Biodegradation of petroleum hydrocarbons based pollutants in contaminated soil by exogenous effective microorganisms and indigenous microbiome.

Microbial remediation is an eco-friendly and promising approach for the restoration of sites contaminated by petroleum hydrocarbons (PHCs). The degradation of total petroleum hydrocarbons (TPHs), semi volatile organic compounds (SVOCs) and volatile organic compounds (VOCs) of the soil samples collected from a petrochemical site by indigenous microbiome and exogenous microbes (Saccharomyces cerevisiae ATCC 204508/S288c, Candida utilis AS2.281, Rhodotorula benthica CBS9124, Lactobacillus plantarum S1L6, Bacillus thuringiensis GDMCC1.817) was evaluated. Community structure and function of soil microbiome and the mechanism involved in degradation were also revealed. After bioremediation for two weeks, the concentration of TPHs in soil samples was reduced from 17,800 to 13,100 mg/kg. The biodegradation efficiencies of naphthalene, benzo[a]anthracene, benzo[b]fluoranthene, benzo[a]pyrene, indeno[1,2,3-cd]pyrene, dibenzo[a,h]anthracene, 1,2,3-trichloropropane, 1,2-dichloropropane, ethylbenzene and benzene in soil samples with the addition of S. cerevisiae were 38.0%, 35.7%, 36.2%, 40.4%, 33.6%, 36.2%, 12.0%, 43.9%, 43.3% and 43.0%, respectively. The microbial diversity and community structure were improved during the biodegradation process. S. cerevisiae supplemented soil samples exhibited the highest relative abundance of the genus Acinetobacter for bacteria and Saccharomyces for yeast. The findings offer insight into the correlation between microbes and the degradation of PHC-based pollutants during the bioremediation process.

Proteome of Saccharomyces cerevisiae under paraquat stress regulated by therapeutic concentration of copper ions.

Paraquat (PQ) is a non-selective herbicide with strong toxicity to humans and mammals. However, the proteome regulation of cells by PQ is still unclear, limiting the development of effective antidotes. Studies have shown that a slight excess of intracellular copper levels could be beneficial to the survival under exposure to PQ. In this study, Saccharomyces cerevisiae was used as a model to explore the regulation effect of copper ions on PQ poisoning by the approach of date independent acquisition proteomics. The results showed that toxic effect of PQ was primarily induced by oxidative damage in the mitochondria and the disorder of gene expression. The addition of Cu2+ involved a series of favorable reactions to cell survival under PQ stress, including activation of the mitogen-activated protein kinase signaling pathway, regulation of processes such as sulfur metabolism, carbon metabolism and gene expression in cells. The generation of glutathione, heme and steroids advantageous to cell growth under stress was also increased. These findings inferred that therapeutic concentration of copper ions could prolong the survival of cells under PQ stress.

Discovering the Importance of ClO• in a Coupled Electrochemical System for the Simultaneous Removal of Carbon and Nitrogen from Secondary Coking Wastewater Effluent.

Inorganic constituents in real wastewater, such as halides and carbonates/bicarbonates, may have negative effects on the performance of electrochemical systems because of their capability of quenching HO•. However, we discovered that the presence of Cl- and HCO3- in an electrochemical system is conducive to the formation of ClO•, which plays an important role in promoting the simultaneous elimination of biorefractory organics and nitrogen in secondary coking wastewater effluent. The 6-h operation of the coupled electrochemical system (an undivided electrolytic cell with a PbO2/Ti anode and a Cu/Zn cathode) at a current density of 37.5 mA cm-2 allowed the removal of 87.8% of chemical oxygen demand (COD) and 86.5% of total nitrogen. The electron paramagnetic resonance results suggested the formation of ClO• in the system, and the probe experiments confirmed the predominance of ClO•, whose steady-state concentrations (8.08 × 10-13 M) were 16.4, 26.5, and 1609.5 times those of Cl2•- (4.92 × 10-14 M), HO• (3.05 × 10-14 M), and Cl• (5.02 × 10-16 M), respectively. The rate constant of COD removal and the Faradaic efficiency of anodic oxidation obtained with Cl- and HCO3- was linearly proportional to the natural logarithm of the ClO• concentration, and the specific energy consumption was inversely correlated to it, demonstrating the crucial role of ClO• in pollutant removal.

