Suitable biochar application practices simultaneously alleviate N2O and NH3 emissions from arable soils: A meta-analysis study.

Nitrogen (N) fertilization profoundly improves crop agronomic yield but triggers reactive N (Nr) loss into the environment. Nitrous (N2O) and ammonia (NH3) emissions are the main Nr species that affect climate change and eco-environmental health. Biochar is considered a promising soil amendment, and its efficacy on individual Nr gas emission reduction has been widely reported. However, the interactions and trade-offs between these two Nr species after biochar addition have not been comprehensively analysed. The influencing factors, such as biochar characteristics, environmental conditions, and management measures, remain uncertain. Therefore, 35 publications (145 paired observations) were selected for a meta-analysis to explore the simultaneous mitigation potential of biochar on N2O and NH3 emissions after its application on arable soil. The results showed that biochar application significantly reduced N2O emission by 7.09% while having no significant effect on NH3 volatilisation. Using biochar with a low pH, moderate BET, or pyrolyzed under moderate temperatures could jointly mitigate N2O and NH3 emissions. Additionally, applying biochar to soils with moderate soil organic carbon, high soil total nitrogen, or low cation exchange capacity showed similar responses. The machine-learning model suggested that biochar pH is a dominating moderator of its efficacy in mitigating N2O and NH3 emissions simultaneously. The findings of this study have major implications for biochar application management and aid the further realisation of the multifunctionality of biochar application in agriculture, which could boost agronomic production while lowering environmental costs.

PointSee: Image Enhances Point Cloud.

There is a prevailing trend towards fusing multi-modal information for 3D object detection (3OD). However, challenges related to computational efficiency, plug-and-play capabilities, and accurate feature alignment have not been adequately addressed in the design of multi-modal fusion networks. In this paper, we present PointSee, a lightweight, flexible, and effective multi-modal fusion solution to facilitate various 3OD networks by semantic feature enhancement of point clouds (e.g., LiDAR or RGB-D data) assembled with scene images. Beyond the existing wisdom of 3OD, PointSee consists of a hidden module (HM) and a seen module (SM): HM decorates point clouds using 2D image information in an offline fusion manner, leading to minimal or even no adaptations of existing 3OD networks; SM further enriches the point clouds by acquiring point-wise representative semantic features, leading to enhanced performance of existing 3OD networks. Besides the new architecture of PointSee, we propose a simple yet efficient training strategy, to ease the potential inaccurate regressions of 2D object detection networks. Extensive experiments on the popular outdoor/indoor benchmarks show quantitative and qualitative improvements of our PointSee over thirty-five state-of-the-art methods.

Retraction Notice to: Long Noncoding RNA OIP5-AS1 Promotes the Progression of Liver Hepatocellular Carcinoma via Regulating the hsa-miR-26a-3p/EPHA2 Axis.

[This retracts the article DOI: 10.1016/j.omtn.2020.05.032.].

The relationship between the molecular composition of dissolved organic matter and bioavailability of digestate during anaerobic digestion process: Characteristics, transformation and the key molecular interval.

In this study, swine wastewater (SW) and cow wastewater (CW) were used for anaerobic digestion (AD). We found the bioavailability of dissolved organic matter (DOM) was affected by the molecular weight ranges and molecular composition during the AD process. The organic substance in the small molecular range (0-5 kDa) accumulated due to a larger molecular fraction (>10 kDa) degradation, which enhanced the bioavailability of the DOM. Moreover, based on the excitation emission matrix-parallel factor (EEM-PARAFAC) analysis, the protein-like component in 0-5 kDa molecular size and humic-like component over 5 kDa are significantly positively correlated with DOM bioavailability. This study indicated that increasing the hydrolysis of larger organic matter and humification degree of molecular weights>5 kDa are critical solutions to improving the bioavailability of DOM. These conclusions can help explain the molecular mechanisms of DOM transformation and the AD process of livestock wastewater.

Exosomal microRNA-15a from mesenchymal stem cells impedes hepatocellular carcinoma progression via downregulation of SALL4.

