Triphenylphosphonium Chloride Research Articles

Ultrasound-assisted oxidative desulfurization of fuel using butyl triphenyl phosphonium chloride as a promising catalyst

The traditional hydrodesulfurization process has severe disadvantages, such as operating at a higher temperature and pressure and the inability to remove refractive sulfur compounds (S-compounds). To overcome these difficulties, the present study reports the synthesis and characterization of ionic liquid (IL), butyl triphenyl phosphonium chloride ([BTPP]Cl) and its application to the S-removal of model fuel (MF) using ultrasound-assisted oxidative desulfurization (UAODS). Ultrasound irradiation enhances the desulfurization efficiency by eliminating resistance to mass transfer between the organic and aqueous phases. The application of ultrasound generates more active free radicals which help in the conversion of S-compounds to their respective sulfones. MF contains dibenzothiophene (DBT) in n-octane (500 ppm), where 78.45% removal of DBT was achieved under optimized conditions of mass ratio of IL to MF:1/1, mole ratio of oxidant to sulfur:20/1, 50 °C, and 30 min under the application of sonication. Moreover, [BTPP]Cl could be regenerated and recycled for six consecutive cycles. The driving force behind the higher desulfurization performance using [BTPP]Cl was supposed to be the interactions between the IL and DBT. Various S-compounds such as thiophene (T), benzothiophene (BT), and 3-methyl thiophene (3-MT) were also studied for their UAODS reactivity. Thus, [BTPP]Cl proved to be a potential catalyst for application in the UAODS of a fuel, and the process can be employed for industrial application.

Cisplatin induces lung cell cilia disruption and lung damage via oxidative stress

BackgroundCisplatin (cis-diamminedichloroplatinum II) is widely used for the treatment of cancer, but its cellular toxicity, especially in the form of oxidative stress, limits its use in multiple organs including the lungs. As a cellular organelle, cilia play an important role in cellular function and can be damaged by oxidative stress. However, the effect of cisplatin-induced lung toxicity on cilia has not yet been defined. Herein, we investigated the association of cilia and oxidative stress with cisplatin-induced lung damage. MethodsMice were administered with cisplatin. Some mice were treated with 2-(2,2,6,6-Tetramethylpiperidin-1-oxyl-4-ylamino)-2-oxoethyl) triphenylphosphonium chloride (Mito-TEMPO, a mitochondria-specific antioxidant) before the administration of cisplatin. Disruption of cilia was evaluated by the detection of ciliary proteins and fragments in the bronchoalveolar lavage fluid (BALF). ResultsCisplatin caused the thickening of interalveolar septa, infiltration of immune cells into the interalveolar septa, and increased protein concentration and total cell number in the BALF. Cisplatin also increased ciliary fragments and proteins in the BALF. In the lungs, cisplatin increased the production of hydrogen peroxide, lipid peroxidation, and apoptosis, while decreasing manganese superoxide dismutase, isocitrate dehydrogenase 2, and catalase expression. Treatment with Mito-TEMPO prevented cisplatin-induced lung damage, ciliary fragmentation, oxidative stress, and apoptosis. ConclusionBy increasing oxidative stress in the lung, cisplatin induces lung cell damage, disruption of cilia, and release of disrupted cilia into the BALF. This suggests that cisplatin-induced lung damage can damage the cilia, manifesting as increased ciliary proteins in the BALF.

Simultaneous use of physical and chemical dispersants for electrical conductivity enhancement in polyamide 6/carbon nanotube/conductive carbon black hybrid nanocomposites

