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PubMed2005

[Fate of matrix-bound phosphine during acidification with anaerobic bacteria].

Matrix-bound phosphine of anaerobic granular sludge was studied during methanogenic and acidogenic stage of anaerobic reactors. Results showed that at methanogenic stage, the concentration of matrix-bound phosphine of anaerobic sludge decreased as the height of reactor increased. But during acidogenic stage, matrix-bound phosphine disappeared when pH of the solution declined to 4-5. Further anaerobic static experiments showed that increased acidification and lower pH value promoted the decrease of matrix-bound phosphine. After cultivation with 2 000 mg x L(-1) glucose synthetic wastewater for two days, the matrix-bound phosphine fell from 1.76 ng x kg(-1) to 0.09 ng x kg(-1); At the same time, the highest disappearing rate of phosphine was reached 0.84 ng x (kg x d)(-1). While the glucose synthetic wastewater was 400 mg x L(-1), the disappearing rate of phosphine was only 0.27 ng x (kg x d)(-1). With further cultivation under acidogenic stage, the phosphine decreasing rate slowed down.

Acids↗
PubMed1996

Glial cell line-derived neurotrophic factor: selective reduction of the intermolecular disulfide linkage and characterization of its disulfide structure.

Glial cell line-derived neurotrophic factor is a protein known to enhance the survival of dopaminergic neurons against several neurotoxins. It has been shown to have therapeutic potential in the treatment of Parkinson's disease and other neurodegenerative diseases. We have determined the inter- and intramolecular disulfide linkages of the dimeric molecule by a combination of direct peptide analysis and peptide analysis after either partial reduction or partial oxidation of the protein. Under an acidic condition, the interchain disulfide bond was selectively cleaved with tris(2-carboxyethyl)phosphine, revealing that Cys101 was involved in the intermolecular disulfide linkage. Three other disulfides, Cys68-Cys131, Cys72-Cys133, and Cys41-Cys102, were identified as intramolecular linkages. The determined disulfide structure is highly homologous to that of transforming growth factor beta 2. Since one intramolecular disulfide points through a ring consisting of eight amino acid residues based on the similarity with transforming growth factor beta 2, the disulfide-linked peptides were not purified by conventional methods. Only the peptides from an N-terminal region (residues -1 to 37) were liberated by proteolytic treatment with trypsin or endoproteinase Lys-C, resulting in a stable cystine-knot protein.

Amino Acid Sequence↗
PubMed2006

Gas-phase synthesis and reactivity of binuclear gold hydride cations, (R3PAu)2H+ (R = Me and Ph).

Electrospray ionization of a mixture of the two gold phosphine chlorides, R3PAuCl (R = Ph and Me), silver nitrate and the amino acid N,N-dimethylglycine (DMG) yields a range of gold containing cluster ions including: (R3P)Au(PR'3)+; (R3PAu)(R'3PAu)Cl+ and (R3PAu)(R'3PAu)(DMG-H)+ (where R = R' = Ph; R = R' = Me; R = Me and R' = Ph). Collision induced dissociation (CID) of the (R3PAu)(R'3PAu)(DMG-H)+ precursor ions yielded the hitherto unknown gold hydride dimers (R3PAu)(R'3PAu)H+. The gas-phase chemistry of these dimers was studied using ion-molecule reactions, collision induced dissociation, electronic excitation dissociation (EED) and DFT calculations on the (H3PAu)2H+ model system. A novel phosphine ligand migration was found to occur prior to fragmentation under CID conditions and this was supported by DFT calculations, which revealed a transition state with a bridging phosphine ligand.

Cations↗
PubMed2005

Efficient solid-phase synthesis of peptide-based phosphine ligands: towards combinatorial libraries of selective transition metal catalysts.