Hepatocellular carcinoma (HCC) is a heterogeneous tumor with an increased incidence worldwide accompanied by high mortality and dismal prognosis. Emerging evidence indicates that mesenchymal stem cells (MSCs)-derived exosomes possess protective effects against various human diseases by transporting microRNAs (miRNAs or miRs). We aimed to explore the role of exosomal miR-15a derived from MSCs and its related mechanisms in HCC. Exosomes were isolated from transduced MSCs and co-incubated with Hep3B and Huh7 cells. miR-15a expression was examined by RT-qPCR in HCC cells, MSCs, and secreted exosomes. CCK-8, transwell, and flow cytometry were used to detect the effects of miR-15a or spalt-like transcription factor 4 (SALL4) on cell proliferative, migrating, invasive, and apoptotic properties. A dual-luciferase reporter gene assay was performed to validate the predicted targeting relationship of miR-15a with SALL4. Finally, in vivo experiments in nude mice were implemented to assess the impact of exosome-delivered miR-15a on HCC. The exosomes from MSCs restrained HCC cell proliferative, migrating, and invasive potentials, and accelerated their apoptosis. miR-15a was expressed at low levels in HCC cells and could bind to SALL4, thus curtailing the proliferative, migrating, and invasive abilities of HCC cells. Exosomes successfully delivered miR-15a to HCC cells. Exosomal miR-15a depressed tumorigenicity and metastasis of HCC tumors in vivo. Overall, exosomal miR-15a from MSCs can downregulate SALL4 expression and thereby retard HCC development.

microRNA-320b suppresses HNF4G and IGF2BP2 expression to inhibit angiogenesis and tumor growth of lung cancer.

We examined the effect of microRNA-320b (miR-320b) on tumor growth and angiogenesis in lung cancer and also determined its downstream molecular mechanisms. Lung cancer tissues and adjacent non-cancerous tissues were collected from 66 patients with lung cancer. miR-320b expression was experimentally determined to be expressed at low level in cancer tissues. The results of gain-of-function experiments suggested that miR-320b overexpression suppressed cancer cell invasion, tube formation, tumor volume and angiogenesis in xenografted nude mice. Hepatocyte nuclear factor 4 gamma (HNF4G) was identified as a target of miR-320b based on in silico analysis. Dual-luciferase reporter gene assays further identified the binding relationship between HNF4G and miR-320b. Lung cancer tissues exhibited increased expression of HNF4G and insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2). Meanwhile, HNF4G knockdown suppressed IGF2BP2 expression, thereby repressing cancer cell invasion and tube formation. Furthermore, IGF2BP2 modified m6A to increase the expression of thymidine kinase 1 (TK1), thus promoting angiogenesis. In nude mice, restoration of TK1 reversed the suppressive effect of miR-320b overexpression on tumor growth rate and CD31 expression. In conclusion, miR-320b suppresses lung cancer growth and angiogenesis by inhibiting HNF4G, IGF2BP2 and TK1.

M2 macrophage-derived exosomal microRNA-155-5p promotes the immune escape of colon cancer by downregulating ZC3H12B.

Previous evidence has highlighted M2 macrophage regulation of cancer cells via exosome shuttling of microRNAs (miRNAs or miRs). The current study set out to explore the possible role of M2 macrophage-derived exosomal miR-155-5p in regard to immune escape of colon cancer cells. Experimental data from quantitative reverse-transcriptase PCR (qRT-PCR) and western blot analysis revealed highly expressed miR-155-5p and interleukin (IL)-6 and poorly expressed ZC3H12B in M2 macrophage-derived exosomes. Additionally, miR-155-5p could be transferred by M2 macrophage-isolated exosomes to colon cancer cells, which targeted ZC3H12B by binding to the 3¢ UTR, as identified by dual luciferase reporter gene. Meanwhile, gain- and loss-of function experimentation on miR-155-5p and ZC3H12B in SW48 and HT29 cells cocultured with M2 macrophage-secreted exosomes demonstrated that miR-155-5p overexpression or ZC3H12B silencing promoted the proliferation and antiapoptosis ability of SW48 and HT29 cells, as well as augmenting the CD3+ T cell proliferation and the proportion of interferon (IFN)-γ+ T cells. Xenograft models confirmed that M2 macrophage-derived exosomal miR-155-5p reduced the ZC3H12B expression to upregulate IL-6, which consequently induced immune escape and tumor formation. Collectively, our findings indicated that M2 macrophage-derived exosomal miR-155-5p can potentially promote the immune escape of colon cancer by impairing ZC3H12B-mediated IL-6 stability reduction, thereby promoting the occurrence and development of colon cancer.

