Highly efficient degradation of 2,2',4,4'-tetrabromodiphenyl ether through combining surfactant-assisted Zn0 reduction with subsequent Fenton oxidation.

2,2',4,4'-tetrabromodiphenyl ether (BDE47) was difficult to be rapidly degraded by common reductive debromination or oxidative decomposition. In this study, the debromination via surfactant-assisted zero valent zinc (Zn0) reduction and subsequent Fenton oxidation was combined to completely degrade BDE47. Firstly, Zn0 integrated with surfactants including cetyltrimethylammonium chloride (CTAC), polyethylene glycol dodecyl ether (Brij35), or 1-dodecanesulfonic acid sodium salt (SDS) were evaluated for their reactivity to debrominate BDE47. CTAC-assisted Zn0 system presented the highest removal efficiency of 98.6% for BDE47 (C0 = 5 mg/L) under the optimized conditions including 0.3 g/L of Zn0 particles and 0.05 g/L of CTAC at 25 °C and pH 4.0 during 1-h reaction. Subsequently, the debromination products as low-brominated BDEs were attacked by hydroxyl radicals (•OH) from Fenton reagent, which were decomposed into short-chain carboxylic acids and even mineralized within 2-h oxidation. In addition, HPLC, GC-MS, LC-MS/MS, and IC were employed to detect intermediates during this reaction/oxidation process and the pathways of debromination and oxidation were proposed according to carbon and bromine balance. The above combination achieved the complete degradation of BDE47 via a relative low-cost method to rapidly remove PBDEs, which provide a new approach for the effective treatment of halogenated organic pollutants.

Efficient removal of acid orange 7 using a porous adsorbent-supported zero-valent iron as a synergistic catalyst in advanced oxidation process.

This study focuses on the synthesis of granular red mud reinforced by zero-valent iron (Fe@GRM) and its application for the removal acid orange 7 (AO7) from aqueous solution. Then ZVI is employed as a catalyst for the activation of persulfate (PS) to produce sulfate radicals (SO4•-) that are produced at 900 °C in an anoxic atmosphere using the direct reduction of iron oxide in the red mud with maize straw as the reductant. Furthermore, scanning electron microscopy (SEM) and energy dispersive spectroscopy (EDS) are used to illustrate the morphology and porous structure of the Fe@GRM. The X-ray diffraction (XRD), Fourier transform infrared spectroscopy (FTIR) and X-ray photoelectron spectroscopy (XPS) revealed that Fe@GRM was loaded with zero-valent iron. This characterization confirmed that the Fe@GRM was a porous structure material that contained zero-valent iron. The influence of conditions for AO7 elimination, including initial pH, Fe@GRM dosage, initial AO7 concentrations, and temperature, is also investigated. The removal efficiency of AO7 was 90.78% using Fe@GRM/PS, while only 18.15% was removed when Fe@GRM was used alone. The degradation kinetics were well fitted to a pseudo-first-order kinetic model, and the rate of removal increased with temperature, demonstrating an endothermic elimination process. The Arrhenius activation energy of the process was 20.77 kJ/mol, which indicated that the reduction of AO7 was a diffusion-mediated reaction. Fe@GRM is a low-cost material that demonstrated outstanding performance with great potential for wastewater treatment.

Bioactivation of Napabucasin Triggers Reactive Oxygen Species-Mediated Cancer Cell Death.

PURPOSE: Napabucasin (2-acetylfuro-1,4-naphthoquinone or BBI-608) is a small molecule currently being clinically evaluated in various cancer types. It has mostly been recognized for its ability to inhibit STAT3 signaling. However, based on its chemical structure, we hypothesized that napabucasin is a substrate for intracellular oxidoreductases and therefore may exert its anticancer effect through redox cycling, resulting in reactive oxygen species (ROS) production and cell death. EXPERIMENTAL DESIGN: Binding of napabucasin to NAD(P)H:quinone oxidoreductase-1 (NQO1), and other oxidoreductases, was measured. Pancreatic cancer cell lines were treated with napabucasin, and cell survival, ROS generation, DNA damage, transcriptomic changes, and alterations in STAT3 activation were assayed in vitro and in vivo. Genetic knockout or pharmacologic inhibition with dicoumarol was used to evaluate the dependency on NQO1. RESULTS: Napabucasin was found to bind with high affinity to NQO1 and to a lesser degree to cytochrome P450 oxidoreductase (POR). Treatment resulted in marked induction of ROS and DNA damage with an NQO1- and ROS-dependent decrease in STAT3 phosphorylation. Differential cytotoxic effects were observed, where NQO1-expressing cells generating cytotoxic levels of ROS at low napabucasin concentrations were more sensitive. Cells with low or no baseline NQO1 expression also produced ROS in response to napabucasin, albeit to a lesser extent, through the one-electron reductase POR. CONCLUSIONS: Napabucasin is bioactivated by NQO1, and to a lesser degree by POR, resulting in futile redox cycling and ROS generation. The increased ROS levels result in DNA damage and multiple intracellular changes, one of which is a reduction in STAT3 phosphorylation.