ABSTRACT Polyamide 6 (PA6)/carbon nanotube (CNT)/conductive carbon black (CCB) nanocomposites with the incorporation of physical and chemical dispersants were prepared via melt blending method to examine the synergistic enhancement of electrical conductivity. Investigation of modified CNT with octadecyl triphenyl phosphonium chloride (OTPC-CNT) as physical dispersant was performed by Fourier transform infrared, nuclear magnetic resonance, Raman spectroscopy, and thermogravimetric analysis. Morphological, electrical, rheological, and mechanical properties of PA6/CNT/CCB nanocomposites were examined by field emission scanning electron microscopy, transmission electron microscopy, digital insulation tester, oscillatory shear rheometer, tensile test, and impact test. The results showed that by the incorporation of physical (OTPC) and chemical (RPS 1005) dispersants to a compound containing 2.5 wt.% CNT and 5 wt.% CCB, electrical conductivity was improved 9 orders of magnitude (S cm−1) compared to those of samples without any dispersants and 6 orders of magnitude compared to those of samples containing 2.5 wt.% CNT and physical dispersants. These results illustrate that by simultaneous incorporation of two different dispersants, it is possible to form a 3D conductive network in such nanocomposites and thus achieve a synergistic enhancement of electrical conductivity. The novelty of this study lies in the simultaneous incorporation of physical and chemical dispersants that lead to desired electrical conductivity without sacrificing mechanical properties besides economical advantage of production. This result is due to the remarkable effect of physical dispersants in improving electrical conductivity along with the low cost of chemical dispersants.

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.

Magnesium Deficiency Causes a Reversible, Metabolic, Diastolic Cardiomyopathy.

BackgroundDietary Mg intake is associated with a decreased risk of developing heart failure, whereas low circulating Mg level is associated with increased cardiovascular mortality. We investigated whether Mg deficiency alone could cause cardiomyopathy.Methods and ResultsC57BL/6J mice were fed with a low Mg (low‐Mg, 15–30 mg/kg Mg) or a normal Mg (nl‐Mg, 600 mg/kg Mg) diet for 6 weeks. To test reversibility, half of the low‐Mg mice were fed then with nl‐Mg diet for another 6 weeks. Low‐Mg diet significantly decreased mouse serum Mg (0.38±0.03 versus 1.14±0.03 mmol/L for nl‐Mg; P<0.0001) with a reciprocal increase in serum Ca, K, and Na. Low‐Mg mice exhibited impaired cardiac relaxation (ratio between mitral peak early filling velocity E and longitudinal tissue velocity of the mitral anterior annulus e, 21.1±1.1 versus 15.4±0.4 for nl‐Mg; P=0.011). Cellular ATP was decreased significantly in low‐Mg hearts. The changes were accompanied by mitochondrial dysfunction with mitochondrial reactive oxygen species overproduction and membrane depolarization. cMyBPC (cardiac myosin‐binding protein C) was S‐glutathionylated in low‐Mg mouse hearts. All these changes were normalized with Mg repletion. In vivo (2‐(2,2,6,6‐tetramethylpiperidin‐1‐oxyl‐4‐ylamino)‐2‐oxoethyl)triphenylphosphonium chloride treatment during low‐Mg diet improved cardiac relaxation, increased ATP levels, and reduced S‐glutathionylated cMyBPC.ConclusionsMg deficiency caused a reversible diastolic cardiomyopathy associated with mitochondrial dysfunction and oxidative modification of cMyBPC. In deficiency states, Mg supplementation may represent a novel treatment for diastolic heart failure.

Unconventional reactivity of epichlorohydrin in the presence of triphenylphosphine: isolation of ((1,4-dioxane-2,5-diyl)-bis-(methylene))-bis-(triphenylphosphonium) chloride

The selective formation of the heterocyclic salt ((1,4-dioxane-2,5-diyl)-bis-(methylene))-bis-(triphenylphosphonium) chloride was observed when epichlorohydrin and triphenylphosphine were reacted in CH2Cl2 at room temperature. Slow evaporation from a mixture of ethanol and ethyl acetate allows to isolate monocrystals of the heterocyclic phosphonium salt. Mechanistic investigations point to the formation of the zwitterionic intermediate 1-chloro-3-(triphenylphosphonio)-propan-2-olate, which can dimerize and generate the 1,4-dioxane derivative. In the exclusive presence of a Bronsted acid as HCl, which usually facilitates epoxide ring opening, the exclusive formation of 1,3-dichloro-2-propanol was although observed. Also, when epichlorohydrin, PPh3, and a stoichiometric amount of HCl were mixed, (2-chloro-3-hydroxypropyl)-triphenylphosphonium chloride was formed and its isolation in pure form provides monocrystals subjectable to X-ray analysis.

Can MitoTEMPO protect rat sciatic nerve against ischemia-reperfusion injury?

