L-AP Alleviates Liver Injury in Septic Mice by Inhibiting Macrophage Activation via Suppressing NF-κB and NLRP3 Inflammasome/Caspase-1 Signal Pathways.

Liver injury and progressive liver failure are severe life-threatening complications in sepsis, further worsening the disease and leading to death. Macrophages and their mediated inflammatory cytokine storm are critical regulators in the occurrence and progression of liver injury in sepsis, for which effective treatments are still lacking. l-Ascorbic acid 6-palmitate (L-AP), a food additive, can inhibit neuroinflammation by modulating the phenotype of the microglia, but its pharmacological action in septic liver damage has not been fully explored. We aimed to investigate L-AP's antisepticemia action and the possible pharmacological mechanisms in attenuating septic liver damage by modulating macrophage function. We observed that L-AP treatment significantly increased survival in cecal ligation and puncture-induced WT mice and attenuated hepatic inflammatory injury, including the histopathology of the liver tissues, hepatocyte apoptosis, and the liver enzyme levels in plasma, which were comparable to NLRP3-deficiency in septic mice. L-AP supplementation significantly attenuated the excessive inflammatory response in hepatic tissues of septic mice in vivo and in cultured macrophages challenged by both LPS and ATP in vitro, by reducing the levels of NLRP3, pro-IL-1ß, and pro-IL-18 mRNA expression, as well as the levels of proteins for p-I-κB-α, p-NF-κB-p65, NLRP3, cleaved-caspase-1, IL-1ß, and IL-18. Additionally, it impaired the inflammasome ASC spot activation and reduced the inflammatory factor contents, including IL-1ß and IL-18 in plasma/cultured superannuants. It also prevented the infiltration/migration of macrophages and their M1-like inflammatory polarization while improving their M2-like polarization. Overall, our findings revealed that L-AP protected against sepsis by reducing macrophage activation and inflammatory cytokine production by suppressing their activation in NF-κB and NLRP3 inflammasome signal pathways in septic liver.

Irisin attenuates vascular remodeling in hypertensive mice induced by Ang II by suppressing Ca2+-dependent endoplasmic reticulum stress in VSMCs.

Vascular remodeling plays a vital role in hypertensive diseases and is an important target for hypertension treatment. Irisin, a newly discovered myokine and adipokine, has been found to have beneficial effects on various cardiovascular diseases. However, the pharmacological effect of irisin in antagonizing hypertension-induced vascular remodeling is not well understood. In the present study, we investigated the protection and mechanisms of irisin against hypertension and vascular remodeling induced by angiotensin II (Ang II). Adult male mice of wild-type, FNDC5 (irisin-precursor) knockout, and FNDC5 overexpression were used to develop hypertension by challenging them with Ang II subcutaneously in the back using a microosmotic pump for 4 weeks. Similar to the attenuation of irisin on Ang II-induced VSMCs remodeling, endogenous FNDC5 ablation exacerbated, and exogenous FNDC5 overexpression alleviated Ang II-induced hypertension and vascular remodeling. Aortic RNA sequencing showed that irisin deficiency exacerbated intracellular calcium imbalance and increased vasoconstriction, which was parallel to the deterioration in both ER calcium dysmetabolism and ER stress. FNDC5 overexpression/exogenous irisin supplementation protected VSMCs from Ang II-induced remodeling by improving endoplasmic reticulum (ER) homeostasis. This improvement includes inhibiting Ca2+ release from the ER and promoting the re-absorption of Ca2+ into the ER, thus relieving Ca2+-dependent ER stress. Furthermore, irisin was confirmed to bind to its receptors, αV/ß5 integrins, to further activate the AMPK pathway and inhibit the p38 pathway, leading to vasoprotection in Ang II-insulted VSMCs. These results indicate that irisin protects against hypertension and vascular remodeling in Ang II-challenged mice by restoring calcium homeostasis and attenuating ER stress in VSMCs via activating AMPK and suppressing p38 signaling.

Difunctional Fluorescent Probes for Iron and Hydrogen Sulfide Detection Based on Diphenyl Derivative.

