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Charge (ion and electron)-transfer reactions at a liquid/liquid interface are critical processes in many important biological and chemical systems. An ion-transfer (IT) process is usually very fast, making it difficult to accurately measure its kinetic parameters. Nano-liquid/liquid interfaces supported at nanopipettes are advantageous approaches to study the kinetics of such ultrafast IT processes due to their high mass transport rate. However, correct measurements of IT kinetic parameters at nanointerfaces supported at nanopipettes are inhibited by a lack of knowledge of the nanometer-sized interface geometry, influence of the electric double layer, wall charge polarity, etc. Herein, we propose a new electrochemical characterization equation for nanopipettes and make a suggestion on the shape of a nano-water/1,2-dichloroethane (nano-W/DCE) interface based on the characterization and calculation results. A theoretical model based on the Poisson-Nernst-Planck equation was applied to systematically study how the electric double layer influences the IT process of cations (TMA

The non-Bornian solvation model has been applied to a theoretical consideration of the Gibbs free energy for the transfer of fluorinated anions, non-fluorinated cations, and non-fluorinated anions at the 2H,3H-decafluoropentane (DFP)/water (W) and 1,2-dichloroethane (DCE)/W interfaces. According to our previous experimental results, the fluorinated anions are more stable in DFP than DCE, while the non-fluorinated cations and anions are less stable in DFP. To understand this characteristic feature of DFP, energy decomposition analyses have been performed for the hypothetical transfer of ions at the DFP/DCE interface. In conclusion, the characteristics of DFP as a fluorous solvent should be explained in terms of the higher repulsive interaction of the solvent molecule with ions, particularly with non-fluorinated ions.

Described herein is a copper-catalyzed oxidative C-H annulation of quinolines with 1,2-chloroethane (DCE), providing a concise synthetic approach to benzoquinoliziniums. In this protocol, DCE not only serves as a solvent and an in situ activation agent of quinoline C2-H but also works as vinyl equivalents to constitute the six-membered azonia ring. Furthermore, the resultant benzoquinolizinium library exhibits good properties of binding to DNA and low cytotoxicity.

The compositions of volatile organic compounds (VOCs) under actual industrial conditions are often complex; especially, the interaction of intermediate products easily leads to more toxic emissions that are harmful to the atmospheric environment and human health. Herein, we report a comparative investigation on 1,2-dichloroethane (1,2-DCE) and (1,2-DCE + toluene) oxidation over the Ru/TiO

This work is focused on the electroanalytical study of a family of five imidazolium-terminated carbosilane dendrimers (from generation G1 to G3) at the polarized liquid-liquid interface formed between water and 1,2-dichloroethane solutions. All dendrimers with permanently and positively charged imidazolium groups located at the periphery within the branched carbosilane core were found to be electrochemically active. Based on the concentration and scan rate dependencies we have concluded that these molecules undergo interfacial ion transfer processes accompanied by interfacial adsorption/desorption rather than the electrochemically induced interfacial formation of the macromolecule-anion (tetrakis(4-chlorophenyl)borate) from the organic phase complex. Also, we report several physicochemical and electroanalytical parameters (e.g. diffusion coefficients, LODs, and detection sensitivities) for the studied family of dendrimers. Our work aims to contribute to the understating of the interaction between branched macromolecules and biomimetic interfaces.

1,2-dichloroethane (1,2-DCA) is a chlorinated hydrocarbon used for polyvinyl chloride plastic production. As such, 1,2-DCA is a common persistent contaminant in saturated zones. While nanoscale zerovalent iron (NZVI) is considered an effective reductant for removing a wide range of chlorinated hydrocarbons, 1,2-DCA is resistant to reduction by NZVI as well as by modified forms of NZVI (e.g., sulfidated-NZVI). Hydroxyl radicals produced in Fenton's reaction can effectively degrade 1,2-DCA, but Fenton's reaction requires the acidification of saturated zones to achieve a groundwater pH of 3 to facilitate the catalytic reaction. To overcome this problem, this study has developed a sequential treatment process using an NZVI-induced Fenton-like reaction that can effectively degrade 1,2-DCA at an initially neutral pH range. The experiments were conducted using a high 1,2-DCA concentration (2000 mg/L) to evaluate the feasibility of using the treatment process at source zones. The process degraded 99% of 1,2-DCA with a pseudo-first-order rate constant of 0.49 h

It has been well recognized that the Fenton reaction requires a rigorous pH control and suffers from the fast self-degradation of H