Metabolic network and recovery mechanism of Escherichia coli associated with triclocarban stress.

Although the toxicity of triclocarban at molecular level has been investigated, the metabolic networks involved in regulating the stress processes are not clear. Whether the cells would maintain specific phenotypic characteristics after triclocarban stress is also needed to be clarified. In this study, Escherichia coli was selected as a model to elucidate the cellular metabolism response associated with triclocarban stress and the recovery metabolic network of the triclocarban-treated cells using the proteomics and metabolomics approaches. Results showed that triclocarban caused systematic metabolic remodeling. The adaptive pathways, glyoxylate shunt and acetate-switch were activated. These arrangements allowed cells to use more acetyl-CoA and to reduce carbon atom loss. The upregulation of NH3-dependent NAD+ synthetase complemented the NAD+ consumption by catabolism, maintaining the redox balance. The synthesis of 1-deoxy-D-xylulose-5-phosphate was suppressed, which would affect the accumulation of end products of its downstream pathway of isoprenoid synthesis. After recovery culture for 12 h, the state of cells returned to stability and the main impacts on metabolic network triggered by triclocarban have disappeared. However, drug resistance caused by long-term exposure to environmentally relevant concentration of triclocarban is still worthy of attention. The present study revealed the molecular events under triclocarban stress and clarified how triclocarban influence the metabolic networks.

Systematic stress adaptation of Bacillus subtilis to tetracycline exposure.

To alleviate the harmful effects of antibiotics on the environment and human health, the stress response and molecular network of Bacillus under tetracycline stress were investigated using a proteomics approach. During the exposure process, Bacillus subtilis exhibited a strong adaptation mechanism. Cell membrane and intracellular reactive oxygen species (ROS) level returned to normal after 5 h. A total of 312 upregulated and 65 downregulated proteins were identified, mainly involved in metabolism and the synthesis of ribosomes, DNA, and RNA. After tetracycline exposure, the core metabolism network was accelerated to supply precursors for the synthesis of DNA, RNA, proteins, peptidoglycans, and saturated fatty acids that were involved in ribosome protection, and strengthened the cell wall and cell membrane. The signal transduction pathways involved were analyzed in association with the stress response of B. subtilis at 15 min of exposure to tetracycline. The primary damage to the ribosome by tetracycline activated a series of response proteins. Antitoxin and heat-shock proteins were activated for the global regulation of transcription and metabolism. Trigger factor Tig was upregulated to ensure proper initiation of transcription and aerobic respiration. Temperature-sensor protein VicR from the two-component system was used by the cell to regulate the composition of the cell wall and cell membrane. The over-consumption of metabolites, such as phosphoribosyl diphosphate (PRPP), purine nucleoside triphosphate (GTP), and acetyl-CoA forced the cells to assimilate more sugar for glycolysis. To this end, methyl-accepting chemotaxis proteins (MCPs) and sugar transportation protein PtsG were upregulated, simultaneously. Ultimately, peroxidase was activated to eliminate the redundant ROS, to minimize cell damage. These findings presented a system-level understanding of adaption processes of bacteria to antibiotic stress.

Metabolic and proteomic mechanism of benzo[a]pyrene degradation by Brevibacillus brevis.