Cancer-associated fibroblast-derived exosomal microRNA-24-3p enhances colon cancer cell resistance to MTX by down-regulating CDX2/HEPH axis.

MicroRNA-24-3p (miR-24-3p) has been implicated as a key promoter of chemotherapy resistance in numerous cancers. Meanwhile, cancer-associated fibroblasts (CAFs) can secret exosomes to transfer miRNAs, which mediate tumour development. However, little is known regarding the molecular mechanism of CAF-derived exosomal miR-24-3p in colon cancer (CC). Hence, this study intended to characterize the functional relevance of CAF-derived exosomal miR-24-3p in CC cell resistance to methotrexate (MTX). We identified differentially expressed HEPH, CDX2 and miR-24-3p in CC through bioinformatics analyses, and validated their expression in CC tissues and cells. The relationship among HEPH, CDX2 and miR-24-3p was verified using ChIP and dual-luciferase reporter gene assays. Exosomes were isolated from miR-24-3p inhibitor-treated CAFs (CAFs-exo/miR-24-3p inhibitor), which were used in combination with gain-of-function and loss-of-function experiments and MTX treatment. CCK-8, flow cytometry and colony formation assays were conducted to determine cell viability, apoptosis and colony formation, respectively. Based on the findings, CC tissues and cells presented with high expression of miR-24-3p and low expression of HEPH and CDX2. CDX2 was a target gene of miR-24-3p and could up-regulate HEPH. Under MTX treatment, overexpressed CDX2 or HEPH and down-regulated miR-24-3p reduced cell viability and colony formation and elevated cell apoptosis. Furthermore, miR-24-3p was transferred into CC cells via CAF-derived exosomes. CAF-derived exosomal miR-24-3p inhibitor diminished cell viability and colony formation and increased cell apoptosis in vitro and inhibited tumour growth in vivo under MTX treatment. Altogether, CAF-derived exosomal miR-24-3p accelerated resistance of CC cells to MTX by down-regulating CDX2/HEPH axis.

KDM5A silencing transcriptionally suppresses the FXYD3-PI3K/AKT axis to inhibit angiogenesis in hepatocellular cancer via miR-433 up-regulation.

Hepatocellular cancer (HCC) has been reported to belong to one of the highly vascularized solid tumours accompanied with angiogenesis of human umbilical vein endothelial cells (HUVECs). KDM5A, an attractive drug target, plays a critical role in diverse physiological processes. Thus, this study aims to investigate its role in angiogenesis and underlying mechanisms in HCC. ChIP-qPCR was utilized to validate enrichment of H3K4me3 and KDM5A on the promotor region of miR-433, while dual luciferase assay was carried out to confirm the targeting relationship between miR-433 and FXYD3. Scratch assay, transwell assay, Edu assay, pseudo-tube formation assay and mice with xenografted tumours were conducted to investigate the physiological function of KDM5A-miR-433-FXYD3-PI3K-AKT axis in the progression of HCC after loss- and gain-function assays. KDM5A p-p85 and p-AKT were highly expressed but miR-433 was down-regulated in HCC tissues and cell lines. Depletion of KDM5A led to reduced migrative, invasive and proliferative capacities in HCC cells, including growth and a lowered HUVEC angiogenic capacity in vitro. Furthermore, KDM5A suppressed the expression of miR-433 by demethylating H3K4me3 on its promoterregion. miR-433 negatively targeted FXYD3. Depleting miR-433 or re-expressing FXYD3 restores the reduced migrative, invasive and proliferative capacities, and lowers the HUVEC angiogenic capacity caused by silencing KDM5A. Therefore, KDM5A silencing significantly suppresses HCC tumorigenesis in vivo, accompanied with down-regulated miR-433 and up-regulated FXYD3-PI3K-AKT axis in tumour tissues. Lastly, KDM5A activates the FXYD3-PI3K-AKT axis to enhance angiogenesis in HCC by suppressing miR-433.