Abdominal ischemia-reperfusion (I/R) is known to cause both structural and functional damage to sciatic nerve which is related to the oxidative stress. We investigated the protective effects of mitochondria-targeted antioxidant (2-(2,2,6,6-tetramethylpiperidin-1-oxyl-4-ylamino)-2-oxoethyl) triphenylphosphonium chloride (MitoTEMPO) on ischemia-reperfusion-induced nerve damage by using the conduction velocity distribution (CVD) calculations from in vitro compound nerve action potential (CNAP) recordings from rat sciatic nerve. Adult male Wistar albino rats were divided into three groups. The IR and IR + MT groups had aortic cross-clamping for 1h followed by 2h reperfusion, while SHAM group had the same procedure without cross-clamping. IR + MT group received 0.7mg/kg/day MitoTEMPO injection for 28days before I/R, while other groups received vehicle alone. Ischemia-reperfusion resulted in a significant decrease (p < .05) in maximum depolarizations (mV), areas (mV.ms), and maximum and minimum upstroke velocities (mV/ms) of CNAPs, while injection of MitoTEMPO showed a complete protective effect on these impairments. The histograms for CVD showed that I/R blocked the contribution of fast-conducting fibers (> 60m/s). MitoTEMPO prevented that blockage and caused a shift in the CVD. Functional nerve damage caused by I/R can be prevented by MitoTEMPO, which can enter mitochondria, the main source of reactive oxygen species (ROS).

Effect of Mitochondrial Antioxidant (Mito-TEMPO) on Burn-Induced Cardiac Dysfunction

Imbalance of oxidants/antioxidants results in heart failure, contributing to mortality after burn injury. Cardiac mitochondria are a prime source of reactive oxygen species (ROS), and a mitochondrial-specific antioxidant may improve burn-induced cardiomyopathy. We hypothesize that the mitochondrial-specific antioxidant, Triphenylphosphonium chloride (Mito-TEMPO), could protect cardiac function after burn. Male rats had a 60% total body surface area (TBSA) scald burn injury and were treated with/without Mito-TEMPO (7 mg/kg-1, intraperitoneal) and harvested at 24 hours post-burn. Echocardiography (ECHO) was used for measurement of heart function. Masson Trichrome and hematoxylin and eosin (H & E) staining were used for cardiac fibrosis and immune response. Qualitative polymerase chain reaction (qPCR) was used for mitochondrial DNA replication and gene expression. Burn-induced cardiac dysfunction, fibrosis, and mitochondrial damage were assessed by measurement of mitochondrial function, DNA replication, and DNA-encoded electron transport chain-related gene expression. Mito-TEMPO partially improved the abnormal parameters. Burn-induced cardiac dysfunction was associated with crosstalk between the NFE2L2-ARE pathway, PDE5A-PKG pathway, PARP1-POLG-mtDNA replication pathway, and mitochondrial SIRT signaling. Mito-TEMPO reversed burn-induced cardiac dysfunction by rescuing cardiac mitochondrial dysfunction. Mitochondria-targeted antioxidants may be an effective therapy for burn-induced cardiac dysfunction.

Age-dependent accumulation of dicarbonyls and advanced glycation endproducts (AGEs) associates with mitochondrial stress