A new methodology for the solid-phase synthesis of peptide-based phosphine ligands has been developed. Solid supported peptide scaffolds possessing either primary or secondary amines were synthesised using commercially available Fmoc-protected amino acids and readily available Fmoc-protected amino aldehydes for reductive alkylation, in standard solid-phase peptide synthesis (SPPS). Phosphine moieties were introduced by phosphinomethylation of the free amines as the final solid-phase synthetic step, immediately prior to complexation with palladium(II), thus avoiding tedious protection/deprotection of the phosphine moieties during the synthesis of the ligands. The extensive use of commercial building blocks and standard SPPS makes this methodology well suited for the generation of solid-phase combinatorial libraries of novel ligands. Furthermore, it is possible to generate several different phosphine ligand libraries for every peptide scaffold library synthesised, by functionalising the scaffold libraries with different phosphine moieties. The synthesised ligands were characterised on solid support by conventional (31)P NMR spectroscopy and, cleaved from the support, as their phosphine oxides by HPLC, (1)H NMR, (31)P NMR and high resolution ESMS. Palladium(II) allyl complexes were generated from the resin bound ligands and to demonstrate their catalytic properties, palladium catalysed asymmetric allylic substitution reactions were performed. Good yields and moderate enantioselectivity was obtained for the selected combination of catalysts and substrate, but most importantly the concept of this new methodology was proven. Screening of ligand libraries should afford more selective catalysts.

Catalysis↗
PubMed2000

Asymmetric conjugate 1,4-addition of arylboronic acids to alpha, beta-unsaturated esters catalyzed by Rhodium(I)/(S)-binap

Arylboronic acids underwent the conjugate 1,4-addition to alpha, beta-unsaturated esters to give beta-aryl esters in high yields in the presence of a rhodium(I) catalyst. The addition of arylboronic acids to isopropyl crotonate resulted in high yields and high enantioselectivity exceeding 90% ee in the presence of 3 mol % of Rh(acac)(C(2)H(4))(2) and (S)-binap at 100 degrees C. The rhodium/(S)-binap complex provided (R)-3-phenylbutanoate in the addition of phenylboronic acid to benzyl crotonate. The effects on the enantioselectivity of chiral phosphine ligands, rhodium precursors, and substituents on alpha,beta-unsaturated esters are discussed, as well as the mechanistic aspect of the catalytic cycle.

Journal Article↗
PubMed2005

Synthesis, characterization and reactivity of tetranuclear ruthenium hydrido clusters containing chiral phosphine ligands.

The chiral clusters [H(4)Ru(4)(CO)(12-n)(L)(n)] (n = 1, 2; L = NMDPP), 1,1-[H(4)Ru(4)(CO)(10)(L-L)] (L-L = DUPHOS, DIPAMP), 1,2-[H(4)Ru(4)(CO)(10)(DIOP)] and [{H(4)Ru(4)(CO)(10)(DIOP)}(2)] have been synthesized by derivatizing the parent carbonyl cluster [H(4)Ru(4)(CO)(12)] with the appropriate mono- or didentate chiral phosphine ligand. The phosphine-substituted clusters were found to be able to catalyze the (asymmetric) hydrogenation of tiglic acid albeit with relatively low selectivity (enantiomeric excesses varying from 0 to 23%). It was found that the stability of the chiral ruthenium hydride clusters and the product distribution obtained in the catalytic reactions are dependent on the nature of the chiral phosphine. The crystal structures of [H(4)Ru(4)(CO)(12-n)(L)(n)] (n = 1, 2; L = NMDPP), 1,1-[H(4)Ru(4)(CO)(10)(L-L)] (L-L = DUPHOS, O-DUPHOS (partially oxygenated ligand), DIPAMP), 1,2-[H(4)Ru(4)(CO)(10)(DIOP)] and [{H(4)Ru(4)(CO)(10)(DIOP)}(2)] are presented.

Journal Article↗
PubMed2004

A differential assay for the reduced and oxidized states of metallothionein and thionein.

In the cellular environment, the sulfur ligands in zinc/thiolate coordination sites of proteins can be oxidized with concomitant mobilization of zinc. The characterization of such "redox zinc switches" requires the determination of three species, i.e., the zinc-containing complex and the zinc-free complex with the thiolate ligands either reduced or oxidized. Differential chemical modification of thiol groups in the presence and absence of either reducing or chelating agents allows the analytical speciation of such systems as demonstrated here for the characterization of the redox and metal-binding states of mammalian metallothionein. Thiol derivatization with 6-iodoacetamidofluorescein in the presence and absence of the reducing agent tris(2-carboxyethyl)phosphine, high-performance liquid chromatographic separation, and photometric detection are employed to determine the reduced and oxidized protein. Because the holoprotein reacts only in the presence of a chelating agent such as ethylenediaminetetraacetate (EDTA) its amount can be determined as the difference between measurements in the presence and the absence of EDTA. This method is applied to the study of the chemical and enzymatic oxidation of metallothionein/thionein. It should also greatly facilitate the characterization of the redox and metal-binding properties of zinc/thiolate coordination environments of other proteins such as zinc finger proteins.

