. Silencing of PPARα alleviated such effects, suggesting participation of PPARα in HFPO-DA induced developmental toxicities in chicken embryo. Moreover, enhanced expression of PPARα downstream genes, cluster of differentiation 36 (CD36) and enoyl-CoA hydratase and 3-hydroxyacyl CoA dehydrogenase (EHHADH), were observed in HFPO-DA exposed animal heart tissues, which can be abolished by PPARα silencing. On the other hand, liver-type fatty acid binding protein (L-FABP) and CD36 expression were effectively enhanced in exposed liver tissues, but not EHHADH, suggesting differential mechanism of toxicity in heart and liver tissues. In summary, developmental exposure to HFPO-DA induced developmental cardiotoxicity and hepatotoxicity in hatchling chickens similar to PFOA, and PPARα still participates in such toxicities, with some differential downstream gene regulations in different organs. Further investigation on HFPO-DA-induced developmental toxicities is guaranteed.

Exposure to heavy metals, such as lead, is a global public health problem. Lead has a long historic relation to several adverse health conditions and was recently classified as an endocrine disruptor. The aim of this study was to investigate the effects of subacute exposure to lead on the thyroid gland function. Adult male and female Wistar rats received a lead acetate solution containing 10 or 25 mg/kg, by gavage, three times a week, for 14 days. One week later, behavioral testing showed no alterations in anxiety and motor-exploratory parameters, as evaluated by Open-Field and Plus-Maze Tests, but impairment in learning and memory was found in the male 25 mg/kg lead-treated group and in both female lead-treated groups, as evaluated by the Inhibitory Avoidance Test. After one week, serum levels of tT3 were reduced in the 25 mg/kg female group and in the 10 mg∕ kg male group. However, tT4 levels were increased in the 25 mg/kg male group and in both female treated groups. TSH levels did not change and lead serum levels were undetectable. Morphologic alterations were observed in the thyroid gland, including abnormal thyroid parenchyma follicles of different sizes, epithelial stratification and vacuolization of follicular cells, decrease in colloid eosinophilia and vascular congestion, accompanied by morphometric alterations. An increase in collagen deposition was also observed. No differences were observed in TPO activity or protein expression, H₂O₂ generation by NADPH oxidases or hepatic D1 mRNA expression. However, thyroid NIS protein expression was considerably decreased in the male and female lead-treated groups, while TSHr expression was decreased in the 25 mg/kg female lead-treated group. These findings demonstrated that subacute exposure to lead acetate disrupts thyroid gland function in both sexes, leading to morphophysiological impairment and to changes in learning and memory abilities.