Systematic analysis using a bioinformatics strategy identifies SFTA1P and LINC00519 as potential prognostic biomarkers for lung squamous cell carcinoma.

Lung cancer has high incidence and mortality rates, in which lung squamous cell carcinoma (LUSC) is a primary type of non-small cell lung carcinoma (NSCLC). The aim of our study was to discover long non-coding RNAs (lncRNAs) associated with diagnose and prognosis for LUSC. RNA sequencing data obtained from LUSC samples were extracted from The Cancer Genome Atlas database (TCGA). Two prognosis-associated lncRNAs (including SFTA1P and LINC00519) were selected from LUSC samples, and the expression levels were also verified to be associated abnormal in LUSC clinical samples. Our findings demonstrate that lncRNAs SFTA1P and LINC00519 exert important functions in human LUSC and may serve as new targets for LUSC diagnosis and therapy.

Comprehensive analysis to identify DLEU2L/TAOK1 axis as a prognostic biomarker in hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is one of the deadliest malignant tumors that are harmful to human health. Increasing evidence has underscored the critical role of the competitive endogenous RNA (ceRNA) regulatory networks among various human cancers. However, the complexity and behavior characteristics of the ceRNA network in HCC were still unclear. In this study, we aimed to clarify a phosphatase and tensin homolog (PTEN)-related ceRNA regulatory network and identify potential prognostic markers associated with HCC. The expression profiles of three RNAs (long non-coding RNAs [lncRNAs], microRNAs [miRNAs], and mRNAs) were extracted from The Cancer Genome Atlas (TCGA) database. The DLEU2L-hsa-miR-100-5p/ hsa-miR-99a-5p-TAOK1 ceRNA network related to the prognosis of HCC was obtained by performing bioinformatics analysis. Importantly, we identified the DLEU2L/TAOK1 axis in the ceRNA by using correlation analysis, and it appeared to become a clinical prognostic model by Cox regression analysis. Furthermore, methylation analyses suggested that the abnormal upregulation of the DLEU2L/TAOK1 axis likely resulted from hypomethylation, and immune infiltration analysis showed that the DLEU2L/TAOK1 axis may have an impact on the changes in the tumor immune microenvironment and the development of HCC. In summary, the current study constructing a ceRNA-based DLEU2L/TAOK1 axis might be a novel important prognostic factor associated with the diagnosis and prognosis of HCC.

Whole-Transcriptome Sequencing Identifies Key Differentially Expressed mRNAs, miRNAs, lncRNAs, and circRNAs Associated with CHOL.

To systematically evaluate the whole-transcriptome sequencing data of cholangiocarcinoma (CHOL) to gain more insights into the transcriptomic landscape and molecular mechanism of this cancer, we performed whole-transcriptome sequencing based on the tumorous (C) and their corresponding non-tumorous adjacent to the tumors (CP) from eight CHOL patients. Subsequently, differential expression analysis was performed on the C and CP groups, followed by functional interaction prediction analysis to investigate gene-regulatory circuits in CHOL. In addition, The Cancer Genome Atlas (TCGA) for CHOL data was used to validate the results. In total, 2,895 differentially expressed messenger RNAs (dif-mRNAs), 56 differentially expressed microRNAs (dif-miRNAs), 151 differentially expressed long non-coding RNAs (dif-lncRNAs), and 110 differentially expressed circular RNAs (dif-circRNAs) were found in CHOL samples compared with controls. Enrichment analysis on those differentially expressed genes (DEGs) related to miRNA, lncRNA, and circRNA also identified the function of spliceosome. The downregulated hsa-miR-144-3p were significantly enriched in the competing endogenous RNA (ceRNA) complex network, which also included 7 upregulated and 13 downregulated circRNAs, 7 upregulated lncRNAs, and 90 upregulated and 40 downregulated mRNAs. Moreover, most of the DEGs and a few of the miRNAs (such as hsa-miR-144-3p) were successfully validated by TCGA data. The genes involved in RNA splicing and protein degradation processes and miR-144-3p may play fundamental roles in the pathogenesis of CHOL.