In order to better monitor the content of Fe3+ and H2S in the biological environment, two new fluorescent probes were designed and synthesized. With the addition of Fe3+, the strong fluorescence emission of two probes was significantly quenched due to the paramagnetic effect of Fe3+. With the further addition of S2-, the fluorescence intensity was quickly restored. Two probes showed high selectivity and strong sensitivity for the detection of Fe3+ and S2-, and the fluorescence intensity "ON-OFF-ON" was accompanied with the interaction process. At the same time, two probes displayed good anti-interference ability which was not interfered by the existence of other ions. In addition, two probes illustrated fast response time to Fe3+, S2- and small cytotoxicity to cells. Therefore, two probes can provide a potential ideal tool for detecting Fe3+ and H2S in organisms and the environment.

Irisin protects against doxorubicin-induced cardiotoxicity by improving AMPK-Nrf2 dependent mitochondrial fusion and strengthening endogenous anti-oxidant defense mechanisms.

Irisin, a new exercise-mediated myokine, plays an important role in cardiovascular diseases by regulating cell energy metabolism. The induction of mitochondrial dysfunction and oxidative stress are the crucial mechanisms involved in doxorubicin-induced cardiomyocyte damage and cardiac dysfunction, but the mitochondria-dependent protective mechanisms of irisin in DOX-impaired cardiomyocytes are poorly understood. In this study, we exposed mouse-FNDC5 (irisin-precursor)-knockout, FNDC5 transgenic mice and their WT littermates, as well as cultured neonatal rat cardiomyocytes to DOX at a dosage of 4 mg/kg (once a week for 4 weeks) in vivo and 2 µM in vitro, respectively, then investigated how irisin alleviated DOX-induced oxidative stress and myocardial injury. Irisin knockout worsened, while irisin overexpression attenuated DOX-induced mortality, body weight loss, myocardial atrophy, damage and oxidative stress, cardiac remodeling and dysfunction in mice. Exogenous irisin supplementation (20 nM) also relieved these DOX-induced damage in cardiomyocytes. Intriguingly, irisin activated AMPK-Nrf2 signaling axis, and then up-regulated the transcription and protein expression of the downstream target genes of Nrf2, including mitochondrial fusion-related genes (mitofusin 1/2 and Optic Atrophy Type 1) and endogenous anti-oxidant genes, to promote mitochondrial fusion, improve mitochondrial dynamics and mitochondrial function, and reduced oxidative stress damage in DOX-induced cardiomyocytes. These results suggest that irisin protects the hearts from DOX-induced cardiotoxicity by improving mitochondrial dynamics and strengthening the endogenous anti-oxidant system through an AMPK-Nrf2 axis dependent manner, thus reducing DOX-induced oxidative stress injury in cardiomyocytes.

Prim-O-glucosycimifugin attenuates liver injury in septic mice by inhibiting NLRP3 inflammasome/caspase-1 signaling cascades in macrophages.

BACKGROUND: Liver dysfunction and liver failure are serious complications of sepsis, directly leading to septic progression and death. Now, there is no specific therapeutics available for sepsis-related liver dysfunction. Prim-O-glucosylcimifugin (POG), a chromone richest in the roots of Saposhnikovia divaricata (Turcz.) Schischk, is usually used to treat headache, rheumatoid arthritis and tetanus. While, the underlying mechanisms of POG against sepsis-induced liver damage and dysfunction are still not clear. PURPOSE: To study the anti-sepsis effect of POG, and its pharmacological mechanism to protect liver injury by weakening the function of macrophages in septic livers through inhibiting NOD-like receptor protein 3 (NLRP3) inflammasome pathway. METHOD: In vivo experiments, septic mouse model was induced by cecal ligation and puncture (CLP), and then the mortality was detected, liver inflammatory damages and plasma biomarkers of liver injury were evaluated by histopathological staining and biochemical assays, respectively. In vitro experiments, mouse primary peritoneal macrophages were treated with lipopolysaccharide (LPS) and ATP, and then the activated-inflammasomes, macrophage migration and polarization were detected by ASC immunofluorescence staining, transwell and flow cytometry assays, respectively. NLRP3 inflammasome components NLRP3, caspase-1, IL-1ß and IL-18 protein expressions were detected using western blot assays, and the contents of IL-1ß and IL-18 were measured by ELISA assays. RESULTS: POG treatment significantly decreased the mortality, liver inflammatory damages, hepatocyte apoptosis and plasma biomarkers of liver injury in CLP-challenged male WT mice, which were comparable to those in ibuprofen (a putative anti-inflammatory drug)-supplemented septic male WT mice and septic NLRP3 deficient-male mice. POG supplementation significantly suppressed NLRP3 inflammasome activation in septic liver tissues and cultured macrophages, by significantly reducing NLRP3, cleaved-caspase-1, IL-1ß and IL-18 levels, the activated-inflammasome ASC specks, and macrophage infiltration and migration, as well as M1-like polarization, but significantly increasing M2-like polarization. These findings were similar to the pharmacological effects of ibuprofen, NLRP3 deficiency, and a special NLRP3 inhibitor, MCC950. CONCLUSION: POG protected against sepsis by inhibiting NLRP3 inflammasome-mediated macrophage activation in septic liver and attenuating liver inflammatory injury, indicating that it may be a potential anti-sepsis drug candidate.