1,2-dichloroethane (DCE or EDC) is a chlorinated hydrocarbon used as a chemical intermediate, including in the synthesis of polyvinyl chloride. Although DCE has induced tumors in both rats and mice, the overall weight-of-evidence suggests a lack of in vivo mutagenicity. The present study was conducted to explore a potential mode of action further for tumor formation in rat mammary tissue. Fischer 344 rats were exposed to target concentrations of 0 or 200 ppm of DCE vapors (6 hours/day, 7 days/week) for at least 28 days; 200 ppm represents a concentration of ~20% higher than that reported to induce mammary tumors. Endpoints examined included DNA damage (via Comet assay), glutathione (reduced, oxidized and conjugated), tissue DNA adducts, cell proliferation and serum prolactin levels. Exposure to DCE did not alter serum prolactin levels with consistent estrous stage, did not cause cell proliferation in mammary epithelial cells, nor result in histopathological alterations in the mammary gland. DNA adducts were identified, including the N7 -guanylethyl glutathione adduct, with higher adduct levels measured in liver (nontumorigenic target) compared with mammary tissue isolated from the same rats; no known mutagenic adducts were identified. DCE did not increase the Comet assay response in mammary epithelial cells, whereas DNA damage in the positive control (N-nitroso-N-methylurea) was significantly increased. Although the result of this study did not identify a specific mode of action for DCE-induced mammary tumors in rats, the lack of any exposure-related genotoxic responses further contributes to the weight-of-evidence suggesting that DCE is a nongenotoxic carcinogen.

Reactivity at phase boundaries is central to many areas of chemistry, from synthesis to heterogeneous catalysis. New tools are necessary to gain a more detailed understanding of processes occurring at these boundaries. We describe a series of experiments to visualize phase boundaries using electrogenerated chemiluminescence (ECL) on glassy carbon electrodes. By taking advantage of the solubilities of the ECL luminophore and the coreactant in different liquid phases, we demonstrate that the interface of various phases (i.e., the boundaries formed between a water microdroplet, 1,2-dichloroethane, and a glassy carbon electrode and the boundaries formed between an oxygen bubble, water, and a glassy carbon electrode) can be evaluated. We measured microdroplet contact radii, the three-phase boundary thickness, and growth dynamics of electrogenerated O2 bubbles. These experimental tools and the fundamental knowledge they yield will find applications in biology, nanoscience, synthesis, and energy storage and conversion, where understanding phase boundary chemistry is essential.

Overexposure to 1,2-dichloroethane (1,2-DCE) can induce brain edema, but the underlying mechanisms remain largely unknown. Aquaporin 4 (AQP4) is the most prevalent water channel in the brain, and the pool of AQP4 facilitates brain edema by controlling the inflow and clearance of brain water. MicroRNAs play an important role in the regulation of brain edema via RNA silencing and post-transcriptional regulation of gene expression. To explore the regulation role of AQP4 and microRNA in 1,2-DCE-induced brain edema, Sprague-Dawley (SD) rats and AQP4 knockout CD-1 mice were exposed to 1,2-DCE by inhalation for 7 days (0, 600, 1,800 mg/m3) and 28 days (0, 100, 350, 700 mg/m3), respectively. The results showed that 1,2-DCE induces brain edema, in both rats and mice, characterized by an increase in brain water content and vacuolations in the brain parenchyma and around the vessels of the cerebral cortex. Notably, 1,2-DCE exposure can down-regulate AQP4 expression, in both rats and mice. Also, deleting AQP4 intensifies 1,2-DCE-induced brain edema in mice. Meanwhile, microRNA-29b-3p (miR-29b) expression increases with 1,2-DCE exposure, in both rats and mice. A negative correlation was found between the expression of miR-29b and AQP4 in vivo. Moreover, the negative regulation of miR-29b by direct targeting to AQP4 was confirmed by dual luciferase reporter assay in vitro. Taken together, our findings indicate that AQP4 plays an important role in balancing water content in 1,2-DCE-induced brain edema. The dysregulation of miR-29b after 1,2-DCE exposure can aggravate brain edema by directly suppressing the expression of AQP4.