Long Noncoding RNA OIP5-AS1 Promotes the Progression of Liver Hepatocellular Carcinoma via Regulating the hsa-miR-26a-3p/EPHA2 Axis.

Numerous studies have suggested that dysregulated long noncoding RNAs (lncRNAs) contributed to the development and progression of many cancers. lncRNA OIP5 antisense RNA 1 (OIP5-AS1) has been reported to be increased in several cancers. However, the roles of OIP5-AS1 in liver hepatocellular carcinoma (LIHC) remain to be investigated. In this study, we demonstrated that OIP5-AS1 was upregulated in LIHC tissue specimens and its overexpression was associated with the poor survival of patients with LIHC. Furthermore, loss-of function experiments indicated that OIP5-AS1 promoted cell proliferation and inhibited cell apoptosis both in vitro and in vivo. Moreover, binding sites between OIP5-AS1 and hsa-miR-26a-3p as well as between hsa-miR-26a-3p and EPHA2 were confirmed by luciferase assays. Finally, a rescue assay was performed to prove the effect of the OIP5-AS1/hsa-miR-26a-3p/EPHA2 axis on LIHC cell biological behaviors. Based on all of the above findings, our results suggested that OIP5-AS1 promoted LIHC cell proliferation and invasion via regulating the hsa-miR-26a-3p/EPHA2 axis.

Bioavailability of dissolved organic matter in biogas slurry enhanced by catalytic ozonation combined with membrane separation.

Large molecular weight pig biogas slurry (L-PBS) and small molecular weight pig biogas slurry (S-PBS) were separated from original pig biogas slurry (O-PBS) using a 100 kDa membrane. The original bioavailability and biosafety of L-PBS was very low. In order to enhance the total bioavailable dissolved organic nitrogen (TB-DON) and total bioavailable dissolved organic phosphorus (TB-DOP), optimum catalytic ozonation of L-PBS conditions were determined using Box-behnken design models (P < 0.0001) and intersection tests. The optimal values for ozone concentration, pH value, active catalyst concentration and reaction time were 2.63 mg·L-1, 6.48, 1.43 g·L-1 and 40 min, respectively. Catalytic ozonation can effectively decompose and transform 68.07% of L-PBS into S-PBS to improve content organic bioavailability, with a molecular weight distribution of 0-1 kDa (13.53%), 1-5 kDa (16.62%), 5-10 kDa (11.16%), 10-30 kDa (11.73%), 30-100 kDa (15.04%). Catalytic ozonation of L-PBS can reduce protein levels from 85.28% to 47.18%, but increases the proportion of fulvic and humic components from 10.22% to 32.67% and 4.51%-20.15%, respectively. Because catalytic ozonation changes the internal components and molecular weights of L-PBS, both saw increases in TB-DON and TB-DOP from 3.33% to 41.12% and 2.43%-37.88%, respectively, with a large number of TB-DON and TB-DOP derived from hydrophilic organic components during catalytic ozonation. These important internal mechanisms changed by catalytic ozonation can effectively reduce the ecotoxicity (IR, from 76.5% to 33.1%) and phytotoxicity (GI, enhanced from 35.4% to 70.3%) of L-PBS. Therefore, catalytic ozonation combined with membrane separation is a choice technology in improving the nutrition of biogas slurry and reduce its ecological risk.