Aging is a strong risk factor for brain dementia and cognitive decline. Age-related accumulation of metabolites such as advanced glycation end products (AGEs) could serve as danger signals to initiate and accelerate disease process and neurodegeneration. The underlying causes and consequences of cerebral AGEs accumulation remain largely unknown. Here, we comprehensively investigate age-related accumulation of AGEs and dicarbonyls, including methylglyoxal (MG), glyoxal (GO), and 3-deoxyglucosone (3-DG), and the effects of mitochondrial reactive oxygen species (ROS) on cerebral AGEs accumulation, mitochondrial function, and oxidative stress in the aging human and mouse brain. We demonstrate that AGEs, including arginine and lysine derived N(6)-carboxymethyl lysine (CML), Nε-(1-Carboxyethyl)-l-lysine (CEL), and methylglyoxal-derived hydroimidazolone-1 (MG-H1), were significantly elevated in the cerebral cortex and hippocampus with advanced age in mice. Accordingly, aging mouse and human brains revealed decrease in activities of mitochondrial respiratory chain complexes I & IV and ATP levels, and increased ROS. Notably, administration of mitoTEMPO (2-(2,2,6,6-Tetramethylpiperidin-1-oxyl-4-ylamino)-2-oxoethyl)triphenylphosphonium chloride (mTEMPO), a scavenger of mitochondrial ROS, not only suppressed ROS production but also reduced aged-induced accumulation of AGEs and dicarbonyls. mTEMPO treatment improved mitochondrial respiratory function and restored ATP levels. Our findings provide evidence linking age-related accumulation of toxic metabolites (AGEs) to mitochondrial oxidative stress. This highlights a novel mechanism by which AGEs-dependent signaling promotes carbonyl stress and sustained mitochondrial dysfunction. Eliminating formation and accumulation of AGEs may represent a new therapeutic avenue for combating cognitive decline and mitochondrial degeneration relevant to aging and neurodegenerative diseases including Alzheimer's disease.

Synthesis and Antimicrobial Activity of (3-Formyl-4-hydroxybenzyl)triphenylphosphonium Chloride Acylhydrazones

In this study, four novel quaternary phosphonium acylhydrazones, derivatives of (3-formyl-4-hydroxybenzyl)triphenylphosphonium chloride, have been synthesized and their structures elucidated from IR and NMR spectra, and elemental analysis. All synthesized compounds have been tested for their antimicrobial activity, and acylhydrazones have demonstrated selective activity against Gram-positive bacteria strains.

Interaction of 1-acylamino-2,2-dichloroethenyl(triphenyl)phosphonium chlorides with alkanolamines

It is shown that the interaction of 1-acylamino-2,2-dichloroethenyl(triphenyl)-phosphonium chlorides with alkanolamines having a primary amino group results in the formation of 4-oxazolylphosphonium salts containing hydroxyalkylamine substituents at position 5 of the oxazole cycle. Under similar conditions the reaction of N-substituted alkanolamines with 1-acylamino-2,2-dichloroethenyl-(triphenyl)phosphonium chlorides leads to the formation of 1,3-oxazolidin-2-ylidene derivatives, in which the triphenylphosphonium group is located in the side chain. The structure of the new synthesized compounds has been reliably proven by elemental analysis, IR, 1Н, 13С, 31Р NMR spectroscopy, mass spectrometry and single crystal X-ray diffraction.

Exposure of Triclosan in Porcine Oocyte Leads to Superoxide Production and Mitochondrial-Mediated Apoptosis During In Vitro Maturation.

While triclosan (TCS) exerts detrimental effects on female reproduction, the effect of TCS-derived toxins on porcine oocytes during in vitro maturation (IVM) is unclear. This study investigated the effects of TCS on mitochondrion-derived reactive oxygen species (ROS) production and apoptosis pathways during porcine oocyte maturation. Porcine oocytes were treated with TCS (1, 10, and 100 μM) and triphenylphosphonium chloride (Mito-TEMPO; 0.1 μM), and matured cumulus oocyte complexes (COCs) were stained with orcein, dichlorofluorescein diacetate (DCF-DA), and Mito-SOX. Proteins and mRNA levels of factors related to cumulus expansion and mitochondrion-mediated apoptosis and antioxidant enzymes were analyzed by western blotting and reverse-transcription polymerase chain reaction (RT-PCR), respectively. Meiotic maturation and cumulus cell expansion significantly decreased for COCs after TCS treatment along with an increase in mitochondrial superoxide levels at 44 h of IVM. Further, mitochondrion-related antioxidant enzymes and apoptosis markers were significantly elevated in porcine COCs following TCS-mediated oxidative damage. The protective effect of Mito-TEMPO as a specific superoxide scavenger from TCS toxin improved the maturation capacity of porcine COCs. Mito-TEMPO downregulated the mitochondrial apoptosis of TCS-exposed porcine COCs by reducing superoxide level. In conclusion, our data demonstrate that TCS mediates toxicity during porcine oocyte maturation through superoxide production and mitochondrion-mediated apoptosis.