1,2-Dichloroethane (1,2-DCE) is a pervasive environmental pollutant, and overexposure to this hazardous material causes brain edema and demyelination in humans. We found that 1,2-DCE inhibits aquaporin 4 (AQP4) and is a primary pathogenic effector of 1,2-DCE-induced brain edema in animals. However, AQP4 down-regulation’s link with cortex demyelination after 1,2-DCE exposure remains unclear. Thus, we exposed wild-type (WT) CD-1 mice and AQP4 knockout (AQP4-KO) mice to 0, 100, 350 and 700 mg/m3 1,2-DCE by inhalation for 28 days. We applied label-free proteomics and a cell co-culture system to elucidate the role of AQP4 inhibition in 1,2-DCE-induced demyelination. The results showed that 1,2-DCE down-regulated AQP4 in the WT mouse cortexes. Both 1,2-DCE exposure and AQP4 deletion induced neurotoxicity in mice, including increased brain water content, abnormal pathological vacuolations, and neurobehavioral damage. Tests for interaction of multiple regression analysis highlighted different effects of 1,2-DCE exposure level depending on the genotype, indicating the core role of AQP4 in regulation on 1,2-DCE-caused neurotoxicity. We used label-free quantitative proteomics to detect differentially expressed proteins associated with 1,2-DCE exposure and AQP4 inhibition, and identified down-regulation in myelin basic protein (MBP) and tyrosine-protein kinase Fyn (FYN) in a dose-dependent manner in WT mice but not in AQP4-KO mice. 1,2-DCE and AQP4 deletion separately resulted in demyelination, as detected by Luxol fast blue staining, and manifested as disordered nerve fibers and cavitation in the cortexes. Western blot and immunofluorescence confirmed the decreased AQP4 in the astrocytes and the down-regulated MBP in the oligodendrocytes by 1,2-DCE exposure and AQP4 inhibition, respectively. Finally, the co-culture results of SVG p12 and MO3.13 cells showed that 1,2-DCE-induced AQP4 down-regulation in the astrocytes was responsible for demyelination, by decreasing MBP in the oligodendrocytes. In conclusion, 1,2-DCE induced cortex demyelination by depressing MBP via AQP4 inhibition in the mice.

Matrix-assisted laser desorption/ionization-based mass spectrometry imaging (MSI) of separated lipids on thin-layer chromatography (TLC) plates or followed by blotted hydrophilic polyvinylidene fluoride (PVDF) membranes has become a powerful tool in lipidomic analyses. However, background peaks in MS spectra often cover lipid peaks in a low amount/ionization effect; consequently, only low intensities/resolutions MSI are obtained. To address the aforementioned problem, we attempted 1,2-dichloroethane pre-washing of TLC plates before development and found that backgrounds could successfully be removed from the TLC plate or PVDF membrane.

Ru-based catalysts for catalytic combustion of high-toxicity Cl-containing volatile organic compounds are inclined to produce Cl

Volatile organic compounds (VOCs) are an important source of air pollution, harmful to human health and the environment, and important precursors of secondary organic aerosols, O3 and photochemical smog. This study focused on the low-temperature catalytic oxidation and degradation of benzene, dichloroethane, methanethiol, methanol and methylamine by ozone. Benzene was used as a model compound, and a molecular sieve was selected as a catalyst carrier to prepare a series of supported active metal catalysts by impregnation. The effects of ozone on the catalytic oxidation of VOCs and catalysts’ activity were studied. Taking benzene as a model compound, low-temperature ozone catalytic oxidation was conducted to explore the influence of the catalyst carrier, the active metal and the precious metal Pt on the catalytic degradation of benzene. The optimal catalyst appeared to be 0.75%Pt–10%Fe/HZSM(200). The catalytic activity and formation of the by-products methylamine, methanethiol, methanol, dichloroethane and benzene over 0.75%Pt–10%Fe/HZSM(200) were investigated. The structure, oxygen vacancy, surface properties and surface acidity of the catalysts were investigated. XRD, TEM, XPS, H2-TPR, EPR, CO2-TPD, BET, C6H6-TPD and Py-IR were combined to establish the correlation between the surface properties of the catalysts and the degradation activity.

Wet scrubbing is a low-cost process for disposing of air pollutants. Nevertheless, this method is rarely used for the treatment of volatile organic compounds (VOCs) because of their poor water solubility. In this study, we used a unique wet scrubbing system containing H

1,2-Dichloroethane (1,2-DCE) is a highly toxic neurotoxicity, and the brain tissue is the main target organ. At present, long-term exposure to 1,2-DCE has been shown to cause cognitive dysfunction in some studies, but the mechanism is not clear. The results of this study showed that long-term 1,2-DCE exposure decreased learning and memory abilities in mice and impaired the structure and morphology of neurons in the hippocampal region. Moreover, except for the mRNA level of PAG, the enzymatic activities and protein levels of GS and PAG, as well as the mRNA level of GS were inhibited. With increasing dose of exposure, the protein and mRNA expression of GLAST and GLT-1 also decreased. Contrarily, there were protein and mRNA expression upregulation of GluN1, GluN2A and GluN2B in the hippocampus, as well as increased levels of extracellular Glu and intracellular Ca