Benzo[a]pyrene (BaP) is a model compound of polycyclic aromatic hydrocarbons. The relationship between its toxicity and some target biomolecules has been investigated. To reveal the interactions of BaP biodegradation and metabolic network, BaP intermediates, proteome, carbon metabolism and ion transport were analyzed. The results show that 76% BaP was degraded by Brevibacillus brevis within 7 d through the cleavage of aromatic rings with the production of 1-naphthol and 2-naphthol. During this process, the expression of xylose isomerase was induced for xylose metabolism, whereas, α-cyclodextrin could no longer be metabolized. Lactic acid, acetic acid and oxalic acid at 0.1-1.2 mg dm-3 were released stemming from their enhanced biosynthesis in the pathways of pyruvate metabolism and citrate cycle, while 5-7 mg dm-3 of PO43- were transported for energy metabolism. The relative abundance of 43 proteins was significantly increased for pyruvate metabolism, citrate cycle, amino acid metabolism, purine metabolism, ribosome metabolism and protein synthesis.

Degradation of 1H-benzotriazole using vacuum ultraviolet: a prospective treatment method for micro-pollutants.

Benzotriazoles (BTs) attract increasing concerns because of abundant presence in environmental water bodies. In this study, degradation of 1H-benzotriazole (1H-BT) was performed by a customized vacuum ultraviolet (VUV) device emitting 185 + 254 nm (VUV/UV-C) irradiation. Degradation of 1H-BT presented an apparent rate constant reached 8.17 × 10-4 s-1. Degradation mechanisms included 185 + 254 nm photodegradation and radical reaction. The later one may be the predominant one, which presented a k·OH-1H-BT at (7.3 ± 0.8) × 109 M-1 s-1. Effects of anions revealed that VUV interception and radical trapping were the dominant restraining factors. Degradation of 1H-BT can be attributed to VUV induced radical-based oxidation. Radical-induced addition, substitution and fracture generated abundant hydroxylated and open-loop products during 10-45 min. Identification using reactive oxygen species and apoptosis in Escherichia coli was conducted. Variations of these two indicators revealed that the incomplete degradation products presented higher toxicities than 1H-BT, and a further mineralization reduced their toxicities. In the pure water solution with little impurities, VUV can induce efficient degradation of 1H-BT, suggesting its potential for eliminating and detoxifying MPs.

Cellular metabolism network of Bacillus thuringiensis related to erythromycin stress and degradation.

Erythromycin is one of the most widely used macrolide antibiotics. To present a system-level understanding of erythromycin stress and degradation, proteome, phospholipids and membrane potentials were investigated after the erythromycin degradation. Bacillus thuringiensis could effectively remove 77% and degrade 53% of 1 µM erythromycin within 24 h. The 36 up-regulated and 22 down-regulated proteins were mainly involved in spore germination, chaperone and nucleic acid binding. Up-regulated ribose-phosphate pyrophosphokinase and ribosomal proteins confirmed that the synthesis of protein, DNA and RNA were enhanced after the erythromycin degradation. The reaction network of glycolysis/gluconeogenesis was activated, whereas, the activity of spore germination was decreased. The increased synthesis of phospholipids, especially, palmitoleic acid and oleic acid, altered the membrane permeability for erythromycin transport. Ribose-phosphate pyrophosphokinase and palmitoleic acid could be biomarkers to reflect erythromycin exposure. Lipids, disease, pyruvate metabolism and citrate cycle in human cells could be the target pathways influenced by erythromycin. The findings presented novel insights to the interaction among erythromycin stress, protein interaction and metabolism network, and provided a useful protocol for investigating cellular metabolism responses under pollutant stress.

Triphenyltin degradation and proteomic response by an engineered Escherichia coli expressing cytochrome P450 enzyme.

Although triphenyltin (TPT) degradation pathway has been determined, information about the enzyme and protein networks involved was severely limited. To this end, a cytochrome P450 hydroxylase (CYP450) gene from Bacillus thuringiensis was cloned and expressed in Escherichia coli BL21 (DE3), namely E. coli pET32a-CYP450, whose dosage at 1gL-1 could degrade 54.6% TPT at 1mgL-1 within 6 d through attacking the carbon-tin bonds of TPT by CYP450. Sequence analysis verified that the CYP450 gene had a 1214bp open reading frame, encoding a protein with 404 amino acids. Proteomic analysis determined that 60 proteins were significantly differentially regulated expression in E. coli pET32a-CYP450 after TPT degradation. The up-regulated proteins enriched in a network related to transport, cell division, biosynthesis of amino acids and secondary metabolites, and microbial metabolism in diverse environments. The current findings demonstrated for the first time that P450 received electrons transferring from NADH could effectively cleave carbon-metal bonds.