Mogrol suppresses lung cancer cell growth by activating AMPK-dependent autophagic death and inducing p53-dependent cell cycle arrest and apoptosis.

Lung carcinoma is the leading cause of cancer-related death worldwide. Chemotherapy remains the cornerstone of lung cancer treatment. Unfortunately, most types of cancer will develop resistance to chemotherapies over the time. One of the efforts to prevent the chemotherapy resistance is to find alternative chemotherapy drugs. Mogrol has been found to have antitumor activity. However, little is known about the pharmacological mechanisms underlying the suppression of mogrol on lung cancers. In this study, we observed that mogrol exposure significantly reduced the tumor volume and weight in tumor-bearing nude mice without obvious effect on body weight and cardiac function. Mogrol also significantly inhibited the proliferation and migration of lung cancer cells, including non-small-cell lung carcinoma cells, A549, H1299, H1975 and SK-MES-1 cells, with no obvious effect on control human bronchial epithelial cells (HBE). Further studies revealed that mogrol stirred excessive autophagy and autophagic flux, and finally, autophagic cell death, in lung cancer cells, which could be attenuated by autophagy inhibitors, 3-MA and chloroquine. Furthermore, mogrol significantly activated AMPK to induce autophagy and autophagic cell death, which could be abrogated by Compound C, an AMPK inhibitor. In addition, mogrol induced a significant increase in p53 activity in lung cancer cells, accompanied with cell cycle arrest and apoptosis, which could be weakened by p53 silence. Our results indicated that mogrol effectively suppressed lung cancer cells in vivo and in vitro by inducing the excessive autophagy and autophagic cell death via activating AMPK signaling pathway, as well as cell cycle arrest and apoptosis via activating p53 pathway.

Proteasome inhibition induces macrophage apoptosis via mitochondrial dysfunction.

Dysfunction of the ubiquitin-proteasome system has been linked to the pathogenesis of a variety of diseases. Proteasome inhibition not only exerts antitumor effects but also affects inflammatory signaling pathways. MG132, a proteasome inhibitor, has been shown to induce tumor cell apoptosis. However, its role in the induction of macrophage apoptosis remains unknown. In our study, we investigated the mechanism of the proapoptotic effects of MG132 in macrophages. Our data showed that MG132 treatment induced mitochondrial reactive oxygen species (ROS) generation and loss of mitochondrial membrane potential in macrophages. We found that proteasome inhibition induced a significant increase in the apoptosis rate, as evidenced by cleavage of caspase-3 and cleavage of poly(ADP-ribose) polymerase (PARP). Moreover, (2-(2,2,6,6-tetramethylpiperidin-1-oxyl-4-ylamino)-2-oxoethyl)triphenyl-phosphonium chloride (Mito-TEMPO) attenuated MG132-induced apoptosis. In conclusion, proteasome inhibition by MG132 can induce macrophage apoptosis by promoting the production of ROS and mitochondrial dysfunction.

New and known phenylpropanoid glycosides from mountain cultivated ginseng.

Two new phenylpropanoid glycosides elucidated as 2,6-dimethoxyphenyl-4-propylene-1-O-ß-D-apiofuranosyl-(1-6)-ß-D-glucopyranoside (1) and 2-methoxyphenyl-4-propylene-1-O-ß-D-apiofuranosyl-(1-6)-ß-D-glucopyranoside (2), along with three known phenylpropanoid glycosides (3-5) were isolated from Mountain Cultivated Ginseng. The structures of compounds 1-5 were elucidated on the basis of comprehensive spectroscopic data including 1D, 2D NMR spectra, and MS. In addition, in vitro cytotoxicity of all the isolated compounds was evaluated against HELA cell.