Spontaneous changes in dissolved organic matter affect the bio-removal of steroid estrogens.

Microbial action is the main pathway removing steroid estrogens (SEs) from both aerobic and anaerobic natural waters. The rate is influenced by other active substances present, particularly dissolved organic matter (DOM). DOM in natural surface waters has unstable components which undergo spontaneous photochemical oxidation, biological oxidation, chemical oxidation changes. How these changes influence the biosorption and bio-removal of SEs was the subject of this research. Photo oxidation-induced DOM increased the proportion of the fluorescence in area V, but biological oxidation and chemical oxidation caused fluorescence area V to decrease. All three oxidation processes can reduce the proportions of molecular weight (MW) > 5 kg·mol-1 and increase the proportions of MW < 5 kg·mol-1. Both the electron transfer capacity decreased monotonically with photo oxidation and chemical oxidation ageing, but biological oxidation ageing increased them. 17ß-estradiol (E2) was the SEs used in the experiments. In aerobic conditions, fresh river humic acids (RHA) and aged RHA had the stronger mediating effect on the rate of E2 bio-removal under aerobic conditions. Its greater effectiveness was probably related to its binding with E2. Binding, biosorption of E2 and bio-removal of E2 were strongly positively correlated with the elemental C (R > 0.8, p ≤ 0.01) and SUVA254 (R > 0.8, p ≤ 0.01) by correlation matrix. Besides, fresh river fulvic acids (RFA) and aged RFA had the bigger mediating effect on E2 bio-removal under anaerobic conditions, and this imply that changes in aged DOM affected by other electron transfer groups in an anaerobic water environment. In anaerobic conditions, biosorption of E2 and binding action could cluster together with SUVA254, p(v), and 1 kg·mol-1 < MW < 5 kg·mol-1 by redundancy analysis, and but bio-removal of E2 could be well polymerized with EAC, EDC, p(iv), and MW > 5 kg·mol-1.

Ecotoxicological effects and removal of 17ß-estradiol in chlorella algae.

17ß-estradiol (E2) is a steroid estrogen able to affect the reproduction of aquatic organisms even at extremely low concentrations. The behavior of E2 in the presence of chlorella algae was investigated in laboratory experiments. The results showed that the algae's growth was inhibited by 26% after 7 days of culturing in a 2.0 mg L-1 solution of E2. The 96 h EC50 value of 21.46 mg L-1 reflected moderate toxicity. Even low concentrations of E2 were found to affect total chlorophyll and carotenoid levels after 7 and 10 days and to alter stress-generated enzymatic activity in the algae. The efficiency of chlorella's E2 degradation decreased with the increasing of E2 concentration, but 92% of the E2 can be removed from a 0.5 mg L-1 solution over 10 days. The degradation mechanism was speculated. The microalgae suffered relatively less growth inhibition at low E2 concentrations, and their removal effectiveness was then better. The data help to elucidate the interaction between chlorella algae and E2 in an aquatic environment.

Intermittent light and microbial action of mixed endogenous source DOM affects degradation of 17ß-estradiol day after day in a relatively deep natural anaerobic aqueous environment.

All kinds of wastewaters containing steroid estrogens (SEs) and mixed endogenous source dissolved organic matter (DOM) enter natural water environments with intermittent illumination where microbial action occurs in a relatively deep natural aqueous environment. The role of mixed endogenous source DOM in SEs' biodegradation and photochemical degradation in such environments was studied using 17ß-estradiol (E2) in laboratory experiments under anaerobic conditions. The experimental results show that microbial action can improve the optical properties and electron transfer capability of mixed endogenous source DOM, promoting photodegradation and biodegradation. Intermittent illumination attenuates DOM's electron transfer capacity and its chromophore groups, but it improves the bioavailability of low molecular weight dissolved organic matter which promotes microbial growth under anaerobic conditions. DOM-mediated co-degradation by light and microbial action over three days was better than either individually. The presence of Fe(III) promoted electron transfer, and Fe(III)-DOM complexes accelerated energy transfer under irradiation, enhancing photodegradation. Any remaining estrogens will continue to degrade, most effectively in well-aerated waters with sufficient illumination.