Biosorption and biodegradation of pyrene by Brevibacillus brevis and cellular responses to pyrene treatment.

Biodegradation has been proposed as an effective approach to remove pyrene, however, the information regarding cellular responses to pyrene treatment is limited thus far. In this study, the biodegradation and biosorption of pyrene by Brevibacillus brevis, along with cellular responses caused by pollutant were investigated by means of flow cytometry assay and scanning electron microscopy. The experimental results showed that pyrene was initially adsorbed by B. brevis and subsequently transported and intracellularly degraded. During this process, pyrene removal was primarily dependent on biodegradation. Cell invagination and cell surface corrugation occurred due to pyrene exposure. Nevertheless, cell regrowth after 96h treatment was observed, and the proportion of necrotic cell was only 2.8% after pyrene exposure for 120h, confirming that B. brevis could utilize pyrene as a sole carbon source for growth. The removal and biodegradation amount of pyrene (1mg/L) at 168h were 0.75 and 0.69mg/L, respectively, and the biosorption amount by inactivated cells was 0.41mg/L at this time.

Pyrene removal and transformation by joint application of alfalfa and exogenous microorganisms and their influence on soil microbial community.

Phytoremediation is an attractive approach for the cleanup of polycyclic aromatic hydrocarbons-contaminated soil. The joint effect of alfalfa and microorganisms, including Arthrobacter oxydans, Staphylococcus auricularis and Stenotrophomonas maltophilia, on pyrene removal was investigated. The results showed that the joint effect primarily contributed to pyrene removal, and the concentration of residual pyrene in rhizosphere soil was lower than that in non-rhizosphere soil. After joint treatment for 45d, pyrene in rhizosphere soils decreased from 11.3, 52.5 and 106.0mg/kg to 2.0-3.0, 15.0-18.7, and 41.2-44.8mg/kg, respectively. These bacteria significantly enhanced pyrene accumulation and microbial community diversity, and increased soil dehydrogenase and polyphenol oxidase activities. Pyrene was initially degraded through ring cleavage. One of the main metabolites 4-dihydroxy-phenanthrene was transformed into naphthol and 1,2-dihydroxynaphthalene, which were further degraded through salicylic acid pathway and phthalic acid pathway, separately.

Magnetic resonance imaging-based prediction models for differentiating intraspinal schwannomas from meningiomas: classification and regression tree and random forest analysis.

Background: Due to the variations in surgical approaches and prognosis between intraspinal schwannomas and meningiomas, it is crucial to accurately differentiate between the two prior to surgery. Currently, there is limited research exploring the implementation of machine learning (ML) methods for distinguishing between these two types of tumors. This study aimed to establish a classification and regression tree (CART) model and a random forest (RF) model for distinguishing schwannomas from meningiomas. Methods: We retrospectively collected 88 schwannomas (52 males and 36 females) and 51 meningiomas (10 males and 41 females) who underwent magnetic resonance imaging (MRI) examinations prior to the surgery. Simple clinical data and MRI imaging features, including age, sex, tumor location and size, T1-weighted images (T1WI) and T2-weighted images (T2WI) signal characteristics, degree and pattern of enhancement, dural tail sign, ginkgo leaf sign, and intervertebral foramen widening (IFW), were reviewed. Finally, a CART model and RF model were established based on the aforementioned features to evaluate their effectiveness in differentiating between the two types of tumors. Meanwhile, we also compared the performance of the ML models to the radiologists. The receiver operating characteristic (ROC) curve, accuracy, sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) were used to evaluate the models and clinicians' discrimination performance. Results: Our investigation reveals significant variations in ten out of 11 variables in the training group and five out of 11 variables in the test group when comparing schwannomas and meningiomas (P<0.05). Ultimately, the CART model incorporated five variables: enhancement pattern, the presence of IFW, tumor location, maximum diameter, and T2WI signal intensity (SI). The RF model combined all 11 variables. The CART model, RF model, radiologist 1, and radiologist 2 achieved an area under the curve (AUC) of 0.890, 0.956, 0.681, and 0.723 in the training group, and 0.838, 0.922, 0.580, and 0.659 in the test group, respectively. Conclusions: The RF prediction model exhibits more exceptional performance than an experienced radiologist in discriminating intraspinal schwannomas from meningiomas. The RF model seems to be better in discriminating the two tumors than the CART model.