Occurrence, Distribution, and Accumulation of Pesticides in Exterior Residential Areas.

Pesticides are commonly applied around residential homes, but their occurrence on exterior surfaces (e.g., pavement) has not been thoroughly evaluated. We collected 360 dust samples from curbside gutters, sidewalks, and street surfaces at 40 houses in southern California to evaluate pesticide occurrence on urban paved surfaces as well as their spatial and temporal distributions. Pesticides and select degradates were ubiquitously detected in dust, with the median concentration of total target analytes at 85 µg kg-1. A total of 75% of samples contained at least five pesticides. As a result of recurring pesticide applications, concentrations increased throughout the summer. The pyrethroids bifenthrin and permethrin accounted for 55% of total pesticides detected in the dust. The highest concentrations in dust were found on the sidewalk and in the gutter. Relative to indoor environments, human exposure risk to pesticides on paved surfaces was estimated to be lower, with the highest potential oral and dermal exposure predicted to be 38 ng day-1 for permethrin. The ubiquitous detection of pesticides on residential outdoor surfaces and the fact that the exterior concentrations did not correlate to the indoor areas highlight the necessity to measure pesticides in both indoor and outdoor areas for complete residential pesticide risk assessment.

Pesticides on residential outdoor surfaces: environmental impacts and aquatic toxicity.

BACKGROUND: Pesticides are routinely applied to residential impervious outdoor surfaces for structural pest control. This residential usage has been linked to the occurrence of toxic levels of pesticides in urban water bodies. It is believed that run-off water transports particles that have sorbed hydrophobic pesticides. However, concentrations of particle-bound pesticides have not been directly measured on impervious surfaces, and the role of these particles as a source of contamination is unknown. RESULTS: Pesticides were detected in 99.4% of samples, with >75% of samples containing at least five pesticides. Assuming all particles were transferred with run-off, the run-off amount of pesticide during each rainfall would be >5 mg. We also used the US EPA Storm Water Management Model and estimated that 43 and 65% of the pesticides would be washed off during two rainfall events, with run-off concentrations ranging from 10.0 to 54.6 ng L(-1) and from 13.3 to 109.1 ng L(-1) respectively. The model-predicted pesticide run-off concentrations were similar to the levels monitored in urban run-off and sediments. Most (78%) particle samples contained aggregate toxicities above the Hyalella azteca LC50 . CONCLUSION: The results suggest that loose particles on residential impervious surfaces are not only carriers but also an important source of hydrophobic pesticides in urban run-off and contribute to downstream aquatic toxicities. © 2015 Society of Chemical Industry.

Determination of cholesterol and four phytosterols in foods without derivatization by gas chromatography-tandem mass spectrometry.

In this study, a method for determination of cholesterol and four phytosterols by gas chromatography coupled with electron impact ionization mode-tandem mass spectrometry without derivatization in general food was developed. The sample was saponified with 7.5% KOH in methanol. After heating on hot plate and reflux for 60 minutes, the saponified portion was extracted with n-hexane/petroleum ether (50:50, v/v). The extracts were evaporated with rotary evaporator and then redissolved with tetrahydrofuran. The tetrahydrofuran layer was transferred into an injection vial and analyzed by gas chromatography on a 30 m VF-5 column. Limit of quantification was 2 mg/kg. Recoveries of cholesterol and four phytosterols from general food were between 91% and 100%.

Fluorescence turn-on detection of hypochlorous acid via HOCl-promoted dihydrofluorescein-ether oxidation and its application in vivo.

We report three new water-soluble dihydrofluorescein-ether probes FCN1, FCN2 and FCN3 for the detection of hypochlorous acid (HOCl), which were designed on the basis of a specific HOCl-promoted oxidation reaction. This work also provided a useful method to monitor the accumulated HOCl in specific organelles using a zebrafish model.