A putative effector UvHrip1 inhibits BAX-triggered cell death in Nicotiana benthamiana, and infection of Ustilaginoidea virens suppresses defense-related genes expression.

Rice false smut (RFS), caused by Ustilaginoidea virens, is one of the most detrimental rice fungal diseases and pose a severe threat to rice production and quality. Effectors in U. virens often act as a set of essential virulence factors that play crucial roles in the interaction between host and the pathogen. Thus, the functions of each effector in U. virens need to be further explored. Here, we performed multiple alignment analysis and demonstrated a small secreted hypersensitive response-inducing protein (hrip), named UvHrip1, was highly conserved in fungi. The predicted SP of UvHrip1 was functional, which guided SUC secreted from yeast and was recognized by plant cells. The localization of UvHrip1 was mainly in the nucleus and cytoplasm monitored through the GFP fusion protein in Nicotiana benthamiana cells. uvhrip1 was drastically up-regulated in the susceptible cultivar LYP9 of rice during the pathogen infection, while did not in the resistant cultivar IR28. We also proved that UvHrip1 suppressed the mammalian BAX-induced necrosis-like defense symptoms in N. benthamiana. Furthermore, patterns of expression of defense-related genes, OsPR1#012 and OsPR10b, were regulated over U. virens infection in rice. Collectively, our data demonstrated that infection of U. virens suppresses defense-related genes expression and UvHrip1 was most likely a core effector in regulating plant immunity.

UvHrip1, an effector secreted by Ustilaginoidea virens, suppresses basal defense and promotes disease development in Arabidopsis thaliana.

Rice false smut (RFS), caused by Ustilaginoidea virens, is one of the most detrimental rice fungal diseases and pose a severe threat to rice production and quality. Effectors in U. virens often act as a set of essential virulence factors that play crucial roles in the interaction between host and the pathogen. Thus, the functions of each effector in U. virens need to be further explored. Here, a conserved small secreted hypersensitive response-inducing protein (hrip) was named UvHrip1. Functional validation was investigated to prove that UvHrip1 suppressed cell death symptom and ROS accumulation in Nicotiana benthamiana triggered by Burkholderia glumae. We performed transgenic technology to demonstrate UvHrip1 remarkably inhibited pathogen-associated molecular pattern-induced defense responses in Arabidopsis seedlings and plants, including the expression of defense-response genes. Furthermore, disease progression caused by the type III secretion system-defective mutant from Pseudomonas syringae pv. tomato DC3000 was strongly facilitated in transgenic Arabidopsis ectopic expressing UvHrip1. Our data demonstrated UvHrip1 suppresses plant innate immunity and promoting disease multiplication in Arabidopsis.

The Conserved Effector UvHrip1 interacts with OsHGW, and Infection of Ustilaginoidea virens Regulates Defense- and Heading Date-Related Signaling Pathway.

Ustilaginoidea virens, which causes rice false smut (RFS), is one of the most detrimental rice fungal diseases and poses a severe threat to rice production and quality. Effectors in U. virens often act as a group of essential virulence factors that play crucial roles in the interaction between host and the pathogen. Thus, the functions of individual effectors in U. virens need to be further explored. Here, we demonstrated a small secreted hypersensitive response-inducing protein (hrip), named UvHrip1, which was highly conserved in U. virens isolates. UvHrip1 was also proven to suppress necrosis-like defense symptoms in N. benthamiana induced by the oomycete elicitor INF1. The localization of UvHrip1 was mainly in the nuclei and cytoplasm via monitoring the UvHrip1-GFP fusion protein in rice cells. Furthermore, Y2H and BiFC assay demonstrated that UvHrip1 interacted with OsHGW, which is a critical regulator in heading date and grain weight signaling pathways in rice. Expression patterns of defense- and heading date-related genes, OsPR1#051 and OsMYB21, were down-regulated over U. virens infection in rice. Collectively, our data provide a theory for gaining an insight into the molecular mechanisms underlying the UvHrip1 virulence function.