We have previously reported that the activation of astrocytes and microglia may lead to the overproduction of proinflammatory mediators, which could induce neuroinflammation and cause brain edema in 1,2-dichloroethane (1,2-DCE)-intoxicated mice. In this research, we further hypothesized that astrocyte–microglia crosstalk might trigger neuroinflammation and contribute to brain edema in 1,2-DCE-intoxicated mice. The present research revealed, for the first time, that subacute intoxication with 1,2-DCE might provoke the proinflammatory polarization of microglia, and pretreatment with minocycline, a specific inhibitor of microglial activation, may attenuate the enhanced protein levels of ionized calcium-binding adapter molecule1 (Iba-1), cluster of differentiation 11b (CD11b), glial fibrillary acidic protein (GFAP), soluble calcium-binding protein 100B (S100B), tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), inducible nitric oxide synthase (iNOS), vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), matrix metalloproteinase-9 (MMP-9), Toll-like receptor 4 (TLR4), MyD88, and p-p65, and ameliorate the suppressed protein expression levels of occludin and claudin 5, we also observed changes in water content and made pathological observations on edema in the brains of 1,2-DCE-intoxicated mice. Moreover, pretreatment with fluorocitrate, an inhibitor of reactive astrocytes, could also reverse the alteration in protein expression levels of GFAP, S100B, Iba-1, CD11b, TNF-α, IL-6, iNOS, VCAM-1, ICAM-1, MMP-9, occludin, and claudin 5 in the brain of 1,2-DCE intoxicated mice. Furthermore, pretreatment with melatonin, a well-known anti-inflammatory drug, could also attenuate the above-mentioned changes in the brains of 1,2-DCE-intoxicated mice. Altogether, the findings from this research indicated that microglial activation might play an important role in triggering neuroinflammation, and hence may contribute to brain edema formation, additionally, the findings suggested that molecular crosstalk between reactive astrocytes and activated microglia may amplify the neuroinflammatory reaction, which could induce secondary brain injury in 1,2-DCE-intoxicated mice.

In this paper, the electrochemical behavior of four fluoroquinolone antibiotics (FAs) [Ciprofloxacin (Cip), Enrofloxacin (Enr), Marbofloxacin (Mar) and Ofloxacin (Ofl)] at a polarized interface between two immiscible electrolyte solutions (ITIES) has been studied using ion–transfer voltammetry (ITV). The measurements were conducted in the traditional macroscopic (macro-ITIES) and a recently developed miniaturized (micro-ITIES) platform. The latter was obtained from fused silica micro-capillaries having an internal diameter of 25 μm. We used macroITIES to obtain a number of analytical parameters such as: standard Galvani potential of ion transfer (ΔΦ0), diffusion coefficients (D), free Gibbs energy of ion transfer (ΔG0) and partition coefficients (logPDCE). The latter were compared with the available literature values of logPoctanol. The effect of concentration of the studied antibiotics on the electrochemical response was investigated with the microITIES platform, setting statistical parameters such as: linear dynamic ranges (LDRs – studied from 1 μM up to 50 μM), lower limit of detections (LODs – around 1 μM) and sensitivity (found in the range from 2.6·10−2 to 6.8·10−2 nA·μM−). MicroITIES were further used to study the effect of pH on the analytical signal and the results are plotted in a form of ion partition diagrams. Working with microITIES supported with the fused silica capillaries significantly reduced the volumes of consumed chemicals and expedite all analytical experiments. The provided results can be successfully applied in pharmacology and electroanalysis for testing and determination of the chosen fluoroquinolone antibiotics.

Flurbiprofen is a kind of nonsteroidal anti‐inflammatory drug, which has been widely used in clinic for treatment of rheumatoid arthritis and osteoarthritis. It has been reported that S‐flurbiprofen shows good performance on clinic anti‐inflammatory treatment, while R‐enantiomer almost has no pharmacological activities. It has important practical values to obtain optically pure S‐flurbiprofen. In this work, chiral ionic liquids, which have good structural designability and chiral recognize ability, were selected as the extraction selector by the assistance of quantum chemistry calculations. The distribution behaviors of flurbiprofen enantiomers were investigated in the extraction system, which was composed of organic solvent and aqueous phase containing chiral ionic liquid. The results show that maximum enantioselectivity up to 1.20 was attained at pH 2.0, 25°C using 1,2‐dichloroethane as organic solvent, 1‐butyl‐3‐methylimidazole L‐tryptophan ([Bmim][L‐trp]) as chiral selector. The racemic flurbiprofen initial concentration was 0.2 mmol L−1, and [Bmim][L‐trp] concentration was 0.02 mol L−1. Furthermore, the recycle of chiral ionic liquids has been achieved by reverse extraction process of the aqueous phase with chiral selector, which is significant for industrial application of chiral ionic liquids and scale‐up of the extraction process.