SYNTHESIS AND STRUCTURE OF (METHOXYMETHYL)TRIPHENYLPHOSPHONIIUM TRICHLORO(DIMETHYLSULFOXIDO)PLATINATE

(Methoxymethyl)triphenylphosphonium trichloro(dimethylsulfoxido)platinate [Ph3PCH2OCH3][PtCl3(dmso-S)] was synthesized by the reaction of hexachloroplatinic acid with (methoxymethyl)triphenylphosphonium chloride in dimethyl sulfoxide. During the reaction, Pt (IV) was reduced to Pt (II). The reactions are accompanied by the ligand exchange in anions with substitution of the S-coordinated dimethyl sulfoxide molecule for one of chlorine atoms. Slow evaporation of the solvent led to the formation of large orange crystals. The product structure was determined by XRDA. The structures were interpreted by the direct method. Positions and temperature parameters of non-hydrogen atoms were refined in isotropic and then in anisotropic approximations by the full-matrix LSM. The X-ray diffraction pattern of crystal I was carried out on a Bruker D8 QUEST diffractometer. According to the data of X-ray analysis the unit cell crystallographic parameters of compound I are [crystal system monoclinic, space group P21/c, M 686.90, a 14.48(2), b 14.48(2), c 19.99(3) Å]. The tetrahedral configuration of the (methoxymethyl)triphenylphosphonium cation approaches the ideal values (CPC angles are 108.5(2)°-110.3(2)°, bond lengths Р-С are slightly differ from each other). Platinum atoms in anions have square coordination (trans-arranged angles ClPtCl are 177.65(5)°, SPtCl are 178.88(6)°, cis-angles approach 90°). The bond lengths Pt–Cl are equal to 2.290(3)–2.314(3) Å, Pt–S are equal to 2.205(3) Å. The platinum atoms are coordinated by three chlorine atoms and dimethyl sulfoxide molecule in the anion. Dimethyl sulfoxide molecule is coordinated to the platinum atoms by sulfur atoms. The geometry of the coordinated dimethyl sulfoxide ligand [OSC and СSC angles, S−O bond] differs from the geometry of a free dimethyl sulfoxide molecule.

Trialkyl Triphenyl Phosphonium Dicyanodibromoaurates [Ph3PAlk][Au(CN)2Br2], Alk = CH2C6H4(OH)-2, CH2C6H11-cyclo, CH2Ph, CH2C6H4CN-4

The crystalline yellow complexes [Ph3PAlk][Au(CN)2Br2], where Alk = CH2C6H4(OH)-2 (I), CH2C6H11-cyclo (II ⋅ 1/2PhH), CH2Ph (III), CH2C6H4CN-4 (IV), have been synthesized from potassium dicyanodibromoaurate and alkyl triphenyl phosphonium chlorides in water and structurally characterized by X-ray diffraction. Crystals of complexes I–IV contain tetrahedral alkyl triphenyl phosphonium cations (CPC, 104.8(2)°–114.1(2)°; P–C, 1.782(6)–1.825(5) A). In square [Au(CN)2Br2]– anions, the CAuC and BrAuBr trans-angles are 178.8(2)°–180.0(5)° and 178.38(3)°–180.00(3)°, and the Au–C and Au–Br bonds are 2.001(7)–2.205(9) A and 2.4086(14)–2.4276(18) A, respectively. The crystal structures are formed by weak hydrogen bonds N⋅⋅⋅Н–С and strong bonds N⋅⋅⋅Н–О in complex I and contacts Br⋅⋅⋅Н–С in dicyano-dibromides I, III, and IV.

PKCβ and reactive oxygen species mediate enhanced pulmonary vasoconstrictor reactivity following chronic hypoxia in neonatal rats.