Pristine S,N-containing Mn-based metal organic framework nanorods enable efficient oxygen reduction electrocatalysis.

Owing to their unique physicochemical properties, metal-organic frameworks (MOFs) are a kind of promising material for electrocatalysis. However, many reports focus on the use of MOFs as precursors to produce efficient electrocatalysts by pyrolysis. The use of pristine MOFs with well-defined structures as efficient electrocatalysts directly is still a challenging problem. Herein, S,N-containing MnII[(Tdc)(4,4'-Bpy)]n with different morphologies have been obtained by using MnII, thiophene-2,5-dicarboxylate (Tdc) and 4,4'-bipyridine (4,4'-Bpy) as raw materials via hydrothermal synthesis. Furthermore, the influences of different hydrothermal reaction times (0, 2 and 4 h) and anions (SO42-, Cl-, NO3- and CH3COO-) on the morphologies, compositions and ORR activity of the resultant Mn-MOFs are also investigated at length. The results indicate that only the reaction of MnSO4 with Tdc and 4,4'-Bpy for 4 h can form relatively uniform one-dimensional (1D) MOF nanorods. The 1D nanorods combine the favorable features towards the oxygen reduction reaction (ORR), such as a high surface area and efficient 1D electron/mass transport capability. Therefore, the MnII[(Tdc)(4,4'-Bpy)]n nanorods display the highest ORR activity with an onset potential of 0.98 V and a half-wave potential of 0.78 V vs. RHE (reversible hydrogen electrode), which is even comparable to that of Pt/C. In addition, the MnII[(Tdc)(4,4'-Bpy)]n nanorods exhibit higher stability, methanol resistance and ORR selectivity than Pt/C. The present study illustrates an efficient fabrication strategy for highly efficient 1D MOF nanorods for energy storage and conversion applications.

Tunable and sustainable photocatalytic activity of photochromic Y-WO3 under visible light irradiation.

Although photochromic and photocatalytic performance are the most significant features of WO3, the effects of photochromism on photocatalytic activities have not been investigated further. Herein, a novel gear-shaped WO3, with high coloration efficiency, fast reversibility, and remarkable photocatalytic performance was successfully prepared via a facile hydrothermal method. The influence of photochromic effects on its photocatalytic properties was evaluated under visible light irradiation. The results showed that the yellow WO3 sample exhibited higher photocatalytic efficiencies toward tetracycline hydrochloride (TCH), oxytetracycline (OTC), rhodamine B (RhB), and ciprofloxacin (CIP) (94.3%, 87.9%, 76%, and 68.6%, respectively, in 60 min). Further research found that the redox conversion between W6+ and W5+ played a key role in separating e-/h+ pairs. Importantly, the rapid and reversible conversion between W6+ and W5+ could be realized through light radiation or H2O2 treatment. Therefore, the gear-shaped WO3 possessed tunable and sustainable photocatalytic properties and maintained a high level of activity after recycling ten times under visible light irradiation. This work provides new insights into practical WO3 applications for environmental remediation based on photochromic regulation.

Potential chiral fluorescent molecular probes based on an α,ß-unsaturated ketone for anion detection.

A series of potential chiral compounds containing an α,ß-unsaturated ketone was developed for anion detection. The interplay of compounds and biological momentous anions (Cl-, H2PO4-, I-, AcO-, HS-, F-, and Br-) was evaluated by UV-vis experiments, fluorescence experiments, and electrochemical tests. By comparison, compound 1 had the best selectivity and compound 5 had the strongest binding ability among the five compounds. And compound 5 had the highest sensitivity to H2PO4- among the measured anions, and it also can be applied to actual samples, the content of H2PO4- tested in the potassium dihydrogen phosphate fertilizer solution reached above 97.5% of the marked content, and the recovery rates were within the range of 98.5-99.1%, attesting that this method was reliable for the test of H2PO4- in fertilizer. Through HRMS titration, circular dichroism and optical rotation experiments, the probable interacted mechanism was proved that the interaction site was the C=C of the α,ß-unsaturated ketone structure. In addition, the interacted mechanism was researched from the perspective of chirality. Furthermore, theoretical investigation analysis was introduced to reveal that the roles of molecular frontier orbitals in molecular interplay were determined. Therefore, this series of potential chiral compounds has potential application prospects in anion recognition.