Although the application of 1,2-dichloroethane (DCE) as a chlorinating reagent in organic synthesis with the concomitant release of vinyl chloride as a useful byproduct is a fantastic idea, it still presents a tremendous challenge and has not yet been achieved because of the harsh dehydrochlorination conditions and the sluggish C-H chlorination process. Here we report a bifunctional electrocatalysis strategy for the catalytic dehydrochlorination of DCE at the cathode simultaneously with anodic oxidative aromatic chlorination using the released HCl as the chloride source for the efficient synthesis of value-added (hetero)aryl chlorides. The mildness and practicality of the protocol was further demonstrated by the efficient late-stage chlorination of bioactive molecules.

1,2-Dichloroethane (1,2-DCE) is a pervasive environmental pollutant found in ambient and residential air, as well as ground and drinking water. Overexposure to it results in cortex edema, in both animals and humans. 1,2-DCE induces apoptosis in the cerebellum, liver and testes. This promotes the hypothesis that 1,2-DCE may induce apoptosis in the cortex as brain edema progresses. To validate our hypothesis, 40 NIH male mice were exposed to 0, 100, 350, 700 mg/m3 1,2-DCE by whole-body dynamic inhalation for 28 consecutive days. MicroRNA (miRNA) and mRNA microarray combined with TdT-mediated dUTP nick-end labeling, flow cytometry, and mitochondrial membrane potential (mtΔΨ) measurement were applied to identify the cortex apoptosis pathways' specific responses to 1,2-DCE, in vitro and in vivo. The results showed that 1,2-DCE caused brain edema and increased apoptosis in the mouse cortexes. We confirmed that 1,2-DCE induced increased apoptosis via mitochondrial pathway, both in vitro and in vivo, as evidenced by increased Caspase-3, cleaved Caspase-3, Cytochrome c and Bax expression, and decreased Bcl-2 expression. Additionally, mtΔΨ decreased after 1,2-DCE treatment in vitro. 1,2-DCE exposure increased miR-182-5p and decreased phospholipase D1 (PLD1) in the cerebral cortex of mice. MiR-182-5p overexpression and PLD1 inhibition reduced mtΔΨ and increased astrocyte apoptosis, yet miR-182-5p inhibition alleviated the 1,2-DCE-induced PLD1 down-regulation and the increased apoptosis. Finally, PLD1 was confirmed to be a target of miR-182-5p by luciferase assay. Taken together, our findings indicate that 1,2-DCE exposure induces apoptosis in the cortex via a mitochondria-dependent pathway. This pathway is regulated by a miR-182-5p⊣PLD1 axie.

A reedbed system planted with Phragmites australis was implemented to treat chlorinated hydrocarbon-contaminated groundwater in an industrial plant area. Reedbed commissioning was conducted from July 2016 to November 2016 to treat contaminated groundwater via a pump-and-treat mechanism. Combination of horizontal and vertical reedbed systems was applied to treat 1,2-dichloroethane (1,2 DCA) under four parallel installations. The 2-acre horizontal and vertical reedbed systems were designed to treat approximately 305 m

The ion-transfer reactions of alkyl and perfluoroalkyl carboxylate ions (CH

Enzymes play a fundamental role in many biological processes. We present a theoretical approach to investigate the catalytic power of the haloalkane dehalogenase reaction with 1,2-dichloroethane. By removing the three main active-site residues one by one from haloalkane dehalogenase, we found two reactive descriptors: one descriptor is the distance difference between the breaking bond and the forming bond, and the other is the charge difference between the transition state and the reactant complex. Both descriptors scale linearly with the reactive barriers, with the three-residue case having the smallest barrier and the zero-residue case having the largest. The results demonstrate that, as the number of residues increases, the catalytic power increases. The predicted free energy barriers using the two descriptors of this reaction in water are 23.1 and 24.2 kcal/mol, both larger than the ones with any residues, indicating that the water solvent hinders the reactivity. Both predicted barrier heights agree well with the calculated one at 25.2 kcal/mol using a quantum mechanics and molecular dynamics approach, and also agree well with the experimental result at 26.0 kcal/mol. This study shows that reactive descriptors can also be used to describe and predict the catalytic performance for enzyme catalysis.