Reactive oxygen species (ROS), mitochondrial dysfunction, and excessive vasoconstriction are important contributors to chronic hypoxia (CH)-induced neonatal pulmonary hypertension. On the basis of evidence that PKCβ and mitochondrial oxidative stress are involved in several cardiovascular and metabolic disorders, we hypothesized that PKCβ and mitochondrial ROS (mitoROS) signaling contribute to enhanced pulmonary vasoconstriction in neonatal rats exposed to CH. To test this hypothesis, we examined effects of the PKCβ inhibitor LY-333,531, the ROS scavenger 1-oxyl-2,2,6,6-tetramethyl-4-hydroxypiperidine (TEMPOL), and the mitochondrial antioxidants mitoquinone mesylate (MitoQ) and (2-(2,2,6,6-tetramethylpiperidin-1-oxyl-4-ylamino)-2-oxoethyl)triphenylphosphonium chloride (MitoTEMPO) on vasoconstrictor responses in saline-perfused lungs (in situ) or pressurized pulmonary arteries from 2-wk-old control and CH (12-day exposure, 0.5 atm) rats. Lungs from CH rats exhibited greater basal tone and vasoconstrictor sensitivity to 9,11-dideoxy-9α,11α-methanoepoxy prostaglandin F2α (U-46619). LY-333,531 and TEMPOL attenuated these effects of CH, while having no effect in lungs from control animals. Basal tone was similarly elevated in isolated pulmonary arteries from neonatal CH rats compared with control rats, which was inhibited by both LY-333,531 and mitochondria-targeted antioxidants. Additional experiments assessing mitoROS generation with the mitochondria-targeted ROS indicator MitoSOX revealed that a PKCβ-mitochondrial oxidant signaling pathway can be pharmacologically stimulated by the PKC activator phorbol 12-myristate 13-acetate in primary cultures of pulmonary artery smooth muscle cells (PASMCs) from control neonates. Finally, we found that neonatal CH increased mitochondrially localized PKCβ in pulmonary arteries as assessed by Western blotting of subcellular fractions. We conclude that PKCβ activation leads to mitoROS production in PASMCs from neonatal rats. Furthermore, this signaling axis may account for enhanced pulmonary vasoconstrictor sensitivity following CH exposure.NEW & NOTEWORTHY This research demonstrates a novel contribution of PKCβ and mitochondrial reactive oxygen species signaling to increased pulmonary vasoconstrictor reactivity in chronically hypoxic neonates. The results provide a potential mechanism by which chronic hypoxia increases both basal and agonist-induced pulmonary arterial smooth muscle tone, which may contribute to neonatal pulmonary hypertension.

Interfacial adsorption behavior of quaternary phosphonium based ionic liquids on metal-electrolyte interface: Electrochemical, surface characterization and computational approaches

In present study two quaternary phosphonium salts namely (1-NapthylMethyl)-triphenylphosphonium Chloride (1-NpMe-TPC) and (4-Methoxybenzyl)-triphenylphosphonium Bromide (4-MeOBz-TPB) are reported as inhibitors for mild steel (MS) corrosion in 0.5MH2SO4 using various electrochemical, theoretical and surface morphological techniques. Inhibitors 1-NpMe-TPC and 4-MeOBz-TPB were prepared by diluting the solution of concentration 10−2 to 10−5M and results are showed maximum efficiencies of 99.72% and 97.76%, respectively at 10−3M concentration (298K). Polarization measurements revealed that both 1-NpMe-TPC and 4-MeOBz-TPB acted as mixed corrosion inhibitors. EIS study revealed that 1-NpMe-TPC and 4-MeOBz-TPB adsorbed at the mild steel/0.5M H2SO4 interfaces and enhanced the magnitude of charge transfer resistances. Adsorption of the 1-NpMe-TPC and 4-MeOBz-TPB at the metallic surface was further supported by SEM and AFM studies. Several thermodynamic parameters (ΔGads0, ΔHads0 and ΔSads0 ), Semi-empirical AM1 and MD parameters were derived in order to describe the adsorption behavior of 1-NpMe-TPC and 4-MeOBz-TPB on metallic surface. The reasonable consistence was found between experimental and theoretical results.

Synthesis of Phosphonium Enamines: Physicochemical Properties of Dimethylsulfoxide Solutions

Dimethylsulfoxide solutions of the products of the condensation of formylmethyl(triphenyl)phosphonium chloride with amines of different nature are studied via densitometry, elemental analysis, and IR, 1H NMR, and UV–Vis spectroscopy. Compounds containing carboxyl groups are found to be capable of forming micelles. It is concluded that the substantial drop in the molar volume as the temperature rises for a compound containing butyl radicals suggests the solution contains only one isomer at elevated temperatures.