The Effector AGLIP1 in Rhizoctonia solani AG1 IA Triggers Cell Death in Plants and Promotes Disease Development Through Inhibiting PAMP-Triggered Immunity in Arabidopsis thaliana.

Rhizoctonia solani, one of the most detrimental necrotrophic pathogens, causes rice sheath blight and poses a severe threat to production. Focus on the function of effectors secreted by necrotrophic pathogens during infection has grown rapidly in recent years. However, little is known about the virulence and mechanisms of these proteins. In this study, we performed functional studies on putative effectors in R. solani and revealed that AGLIP1 out of 13 putative effectors induced cell death in Nicotiana benthamiana. AGLIP1 was also demonstrated to trigger cell death in rice protoplasts. The predicted lipase active sites and signal peptide (SP) of this protein were required for the cell death-inducing ability. AGLIP1 was greatly induced during R. solani infection in rice sheath. The AGLIP1's virulence function was further demonstrated by transgenic technology. The pathogenesis-related genes induced by pathogen-associated molecular pattern and bacteria were remarkably inhibited in AGLIP1-expressing transgenic Arabidopsis lines. Ectopic expression of AGLIP1 strongly facilitated disease progression in Arabidopsis caused by the type III secretion system-defective mutant from Pseudomonas syringae pv. tomato DC3000. Collectively, these results indicate that AGLIP1 is a possible effector that plays a significant role in pathogen virulence through inhibiting basal defenses and promoting disease development in plants.

Synchronous detoxification and reduction treatment of tannery sludge using Cr (VI) resistant bacterial strains.

This investigation focused on the simultaneous decrease of tannery sludge and the reduction of its high chromium (Cr(VI)) content. This was accomplished through the addition of mixed bacterial strains that were cultured in the laboratory, subsequent to their isolation from tannery sludge. The results indicated that under anaerobic conditions, the amount of the tannery sludge was decreased by 27% with these mixed bacteria. The impacts of various parameters were explored, such as pH, processing duration, strain inoculation, and temperature. Along with the decreased volume of sludge, the Cr(VI) concentration was lowered as well. Among the isolated bacterial strains, WY601 (belonging to Stenotrophomonas sp.) demonstrated the highest Cr(VI) resistance; from an initial concentration of 300 mg L-1, the Cr(VI) level was decreased by 90% within 65 h. Hexavalent chromate reductase was found to be localized primarily within the extracellular membrane or adsorbed to its surface, and a mechanism was proposed for the removal of Cr(VI) via WY601. Further, the WY601 isolate was found to be tolerant to other toxic heavy metals. In summary, the isolated mixed bacterial strains in our study demonstrated a strong potential for the treatment of tannery sludge, as they could simultaneously decrease its volume while lowering high Cr(VI) levels.

Cathodic photoelectrochemical detection of PCB101 in environmental samples with high sensitivity and selectivity.

A novel cathodic photoelectrochemical (PEC) sensing method was developed for fast and convenient detection of PCB101 taking advantages of the excellent PEC reducibility of Pd quantum dots (QDs) modified molecularly imprinted TiO2 nanorods (NRs). Attributed to the efficient PEC reduction of PCB101 on the cathode surface, sensitive cathodic photocurrent would be produced with increasing PCB101 concentration under a negative bias potential, giving a low PCB101 detection limit of 5×10-14molL-1. Meanwhile, molecular imprinting (MI) technique was integrated by in situ introduction of MI sites on the surface of TiO2 NRs, so that highly specific adsorption and reduction of PCB101 congener could be obtained. The results indicated that the PEC sensor presented excellent selectivity toward PCB101 with the coexistance of 100-fold excess of other pollutants including the PCBs congeners, other aromatic pollutants, and heavy metal ions. The cathodic PEC sensor was sucessfully applied in determination of PCB101 in real water and soil samples, and the results had good consistency with that obtained by the traditional GC-MS. This work provides a new concept and research basis for fabricating cathodic PEC sensor for the environmental pollutants with specific structures that were easily reduced.

Oxidative treatment of diclofenac via ferrate(VI) in aqueous media: effect of surfactant additives.