The existence of ferric hydroxide links the carbon and nitrogen cycles by promoting nitrite-coupled methane anaerobic oxidation.

Microorganism-mediated anaerobic oxidation of methane can efficiently mitigate methane atmospheric emissions and is a key process linking the biogeochemical cycles of carbon, nitrogen, and iron. The results showed that methane oxidation and nitrite removal rates in the CF were 1.12 and 1.28 times higher than those in CK, respectively, suggesting that ferric hydroxide can enhance nitrite-driven AOM. The biochemical process was mediated by the enrichment of methanogens, methanotrophs, and denitrifiers. Methanobacterium and Methanosarcina were positively correlated with Fe3+ and Fe2+, whereas Methylocystis and Methylocaldum were positively correlated with methane, and denitrifiers were positively correlated with nitrite. Metagenomic analysis revealed that the genes related to methane oxidation, nitrogen reduction, and heme c-type cytochrome were upregulated in CF, indicating that a synergistic action of bacteria and methanogens drove AOM via diverse metabolic pathways, within which ferric hydroxide played a crucial role. This study provides novel insights into the synergistic mechanism of ferric iron and nitrite-driven AOM.

Metabolic Mechanism of Bacillus sp. LM24 under Abamectin Stress.

Abamectin (ABM) has been recently widely used in aquaculture. However, few studies have examined its metabolic mechanism and ecotoxicity in microorganisms. This study investigated the molecular metabolic mechanism and ecotoxicity of Bacillus sp. LM24 (B. sp LM24) under ABM stress using intracellular metabolomics. The differential metabolites most affected by the bacteria were lipids and lipid metabolites. The main significant metabolic pathways of B. sp LM24 in response to ABM stress were glycerolipid; glycine, serine, and threonine; and glycerophospholipid, and sphingolipid. The bacteria improved cell membrane fluidity and maintained cellular activity by enhancing the interconversion pathway of certain phospholipids and sn-3-phosphoglycerol. It obtained more extracellular oxygen and nutrients to adjust the lipid metabolism pathway, mitigate the impact of sugar metabolism, produce acetyl coenzyme A to enter the tricarboxylic acid (TCA) cycle, maintain sufficient anabolic energy, and use some amino acid precursors produced during the TCA cycle to express ABM efflux protein and degradative enzymes. It produced antioxidants, including hydroxyanigorufone, D-erythroascorbic acid 1'-a-D-xylopyranoside, and 3-methylcyclopentadecanone, to alleviate ABM-induced cellular and oxidative damage. However, prolonged stress can cause metabolic disturbances in the metabolic pathways of glycine, serine, threonine, and sphingolipid; reduce acetylcholine production; and increase quinolinic acid synthesis.

Triclocarban triggers osteoarthritis via DNMT1-mediated epigenetic modification and suppression of COL2A in cartilage tissues.

Triclocarban (TCC) is a widely used environmental endocrine-disrupting chemical (EDC). Articular injury of EDCs has been reported; however, whether and how TCCs damage the joint have not yet been determined. Herein, we revealed that exposure to TCC caused osteoarthritis (OA) within the zebrafish anal fin. Mechanistically, TCC stimulates the expression of DNMT1 and initiates DNA hypermethylation of the type II collagen coding gene, which further suppresses the expression of type II collagen and other extracellular matrices. This further results in decreased cartilage tissue and narrowing of the intraarticular space, which is typical of the pathogenesis of OA. The regulation of OA occurrence by TCC is conserved between zebrafish cartilage tissue and human chondrocytes. Our findings clarified the hazard and potential mechanisms of TCC towards articular health and highlighted DNMT1 as a potential therapeutic target for OA caused by TCC.