Regulation of MITF stability by the USP13 deubiquitinase.

The microphthalmia-associated transcription factor (MITF) is essential for melanocyte development. Mutation-induced MAPK pathway activation is common in melanoma and induces MITF phosphorylation, ubiquitination, and proteolysis. Little is known about the enzymes involved in MITF ubiquitination/deubiquitination. Here we report the identification of a deubiquitinating enzyme, named ubiquitin-specific protease 13 (USP13) that appears to be responsible for MITF deubiquitination, utilizing a short hairpin RNA library against known deubiquitinating enzymes. Through deubiquitination, USP13 stabilizes and upregulates MITF protein levels. Conversely, suppression of USP13 (through knockdown) leads to dramatic loss of MITF protein, but not messenger RNA. Through its effects on MITF deubiquitination, USP13 was observed to modulate expression of MITF downstream target genes and, thereby, to be essential for melanoma growth in soft agar and in nude mice. These observations suggest that as a potentially drugable protease, USP13 might be a viable therapeutic target for melanoma.

Visualization of nitroxyl in living cells by a chelated copper(II) coumarin complex.

The coumarin-based probe Cu(II)-COT1 was successfully developed for the detection of HNO on the basis of the reduction reaction. In addition, highly selective "turn on" type fluorogenic behavior upon the addition of Angeli's salt (Na(2)N(2)O(3)) was also applied to bioimaging in A375 cells.

A thiophen-thiooxorhodamine conjugate fluorescent probe for detecting mercury in aqueous media and living cells.

A rhodamine-based sensor RB-S2 was designed and synthesized by combination of the thiospirolacton chromophore and the thiophen ring block with high affinity to Hg(2+). Probe RB-S2 exhibits high selectivity and excellent sensitivity in both absorbance and fluorescence detection of Hg(2+) in aqueous solution. In addition, fluorescent imaging of Hg(2+) in MCF-7 cells is also successfully demonstrated.

Negative regulation of Vps34 by Cdk mediated phosphorylation.

Vacuolar protein sorting 34 (Vps34) complexes, the class III PtdIns3 kinase, specifically phosphorylate the D3 position of PtdIns to produce PtdIns3P. Vps34 is involved in the control of multiple key intracellular membrane trafficking pathways including endocytic sorting and autophagy. In mammalian cells, Vps34 interacts with Beclin 1, an ortholog of Atg6 in yeast, to regulate the production of PtdIns3P and autophagy. We show that Vps34 is phosphorylated on Thr159 by Cdk1, which negatively regulates its interaction with Beclin 1 during mitosis. Cdk5/p25, a neuronal Cdk shown to play a role in Alzheimer's disease, can also phosphorylate Thr159 of Vps34. Phosphorylation of Vps34 on Thr159 inhibits its interaction with Beclin 1. We propose that phosphorylation of Thr159 in Vps34 is a key regulatory mechanism that controls the class III PtdIns3 kinase activity in cell-cycle progression, development, and human diseases including neurodegeneration and cancers.

Caspase-11 regulates cell migration by promoting Aip1-Cofilin-mediated actin depolymerization.

Coordinated regulation of cell migration, cytokine maturation and apoptosis is critical in inflammatory responses. Caspases, a family of cysteine proteases, are known to regulate cytokine maturation and apoptosis. Here, we show that caspase-11, a mammalian pro-inflammatory caspase, regulates cell migration during inflammation. Caspase-11-deficient lymphocytes exhibit a cell-autonomous migration defect in vitro and in vivo. We demonstrate that caspase-11 interacts physically and functionally with actin interacting protein 1 (Aip1), an activator of cofilin-mediated actin depolymerization. The caspase-recruitment domain (CARD) of caspase-11 interacts with the carboxy-terminal WD40 propeller domain of Aip1 to promote cofilin-mediated actin depolymerization. Cells with Aip1 or caspase-11 deficiency exhibit defects in actin dynamics. Using in vitro actin depolymerization assays, we found that caspase-11 and Aip1 work cooperatively to promote cofilin-mediated actin depolymerization. These data demonstrate a novel cell autonomous caspase-mediated mechanism that regulates actin dynamics and mammalian cell migration distinct from the receptor mediated Rho-Rac-Cdc42 pathway.