The potential reaction of diclofenac (DCF) with ferrate(VI) and influences of coexisting surfactants have not been investigated in depth, and are the focus of this study. The results demonstrated that DCF reacted effectively and rapidly with Fe(VI) and approximately 75% of DCF (0.03 mM) was removed by excess Fe(VI) (0.45 mM) within 10 min. All of the reactions followed pseudo first-order kinetics with respect to DCF and Fe(VI), where the apparent second-order rate constant (kapp) was 5.07 M-1 s-1 at pH 9.0. Furthermore, the degradation efficiencies of DCF were clearly dependent on the concentrations of dissolved organic matter additives in the substrate solution. Primarily, inhibitory effects were observed with the samples that contained anionic (sodium dodecyl-benzene sulfonate, SDBS) or non-ionic (Tween-80) surfactants, which have been attributed to the side reactions between Fe(VI) and surfactants, which led to a reduction in the available oxidant for DCF destruction. Furthermore, the addition of a cationic surfactant (cetyltrimethyl ammonium bromide, CTAB) and humic acid (HA) conveyed significantly promotional effects on the DCF-Fe(VI) reaction. The rate enhancement effect for CTAB might be due to micellar surface catalysis, through the Coulomb attraction between the reactants and positively charged surfactants, while the catalytic action for HA resulted from the additional oxidation of Fe(V)/Fe(IV) in the presence of HA. The results provided the basic knowledge required to understand the environmental relevance of DCF oxidation via Fe(VI) in the presence of surfactant additives.

A highly selective and picomolar level photoelectrochemical sensor for PCB 101 detection in environmental water samples.

A highly selective and sensitive photoelectrochemical (PEC) sensor was fabricated for fast and convenient detection of PCB 101 in environmental water samples with a low detection limit of 1.0×10(-14)molL(-1) based on single crystalline TiO2 nanorods (NRs). By integration with molecular imprinting (MI) technique, the PEC sensor's selectivity towards PCB 101 was significantly improved, so that the interference caused by 100-fold excess of PCB 126 and PCB 77 which had similar structure with PCB 101 was below 37%, not to mention other coexisted pollutants. This high selectivity could be attributed to the high-quality expression of the molecular imprinting sites on the rigid and smooth surface of single crystalline TiO2 NRs on which PCB 101 could be selectively and preferentially adsorbed. The oriented and multiple halogen bonds formed between PCB 101 and the molecular imprinting sites played a critical role in improving the recognition ability of the PEC sensor. Meanwhile, the one dimensional nanorods structure of TiO2 was beneficial for the efficient separation of photogenerated electrons and holes, leading to enhanced photocurrent response and further improving the sensitivity of the PEC sensor.

Oxidation of diclofenac with chlorine dioxide in aquatic environments: influences of different nitrogenous species.

The oxidation of diclofenac (DCF), a non-steroidal anti-inflammatory drug and emerging water pollutant, with chlorine dioxide was investigated under simulated water disinfection conditions. The reaction kinetics as functions of the initial concentrations of DCF, different nitrogenous species, and different pE values were experimentally determined. The results demonstrated that DCF reacted rapidly with ClO2, where more than 75 % of DCF (≤3.00 µM) was removed by 18.94 µM ClO2 within 60 s. All of the reactions followed pseudo first-order kinetics with respect to DCF, and the rate constant, k obs, exhibited a significant decrease from 4.21 × 10(-2) to 8.09 × 10(-3) s(-1), as the initial DCF concentration was increased from 1.00 to 5.00 µM. Furthermore, the degradation kinetics of DCF was clearly dependent on nitrogen-containing ion concentrations in the reaction solution. Ammonium and nitrite ions inhibited the DCF degradation by ClO2, whereas nitrate ion clearly initiated its promotion. In contrast, the inhibitory effect of NO2 (-) was more robust than that of NH4 (+). When the values of pE were gradually increased, the transformation of NH4 (+) to NO2 (-), and subsequently to NO3 (-), would occur, the rate constants were initially decreased, and then increased. When NH4 (+) and NO2 (-) coexisted, the inhibitory effect on the DCF degradation was less than the sum of the partial inhibitory effect. However, when NO2 (-) and NO3 (-) coexisted, the actual inhibition rate was greater than the theoretical estimate. These results indicated that the interaction of NH4 (+) and NO2 (-) was antagonistic, while the coexistence of NO2 (-) and NO3 (-) was observed to have a synergistic effect in aqueous environments.