The synergy of Fe(III) and NO2- drives the anaerobic oxidation of methane.

The anaerobic oxidation of methane (AOM) driven by NO2- or Fe(III) alone was limited by slow electron delivery and ineffective enrichment of microbes. The flexible coupling between Fe(III) and NO2- potentially cooperated to accelerate AOM. One negative control was fed CH4 and NO2-, and four treatment reactors were supplemented with CH4, NO2- and ferric citrate (FC)/ferric chloride (FCH)/ chelate iron (FCI)/ferric hydroxide (FH) and were anaerobically operated for 1200 days to verify the synergy and promicrobial roles of Fe(III) and NO2- in improving AOM. The changes in gas and ion profiles were observed in the reactors, and microbial development was studied using 16S rRNA gene sequencing with the Illumina platform. The results indicated that the combined Fe(III) and NO2- treatment improved AOM, and their synergy followed the order of FC > FCI > FCH > FH. The biochemical reaction of Fe3+ with NO2- and its secondary process accelerated electron transfer to microbial cells and subsequently enhanced AOM in the reactors. The total organic carbon (TOC) content, NH4+ content, NO3- content, and pH value altered the dominant bacteria the most in the FC reactor, FCI, FCH, and FH groups, respectively. Several dominant bacterial species were enriched, whereas only two archaea were highly concentrated in the FC and FCI groups. Only bacteria were detected in the FCH group, and archaea contributed substantially to the FH group. These findings contribute to an improved understanding of the interactions among nitrogen, iron and CH4 that are paramount to accelerating the process of AOM for engineering applications.

Novel perspectives of environmental proteomics.

The connection among genome expression, proteome alteration, metabolism regulation and phenotype change under environmental stresses is very vague. It is a tough task for the traditional research approaches to reveal the related scientific mechanisms of the above connection at molecular and systematic levels. Proteomics approach is an insightful tool for revealing the biological functions, metabolic networks and functional protein interaction networks of cells and organisms under stresses at the systematic level. The purpose of this review is to provide an insightful guideline on how to set up a proteomic investigation for revealing biomolecule mechanisms, protein biomarkers and metabolism networks related to stress response, pollutant recognition, transport and biodegradation, and providing an insightful high-throughput approach for screening functional enzymes and effective microbes based on bioinformatics and functional verification method. Furthermore, the toxicity evaluation of pollutants and byproducts by proteomics approaches provides a scientific insight for early diagnosis of ecological risk and determination of the effectiveness of pollutant treatment techniques.

Disrupted metabolic pathways and potential human diseases induced by bisphenol S.

Although the toxicity of bisphenol S has been studied in some species, the global metabolic network disrupted by bisphenol S remains unclear. To this end, published datasets related to the genes, proteins, and metabolites disturbed by bisphenol S were investigated through omics methods. The dataset revealed that bisphenol S at high concentrations tended to downregulate biomolecules, while low concentrations of bisphenol S tended to enhance metabolic reactions. The results showed that exposure to bisphenol S upregulated estrogen and downregulated androgen metabolism in humans, mice, rats, and zebrafish. Fatty acid metabolism and phospholipid metabolism in mice were upregulated. Reactions in amino acid metabolism were upregulated, with the exception of the suppressive conversion of arginine to ornithine. In zebrafish, fatty acid synthesis was promoted, while nucleotide metabolism was primarily depressed through the downregulation of pyruvate 2-o-phosphotransferase. The interference in amino acid metabolism by bisphenol S could trigger Alzheimer's disease, while its disturbance of glucose metabolism was associated with type II diabetes. Disturbed glycolipid metabolism and vitamin metabolism could induce Alzheimer's disease and diabetes. These findings based on omics data provide scientific insight into the metabolic network regulated by bisphenol S and the diseases triggered by its metabolic disruption.