Spontaneous S-alkylation of methimazole (1) with 1,2-dichloroethane (DCE) into 1,2-bis[(1-methyl-1H-imidazole-2-yl)thio]ethane (2), that we have described recently, opened the question about its formation pathway(s). Results of the synthetic, NMR spectroscopic, crystallographic and computational studies suggest that, under given conditions, 2 is obtained by direct attack of 1 on the chloroethyl derivative 2-[(chloroethyl)thio]-1-methyl-1H-imidazole (3), rather than through the isolated stable thiiranium ion isomer, i.e., 7-methyl-2H, 3H, 7H-imidazo[2,1-b]thiazol-4-ium chloride (4a, orthorhombic, space group Pnma), or in analogy with similar reactions, through postulated, but unproven intermediate thiiranium ion 5. Furthermore, in the reaction with 1, 4a prefers isomerization to the N-chloroethyl derivative, 1-chloroethyl-2,3-dihydro-3-methyl-1H-imidazole-2-thione (7), rather than alkylation to 2, while 7 further reacts with 1 to form 3-methyl-1-[(1-methyl-imidazole-2-yl)thioethyl]-1H-imidazole-2-thione (8, monoclinic, space group P 21/c). Additionally, during the isomerization of 3, the postulated intermediate thiiranium ion 5 was not detected by chromatographic and spectroscopic methods, nor by trapping with AgBF4. However, trapping resulted in the formation of the silver complex of compound 3, i.e., bis-{2-[(chloroethyl)thio]-1-methyl-1H-imidazole}-silver(I)tetrafluoroborate (6, monoclinic, space group P 21/c), which cyclized upon heating at 80 °C to 7-methyl-2H, 3H, 7H-imidazo[2,1-b]thiazol-4-ium tetrafluoroborate (4b, monoclinic, space group P 21/c). Finally, we observed thermal isomerization of both 2 and 2,3-dihydro-3-methyl-1-[(1-methyl-1H-imidazole-2-yl)thioethyl]-1H-imidazole-2-thione (8), into 1,2-bis(2,3-dihydro-3-methyl-1H-imidazole-2-thione-1-yl)ethane (9), which confirmed their structures.

Among the chlorinated aliphatic hydrocarbons, 1,2-dichloroethane (1,2-DCA) is widely used for the synthesis of vinyl chloride monomers. Despite the high demand for 1,2-DCA, it poses a risk to the environment because it is persistent and carcinogenic. Therefore, in this study, several reagents (dithionite, hydrosulfide, sulfite, persulfate, sulfate radicals, and hydroxyl radicals) were evaluated for the degradation of 1,2-DCA. Among these, the hydroxyl radicals generated by the Fenton reaction were the most suitable oxidant, decomposing 92% of 1,2-DCA. Chloride, one of the final oxidized products, was observed, which supported the oxidation reaction. Moreover, with an increasing concentration of hydroxyl radicals, the degradation of 1,2-DCA increased. Furthermore, sufficient amounts of hydrogen peroxide were more important than Fe(II) in the decomposition of 1,2-DCA. The radical reaction can generate larger molecules via the degradation of 1,2-DCA, which are degraded over time. The applicability of Fenton oxidation was evaluated using real 1,2-DCA-contaminated groundwater. Although the degradation of target contaminant was lowered due to the alkaline pH and the presence of chloride and bicarbonate ions in groundwater, the Fenton reaction was still efficient to oxidize 1,2-DCA. These results indicate that Fenton oxidation is an effective technique for the treatment of 1,2-DCA in contaminated groundwater.

In this work, we have examined an electrochemical behavior of the ephedrine at the polarized liquid-liquid interface (water/1,2-dichloroethane). In this respect, we first designed and then 3D printed polyamide-based electrochemical cell that was used as the liquid-liquid interface support during electroanalytical measurements. The protonated ephedrine undergoes a reversible ion transfer reaction with the standard Galvani potential difference equal to +0.269 V. This value was used to calculate the water - 1,2-dichloroethane logP equal to -4.6. Ion transfer voltammetry was used to build the calibration curve and allowed for the ephedrine detection from concentration equal to 20 μM. By varying the pH of the aqueous phase from 2 up to 12 we were able to plot the ion partition diagram that was further analyzed and provided several pharmacochemical information. To further push this work towards practical utility, we have formulated the artificial urine and studied the interfacial behavior of all its components at the polarized liquid-liquid interface. Ephedrine detection from real spiked urine samples was also performed.