MOMTPPC improved Cu-based heterogeneous catalyst with high efficiency for acetylene hydrochlorination

The development of environmentally friendly nonmercuric catalysts for acetylene hydrochlorination reaction mainly focuses on precious metal like Au, Pd and Ru. Non-precious metal based catalyst had much lower activity and stability in this reaction, limiting its practical application. In this work, a novel ionic liquid improved Cu-based heterogeneous catalyst has been designed and successfully synthesized, and it showed the highest catalytic activity and stability among the reported non-precious metal based catalyst used in the reaction of acetylene hydrochlorination. Among many ionic liquids, the (Methoxymethyl) triphenylphosphonium chloride (MOMTPPC) ionic liquid improved Cu-based heterogeneous catalysts has the highest catalytic performance. The optimal 15%Cu@15%MOMTPPC/SAC achieved the conversion of C2H2 of 92.2% under the reaction condition of T=180℃, GHSV (C2H2) of 180 h−1 and VHCl/VC2H2 = 1.2. And under the industrial GHSV (C2H2) of 36 h−1, C2H2 conversion maintains above 98.7% within 360 h. A series of experimental characterizations combined with theoretical calculations indicated that the addition of MOMTPPC ionic liquid can inhibit carbon deposition, prevent the aggregation of Cu species, enhance the dispersion of Cu species and the adsorption of HCl reactant. The stabilization effect of MOMTPPC to Cu is mainly through the hydrogen bond, steric hindrance of MOMTPPC cation and electrostatic effect. The development of Cu@MOMTPPC/SAC catalyst with high efficiency shed light on the potential of replacing the toxic mercuric catalyst with non-precious Cu-based catalyst in the polyvinyl chloride (PVC) industry.

Phosphonium Polyelectrolyte Complexes for the Encapsulation and Slow Release of Ionic Cargo.

Polyelectrolyte complexation, the combination of anionically and cationically charged polymers through ionic interactions, can be used to form hydrogel networks. These networks can be used to encapsulate and release cargo, but the release of cargo is typically rapid, occurring over a period of hours to a few days and they often exhibit weak, fluid-like mechanical properties. Here we report the preparation and study of polyelectrolyte complexes (PECs) from sodium hyaluronate (HA) and poly[tris(hydroxypropyl)(4-vinylbenzyl)phosphonium chloride], poly[triphenyl(4-vinylbenzyl)phosphonium chloride], poly[tri(n-butyl)(4-vinylbenzyl)phosphonium chloride], or poly[triethyl(4-vinylbenzyl)phosphonium chloride]. The networks were compacted by ultracentrifugation, then their composition, swelling, rheological, and self-healing properties were studied. Their properties depended on the structure of the phosphonium polymer and the salt concentration, but in general, they exhibited predominantly gel-like behavior with relaxation times greater than 40 s and self-healing over 2-18 h. Anionic molecules, including fluorescein, diclofenac, and adenosine-5'-triphosphate, were encapsulated into the PECs with high loading capacities of up to 16 wt %. Fluorescein and diclofenac were slowly released over 60 days, which was attributed to a combination of hydrophobic and ionic interactions with the dense PEC network. The cytotoxicities of the polymers and their corresponding networks with HA to C2C12 mouse myoblast cells was investigated and found to depend on the structure of the polymer and the properties of the network. Overall, this work demonstrates the utility of polyphosphonium-HA networks for the loading and slow release of ionic drugs and that their physical and biological properties can be readily tuned according to the structure of the phosphonium polymer.

Synthesis and characterization of a new zwitterionic palladium complex as an environmentally friendly catalyst for the Heck-Mizoroki coupling reaction in GVL

A new zwitterionic Palladium (II) complex has been synthesized by the one-pot mixing of Pd(OAc)2, 2-aminophenol and (3-formyl-4-hydroxy-5-methylbenzyl) triphenylphosphonium chloride, in refluxing ethanol. The metal complex formed was characterized by 1H NMR, 13C NMR, 31P NMR and X-ray crystallographic technique and its efficiency tested as a homogeneous pre-catalyst in Heck-Mizoroki cross coupling reaction using γ-Valerolactone (GVL) as a biomass-derived green medium. All the products were obtained in good to excellent yields.