Comparative toxicity reduction potential of UV/sodium percarbonate and UV/hydrogen peroxide treatments for bisphenol A in water: An integrated analysis using chemical, computational, biological, and metabolomic approaches.

Bisphenol A (BPA) is a common industrial chemical with significant adverse impacts on biological systems as an environmental contaminant. UV/hydrogen peroxide (UV/H2O2) is a well-established technology for BPA treatment in water while UV/sodium percarbonate (UV/SPC) is an emerging technology with unclear biological impacts of treated effluent. Therefore, in this study, the toxicity evaluation of BPA solution treated with UV/H2O2 and UV/SPC was preformed and compared based on transformation products (TPs) profile, quantitative structure-activity relationship (QSAR), Escherichia coli (E. coli) toxicity assays, and metabolomic analysis. TPs with hydroxylation, double-ring split, and single-ring cleavage were generated from BPA during the treatments with both technologies, but TPs with quinonation were specifically detected in UV/H2O2 treated solution at the UV dose of 1470 mJ cm-2. QSAR prediction based on TPs profile (excluding benzoquinone TPs) suggested that UV/H2O2 and UV/SPC treatments of BPA may increase matrix toxicity due to the formation of multi-hydroxylated TPs; however decreased bioaccumulation potential of all TPs may mitigate the increase of toxicity by reducing the chance of TPs to reach the concentration of toxicity threshold. In vivo assays with E. coli showed inhibited cell growth, arrested cell cycle, and increased cell death in BPA solution treated with UV/H2O2 at the UV dose of 1470 mJ cm-2. Metabolomic analysis indicated that BPA solution treated with UV/H2O2 at UV dose of 1470 mJ cm-2 impacted E. coli metabolism differently than other solutions with unique inhibition on glycerolipid metabolism. Moreover, BPA interfered in various metabolic pathways including alanine, aspartate and glutamate metabolism, starch and sucrose metabolism, pentose phosphate pathway, and lysine degradation, which were mitigated after the treatments. UV/SPC showed advantage over UV/H2O2 of attenuated impact on butanoate metabolism with UV irradiation. This study has generated valuable data for better understanding of biological impacts of BPA and its solutions treated with UV/H2O2 or UV/SPC, thus providing insights for their application prospect for water and wastewater treatment.

Circulating metabolomics profiling reveals novel pathways associated with cognitive decline in patients with hypertension.

BACKGROUND: Hypertension is a significant risk factor for cardiovascular disease, and it is associated with dementia, including Alzheimer's disease (AD). Although it may be correlated with AD in terms of symptoms, the link between hypertension and AD pathological biomarkers, and the potential underlying mechanism of hypertension with cognitive decline, are still not well understood. METHODS: The Mini-Mental State Examination (MMSE) scores were used to evaluate cognitive function. Enzyme-linked immunosorbent assays were used to examine plasma amyloid-beta (Aß)40, Aß42, and tau concentration in hypertensive patients. Metabolomics and metagenomics were performed to identify the significantly changed circulating metabolites and microbiota between healthy individuals and hypertensive patients. Pearson's correlation was used to examine the association between cognitive indicators and differential metabolites. RESULTS: We found significantly decreased MMSE scores, elevated plasma Aß40, and decreased Aß42/Aß40 ratio in hypertensive patients, which are critically associated with AD pathology. Based on metabolomics, we found that significantly altered metabolites in the plasma of hypertensive patients were enriched in the benzoate degradation and phenylpropanoid biosynthesis pathways, and they were also correlated with changes in MMSE scores and Aß42/Aß40 ratio. In addition, metabolomics signaling pathway analysis suggested that microbial metabolism was altered in hypertensive patients. We also identified altered blood microbiota in hypertensive patients compared with the controls. CONCLUSIONS: Our study provides a novel metabolic and microbial mechanism, which may underlie the cognitive impairment in hypertensive patients.