Microbially reduced humic acid promotes the anaerobic photodegradation of 17α--ethinylestradiol.

Photolysis and microbial activity are relatively obvious in shallow, eutrophic waters with low dissolved oxygen content. Ubiquitous humic acid (HA) can act as electron acceptor and be reduced by bacterial under such conditions, and the reduced form of humic acid (RHA) plays an important role in the photolysis contaminants. In this study, anaerobic 17α-ethinylestradiol (EE2) photodegradation was performed along with biodegradation by Shewanella putrefaciens mediated by HA. The mechanism of such coupled photolysis and biodegradation of EE2 was thus elucidated. The removal rate in such coupled degradation in the presence of 10 mgC L-1 of HA at pH 8.0 was greater than that of either photolysis or biodegradation alone. HA which had been reduced in a double-chamber microbial fuel cell showed better promotion to EE2 photodegradation than fresh HA. Reactive species scavenging experiments indicated that hydroxyl radical and excited triplet states of HA were primary contributors to EE2 photodegradation in anaerobic conditions. More of them were produced from RHA than from pristine HA. Besides, the degraded EE2 solutions inhibited the proliferation of MCF-7 human cancer Cells. These findings improve our understanding of the environmental transformation of EE2 in the shallow, anoxic waters.

The microbial transformation of 17ß­estradiol in an anaerobic aqueous environment is mediated by changes in the biological properties of natural dissolved organic matter.

Dissolved organic matter (DOM) is shown to act as an electron shuttle mediator which enhances the microbial degradation of steroid estrogens in natural water. Batch studies were conducted with 17ß­estradiol (E2), quinone-reducing bacteria, DOM, and Fe(III) as a terminal electron acceptor. The results show that anthraquinone­2­disulfonate (AQS) approximately doubles the microbial degradation of E2 by DOM alone. The effect decreases sharply at AQS concentrations above 1.0mmol·L-1. Over three oxidation-reduction cycles, the electron-shuttling ability of AQS and the E2 biodegradation rate decreased step by step. Changes in the biological properties of the dissolved organic matter increased its aromaticity, its quinone content, and its fulvic-like fluorescence while significantly improving the electron transfer between DOM and the microbes, which made the degradation more effective. This explains why steroid estrogens do not accumulate in natural aqueous environments. Moreover, the estrogenic activity of steroid estrogens is inhibited at low concentrations through the activity of DOM.

Dissolved organic matter as a terminal electron acceptor in the microbial oxidation of steroid estrogen.

Steroid estrogen in natural waters may be biodegraded by quinone-reducing bacteria, dissolved organic matter (DOM) may serve as a terminal electron acceptor in this process. The influence of temperature, pH, dissolved oxygen and light illumination on the reduction efficiency of anthraquinone-2-disulfonate (AQS) was investigated using 17ß-estradiol (E2) as the target species. The optimum reduction conditions were found to be in the dark under anaerobic conditions at pH 8.0 and 30 °C. Quinone-reducing bacteria can use the quinone structure of DOM components as a terminal electron acceptor coupling with microbial growth to promote biodegradation. Compared with other DOM models, AQS best stimulated E2 biodegradation and the mediating effect was improved as the AQS concentration increased from 0 to 0.5 mM. However, further increase had an inhibiting effect. Natural DOM containing lake humic acid (LHA) and lake fulvic acid (LFA) had a very important accelerating effect on the degradation of E2, the action mechanism of which was consistent with that defined using DOM models. The natural DOM contained more aromatic compounds, demonstrating their greater electron-accepting capacity and generally more effective support for microorganism growth and E2 oxidation than Aldrich humic acid (HA). These results provide a more comprehensive understanding of microbial degradation of steroid estrogens in anaerobic environments and confirm DOM as an important terminal electron acceptor in pollutant transformation.