The understanding of the relationship between exposure to carcinogenic vinyl chloride (VCM) and ethylene dichloride (EDC) and liver fibrosis is limited.This study aimed to investigate the associations between the urinary metabolite levels of VCM and EDC and the risk of liver fibrosis in residents living near a petrochemical complex.Our study comprised 447 adult residents of two townships with questionnaire survey and health examination near the largest petrochemical complex in central Taiwan. The urinary levels of thiodiglycolic acid (TdGA), the metabolite of VCM and EDC, were detected in study subjects. We utilized fibrosis-4 (FIB-4) as the noninvasive liver fibrosis index. Adjusted linear model was applied to evaluate the associations between the distance from the complex and the urinary TdGA levels. Adjusted logistic regression model was applied to evaluate the associations between the urinary TdGA levels and the risk of liver fibrosis.The study subjects living in the closer township had significant higher urinary TdGA levels than those living in the more distant township (269.6 ± 200.7 vs. 199.2 ± 164.7 μg/g creatinine) (p 0.001). It showed that urinary TdGA levels were decreased 0.53-fold when the distances from the complex were increased 1-fold after adjusting for confounding factors. It demonstrated that the study subjects with the highest TdGA levels (343.3 μg/g creatinine) had a higher risk of FIB-41.29 (OR = 2.09; 95% CI: 1.17, 3.78), and those with higher TdGA levels (232.7 to 343.3 μg/g creatinine) had a marginally higher risk of FIB-41.29 (OR = 1.65; 95% CI: 0.94, 2.90).The residents living closer to the VCM/PVC plant in the petrochemical complex had higher urinary TdGA levels, which were associated with an increased risk of fibrosis. This confirmed that the EDC and VCM potentially emitted from the petrochemical industry may have an impact on the liver health of nearby residents.

金沢大学理工研究域物質化学系, Molecular association between biocompatible dendritic polymers, dendrigraft poly-l-lysines (DGLs), and an anionic fluorescent probe, 8-anilino-1-naphthalenesulfonate (ANS-), was studied at the polarized water|1,2-dichloroethane (DCE) interface. The fluorescence intensity of ANS measured in aqueous solution was enhanced by the coexistence of DGLs over a wide pH range (2 < pH < 10), where ANS and DGL exist as a monoanionic form and a polycation, respectively. The voltammetric responses indicated that the positively charged DGLs were adsorbed at the water|DCE interface, whereas ANS- was transferred across the interface accompanied by the adsorption process. The interfacial behavior of the DGL-ANS associates was analyzed by potential-modulated fluorescence (PMF) spectroscopy. The PMF results demonstrated that the ion association between DGLs and ANS at the water|DCE interface is strongly affected by the applied potential and the dendritic generation of DGL. By applying appropriate potentials, the ANS anion was dissociated from its ion associate with DGLs at the interface and transferred into the organic phase, whereas DGLs remained in the aqueous phase. The Gibbs free energy of ion association (ΔGD···ANS) was estimated for the second-fourth generation DGLs (DGL-G2-G4) and the G4 polyamidoamine (PAMAM) dendrimer as a control. The highest stability of the DGL-G4-ANS associate manifested itself through ΔGD···ANS: DGL-G4-ANS (>G4 PAMAM dendrimer-ANS) > DGL-G3-ANS > DGL-G2-ANS. The results elucidated the efficient anion-binding ability of higher generation DGLs and its potential dependence at the liquid|liquid interface. © 2018 American Chemical Society., Embargo Periods 12 Months

A gas chromatographic procedure has been developed for the trace determination of chloroacetyl chloride (CAC) and two of its impurities: methyl chloroacetate (MCA) and chloroacetic acid (CAA). All three compounds are derivatized using piperidine in dichloroethane prior to their analysis via gas chromatography coupled with a flame ionization detection (GC-FID). Recoveries of each compound were assessed in two different pharmaceutical matrices (intermediate and final active pharmaceutical ingredient) and ranged from 75 to 125%. The limit of quantitation has been determined to be 0.10% wt/wt for CAA and 0.03% wt/wt for CAC and MCA. The linearity ranged from 0.03 to 5.00% wt/wt for CAC and MCA and from 0.10 to 5.00% wt/wt for CAA, with correlation coefficients from 0.9995 to 1.0000. Repeatability was evaluated at LOQ and at 5.00% wt/wt and was found to be between 1.4-3.0%.