Animals↗
PubMed2005

Taurine chloramine, an oxidant derived from neutrophils, induces apoptosis in human B lymphoma cells through mitochondrial damage.

Taurine chloramine (TN-Cl) is one of the most abundant compounds generated by activated neutrophils. In contrast to HOCl, which causes necrosis, TN-Cl is a potent inducer of apoptosis in tumor cells. Here we show that the apoptosis induced by TN-Cl in human B lymphoma cells is dependent upon oxidant-mediated mitochondrial damage, a decrease in mitochondrial membrane potential, and caspase-9 activation. Further, we show that TN-Cl is taken up into the cells and is concentrated in the mitochondria, where it induces opening of the permeability transition pore and mitochondrial swelling. Identical activity is seen upon treatment of isolated mitochondria with TN-Cl and is blocked by the permeability transition pore inhibitors bongkrekic acid and cyclosporin A, as well as by the sulfhydryl-reducing agent tris(2-carboxyethyl)-phosphine. The data suggest that TN-Cl causes apoptosis through direct damage to the mitochondria.

Anti-Bacterial Agents↗
PubMed2003

Effects of phthalic anhydride modification on horseradish peroxidase stability and activity.

Phthalic anhydride (PA) modification stabilizes horseradish peroxidase (HRP) by reversal of the positive charge on two of HRP's six lysine residues. Native and PA-HRP had half-inactivation temperatures of 51 and 65 degrees C and half-lives at 65 degrees C of 4 and 17 min, respectively. PA-HRP was more resistant to dimethylformamide at room temperature and tetrahydrofuran at 60 degrees C and to unfolding by heat, guanidine chloride, EDTA, and the reducing agent tris(2-carboxyethyl)phosphine hydrochloride. Binding of the hydrophobic probe Nile Red to the native enzyme and to PA-HRP was similar. The kinetics of both HRPs with the substrates ABTS, ferrocyanide, ferulic acid, and indole-3-propionic acid were measured, as was binding of the inhibitor benzhydroxamic acid. Small improvements in the catalytic properties were detected.

Binding Sites↗
PubMed1996

Enhanced NMDAR-dependent epileptiform activity is controlled by oxidizing agents in a chronic model of temporal lobe epilepsy.

1. Graded N-methyl-D-aspartate receptor (NMDAR)-dependent epileptiform discharges were recorded from ex vivo hippocampal slices obtained from rats injected a week earlier with an intracerebroventricular dose of kainic acid. Intracellular recordings from pyramidal cells of the CA1 area showed that glutamate NMDAR actively participated in synaptic transmission, even at resting membrane potential. When NMDAR were pharmacologically isolated, graded burst discharges could still be evoked. 2. The oxidizing reagent 5,5'-dithiobis(2-nitrobenzoic acid) (DTNB, 200 microM, 15 min) suppressed the late part of the epileptiform burst that did not recover after wash but could be reinstated by the reducing agent tris (2-carboxyethyl) phosphine (TCEP, 200 microM, 15 min) and again abolished with the NMDA antagonist D-2-amino-5-phosphonovaleric acid (D-APV). 3. Pharmacologically isolated NMDAR-mediated responses were decreased by DTNB (56 +/- 10%, mean +/- SD, n = 6), an effect reversed by TCEP. 4. When only the fast glutamateric synaptic component was blocked, NMDA-dependent excitatory postsynaptic potentials (EPSPs) could be evoked despite the presence of underlying fast and slow inhibitory postsynaptic potentials (IPSPs). DTNB decreased EPSPs to 48 +/- 12% (n = 5) of control. 5. Since a decrease of the NMDAR-mediated response by +/- 50% is sufficient to suppress the late part of the burst, we suggest that epileptiform activity can be controlled by manipulation of the redox sites of NMDAR. Our observations raise the possibility of developing new anticonvulsant drugs that would spare alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-R (AMPAR)-mediated synaptic responses and decrease NMDAR-mediated synaptic transmission without blocking it completely.

Animals↗
PubMed1983

Potential occupational health hazards in the microelectronics industry.