With the increasing demand for typical hazardous and noxious substances (HNS) in chemical industry, there is an increased leakage risk of these HNS during transportation by vessel and storage nearby seashore. In this study, the acute toxicity of nonylphenol, butyl acrylate and 1, 2-dichloroethane to Phaeodactylum tricornutum (P. tricornutum) and Platymonas subcordiformis (P. subcordiformis), was investigated to assess their ecological risk. The results showed that the three kinds of HNS showed significant time- and dose-dependent patterns on the growth inhibition of two marine microalgae. The 96 h-EC50 of nonylphenol, butyl acrylate and 1, 2-dichloroethane on P. tricornutum was 1.088, 45.908 and 396 mg L−1, respectively, and the 96 h-EC50 of that on P. subcordiformis was 0.851, 52.621 and 389 mg L−1, respectively. It was a common method to evaluate the harm of pollutants to organisms by calculating HC5 value (the minimum pollutant concentration value harmful to 95 % of the studied species, which was no-effect concentration) with Species Sensitivity Distribution (SSD). On the basis of EC50, the ecological risk assessment was further carried out, and HC5 value of nonylphenol and 1, 2-dichloroethane to aquatic organism was 0.079 and 44 mg L−1, respectively.

The identification of aberrant microRNA (miRNA) expression during chemical-induced hepatic dysfunction will lead to a better understanding of the substantial role of miRNAs in liver diseases. 1,2-Dichloroethane (1,2-DCE), a chlorinated organic toxicant, can lead to hepatic abnormalities in occupationally exposed populations. To explore whether aberrant miRNA expression is involved in liver abnormalities mediated by 1,2-DCE exposure, we examined alterations in miRNA expression patterns in the livers of NIH Swiss mice after dynamic inhalation exposure to 350 or 700 mg m-3 1,2-DCE for 28 days. Using a microarray chip, we discovered that only mmumiR-451a was significantly upregulated in the liver tissue of mice exposed to 700 mg m-3 1,2-DCE; this finding was validated by quantitative real-time polymerase chain reaction. In vitro study revealed that it was metabolite 2-chloroacetic acid, not 1,2-DCE that resulted in the upregulation of mmu-miR-451a in the mouse AML12 cell line. Furthermore, our data showed that the upregulation of mmu-miR-451a induced by 2-chloroacetic acid could suppress the expression of glycerol kinase and lead to the inhibition of glycerol gluconeogenesis in mouse liver tissue and AML12 cells. These observations provide evidence that hepatic mmu-miR-451a responds to 1,2-DCE exposure and might induce glucose metabolism disorders by suppressing the glycerol gluconeogenesis process.

Reductive dehalogenases (RDases) of organohalide-respiring bacteria are cobamide-containing iron–sulfur proteins that catalyze different reductive dehalogenation reactions. Here, we report a functional analysis of two recombinant RDases, the tetrachloroethene (PCE) reductive dehalogenase (PceA) of Desulfitobacterium hafniense Y51 and the 1,2-dichloroethane (1,2-DCA) reductive dehalogenase (DcaA) of Desulfitobacterium dichloroeliminans DCA1. Both enzymes share 88% protein sequence identity, but appeared to have divergent mechanisms. In this study, the heterologously produced DcaA converted 1,2-DCA and 1,1,2-trichloroethane (1,1,2-TCA) via dihaloelimination to ethene and vinyl chloride, respectively. In addition, halogen substitution at PCE, trichloroethene (TCE) and tribromoethene (TBE) was observed, but only at low rates. In contrast, recombinant PceA exclusively converted halogenated ethenes and showed no dihaloelimination activity. In silico structural analysis of both RDases revealed similar architectures of their active site cavities. Exchange of the highly conserved Tyr298 to Phe led to a complete loss of the PCE, TCE and TBE conversion by both RDases, strengthening the assumption that Tyr298 functions as proton donor in the course of halogen substitution. The exchange did not affect the ability of DcaA to convert 1,2-DCA and 1,1,2-TCA. This result makes the involvement of a proton transfer in the dihaloelimination reaction unlikely and allows for a clear differentiation between two mechanisms working in DcaA and PceA. The analysis of the role of the active site structure for RDase function was extended to the mutations W118F that had a negative effect on DcaA function and W432F or T294V that caused alterations in the substrate specificity of the enzyme. Enzymes Tetrachloroethene reductive dehalogenase (EC 1.21.99.5), DCA -RDase.