The microelectronics industry is a major user of a wide variety of chemicals and other toxic materials. In the recent past semiconductor manufacturers have located in many countries and brought a new set of challenging clinical problems to occupational physicians. California, an area with a significant history in the statistical study of health and safety in the microelectronics industry, presents some evidence of potential health hazards in the semiconductor manufacturing process. The Semiconductor Industry Study done in California in 1981 explains the application of many toxic materials in the semiconductor manufacturing process, including a variety of solvents, acids, and metals such as arsenic. The Study documents the extensive use of dopant gases, primarily arsine, phosphine and diborane. Further study is necessary to assure the health and safety of microelectronics workers, particularly in the application of dopant gases.

Acids↗
PubMed1993

Radiometric assay of red cell and plasma cholinesterase in pesticide appliers from Minnesota.

In this study we demonstrate the uses of radiometric assay to detect anticholinesterases in a human population (N = 80) exposed to a broad spectrum of pesticides. The assay is nondilutional. Therefore, anticholinesterase (AChE) agents with low binding affinity can be detected. Our initial results show statistically significant exposure-related decreases in either red cell (AChE) or plasma cholinesterase activity ((butyrl)cholinesterase; BuChE) occurred not only among pesticide appliers who use organophosphates, but also among appliers of the fumigant phosphine. These data extend earlier observations made in laboratory animals exposed to this fumigant. Significant exposure-related decreases in AChE activity were seen in herbicide appliers and appear to be associated with exposure to the herbicide 2-methoxy-3,6-dichlorobenzoic acid. There was no evidence of exposure-related decreases in BuChE activity in herbicide appliers. Our in vivo data, coupled with preliminary in vitro studies of phosphine (50% AChE inhibition, 10 ppm) and 2-methoxy-3,6-chlorobenzoic acid (50% AChE and BuChE inhibition, 70 ppm), suggest that the radiometric assay may be used to detect a broader spectrum of biologically active anticholinesterase agents.

Acetylcholinesterase↗
PubMed2000

Impurity annihilation: chromatography-free parallel Mitsunobu reactions.

Mitsunobu reaction of an alcohol ROH with a carboxylic acid, phthalimide, or N-hydroxyphthalimide (NuH) using DNAD (4) and (diphenylphosphino)polystyrene (11) gave the products RNu. Ring-opening metathetic polymerization of the side product DNADH(2) (3) using Cl(2)(Cy(3)P)(2)Ru=CHPh (13) and filtration, to remove poly(DNADH(2)), (diphenylphosphino)polystyrene 11, its oxide, and its adduct with excess DNAD, gave RNu (43-100%, 86-96% purity) without recourse to chromatography.

Chromatography↗
PubMed2005

Mercury compounds disrupt neuronal glutamate transport in cultured mouse cerebellar granule cells.

Cerebellar granule cells are targeted selectively by mercury compounds in vivo. Despite the affinity of mercury for thiol groups present in all cells, the molecular determinant(s) of selective cerebellar degeneration remain to be elucidated fully. We studied the effect of mercury compounds on neuronal glutamate transport in primary cultures of mouse cerebellar granule cells. Immunoblots probed with an antibody against the excitatory amino acid transporter (EAAT) neuronal glutamate transporter, EAAT3, revealed the presence of a specific band in control and mercury-treated cultures. Micromolar concentrations of both methylmercury and mercuric chloride increased the release of endogenous glutamate, inhibited glutamate uptake, reduced mitochondrial activity, and decreased ATP levels. All these effects were completely prevented by the nonpermeant reducing agent Tris-(2-carboxyethyl)phosphine (TCEP). Reduction of mitochondrial activity by mercuric chloride, but not by methylmercury, was inhibited significantly by 4,4'-diisothiocyanato-stilbene-2,2'-disulfonic acid (DIDS) and by reduced extracellular Cl- ion concentration. In addition, DIDS and low extracellular Cl- completely inhibited the release of glutamate induced by mercuric chloride, and produced a partial although significant reduction of that induced by methylmercury. We suggest that a direct inhibition of glutamate uptake triggers an imbalance in cell homeostasis, leading to neuronal failure and Cl(-)-regulated cellular glutamate efflux. Our results demonstrate that neuronal glutamate transport is a novel target to be taken into account when assessing mercury-induced neurotoxicity.

Adenosine Triphosphate↗