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PubMed1981

Determination of some pyridinium aldoxime compounds by means of ion-pair reversed-phase high-performance liquid chromatography: application in biological material.

Two reversed-phase high-performance liquid chromatographic systems are presented for the separation and assay of the pyridinium aldoximes benzyl-P2A, HI-6 and obidoxime in aqueous solutions and biological samples. The systems involve a 5-micrometer C18 silica gel stationary phase. The eluent consists of methanol, acetic acid buffer (pH 4.80), a counter ion (per-chlorate or n-octanesulphonate) and a surfactant. The compounds were detected spectrophotometrically at 304 nm. In the concentration range used, linear plots of concentration versus extinction were obtained, both in blood and in water. Detection limits plots of concentration versus extinction were obtained, both in blood and in water. Detection limits, even in blood are satisfactory (0.5-1 microM). Evidence of presented that, at least for HI-6, the addition of counter ions to the system does not lead to the formation of ion pairs to be retained by partition, but rather to a mechanism based on adsorption chromatography.

2,2'-Dipyridyl↗
PubMed1999

Uptake of vitamin A in macrophages from physiologic transport proteins: role of retinol-binding protein and chylomicron remnants.

Vitamin A plays an important role in reducing infectious disease morbidity and mortality by enhancing immunity, an effect that is partly mediated by macrophages. Thus, knowing how these cells take up vitamin A is important. The results in the present study demonstrate that J774 macrophages efficiently take up chylomicron remnant retinyl esters and retinol-binding protein (retinol-RBP) bound retinol by specific and saturable mechanisms. The binding of (125)I-RBP to plasma membrane vesicles demonstrated that the macrophage receptor had a similar binding affinity, as was discovered previously for other cells. The B(max) for the macrophages was smaller than the values reported for placenta, bone marrow, and kidney, but larger than that reported for liver. The J774 cells also bound and took up [(3)H]retinol-RBP. Approximately 50 to 60% of the uptake may compete with excess unlabeled retinol-RBP and approximately 30 to 40% with excess transtyrethin. Following the uptake of [(3)H]retinol-RBP, an extensive esterification occurred: After 5 hours of incubation, 77.8 +/- 3.9% (SD; n = 3) of the cellular radioactivity was recovered as retinyl esters. The J774 cells also demonstrated saturable binding of chylomicron remnant [(3)H]retinyl esters, and a continuous uptake at 37 degrees C followed by an extensive hydrolysis of the retinyl esters. Binding could be inhibited by approximately 50% by excess unlabeled low density lipoprotein (LDL). In addition, lipoprotein lipase increased the binding of chylomicron remnant [(3)H]retinyl esters by approximately 30% and the uptake of chylomicron remnant [(3)H]retinyl ester by more than 300%. Furthermore, because sodium chlorate reduced binding with 40% and uptake with 55%, the results suggest that proteoglycans are involved in the uptake. Thus, the results suggest that both LDL receptor and LDL-related protein are involved in the uptake of chylomicron remnant [(3)H]retinyl ester in macrophages.

Journal Article↗
PubMed2000

Clinical application of therapeutic erythrocytapheresis (TEA).

Therapeutic erythrocytapheresis (TEA) has been used in different diseases such as polycythemia vera (PV), secondary erythrocytosis or hemochromatosis as a process of the less cumbersome but more expensive phlebotomy. TEA is preferred in emergency conditions such as thrombocytosis or in conditions such as porphyria cutanea tarda (PCT) or erythropoietic porphyria when plasma exchange (PEX) is often combined with TEA to reduce extracellular levels of uroporphyrin which contribute to plasma hyperviscosity. TEA is often combined with drug therapy that varies from etoposide in PV to EPO and desferoxamine which are used to mobilize and reduce iron stores in hemochromatosis. Benefits from this combination may be more long lasting than expected. Nonetheless for TEA, there is no standard protocol and, clinical experience with this therapy remains highly anecdotal. Therapeutic red cell-exchange (TREX) has been used with much interest over the years, starting with the management of hemolytic disease of the newborn and later used to correct severe anemia in thalassemia patients thereby preventing iron overload. It has also been used for the management of complications of sickle cell disease such as priapism, chest syndrome, stroke, retinal, bone, splenic and hepatic infarction or in preparation for surgery by reducing HbS to less than 30%. Automated apheresis has also favored the use of TREX in conditions such as paroxysmal nocturnal hemoglobinuria and aniline poisoning, arsenic poisoning, Na chlorate intoxications and CO intoxications, hemoglobinopathies, autoimmune hemolytic anemia, reactions due to ABO incompatibility, in preparation for ABO incompatible bone marrow transplantation or for preventing anti-D immunization after the transfusion of D(+) cells to D(-) recipients. Another field of application has been in the emergency management of intraerythrocytic parasite infections such as malaria and babesiosis. Application of TREX may be wide but its real use remains limited. In our personal experience, in 16 years, only 167 TREX procedures have been carried out in a total of 13,747 therapeutic procedures. This represents only 1.21% of the total.

Anemia, Sickle Cell↗
PubMed1997

Developmental response by Leydig cells to acidic and basic fibroblast growth factor.

The present study examines the effects of acidic (FGF-1) and basic (FGF-2) fibroblast growth factors on Leydig cell steroidogenesis by cells from 5-, 21- and 90-day-old rats. These ages represent three distinct time points in Leydig cell development: fetal Leydig cells (day 5), immature Leydig cells (day 21) and adult Leydig cells (day 90). The results demonstrate that the actions of the two growth factors on steroidogenesis are developmentally regulated, and require the presence of heparan sulphate proteoglycans (HSPG). FGF-1 and FGF-2 both had stimulatory effects on basal, but not maximally LH-stimulated, testosterone production by fetal Leydig cells, and both growth factors stimulated basal 5 alpha-androstane-3 alpha, 17 beta-diol production by immature Leydig cells. These effects were mediated by heparan sulphate-proteoglycans (HSPG), as they were blocked by the addition of protamine sulphate and sodium chlorate. FGF-1 and FGF-2 had no effect on basal testosterone production by adult Leydig cells, however, FGF-1 alone inhibited LH-stimulated testosterone production by adult Leydig cells in a dose-dependent manner. These data demonstrate that the effects of FGF-1 and FGF-2 are dependent on the specific stage of Leydig cell differentiation and development and may vary accordingly. Furthermore, although FGF-1 and FGF-2 are closely related structurally, a different effect of these two growth factors can be observed on the same type of Leydig cells. The data therefore suggest that these growth factors may have different but specific roles in the regulation of Leydig cell steroidogenesis, at different stages of development.

Age Factors↗
PubMed2003

Low density lipoprotein receptor-related protein (LRP) is a heparin-dependent adhesion receptor for connective tissue growth factor (CTGF) in rat activated hepatic stellate cells.

Connective tissue growth factor (CTGF) is a cysteine-rich, extracellular matrix-associated heparin-binding protein implicated in a variety of fibrotic disorders. CTGF is initially synthesized as a mosaic protein containing four discrete structural modules (CTGF(1-4)) but this is susceptible to proteolytic cleavage yielding isoforms comprising modules 3 and 4 (CTGF(3-4)) or module 4 alone (CTGF(4)). In this study, we show that cultured rat hepatic stellate cells (HSCs) produce CTGF(1-4) and CTGF(3-4) following treatment with transforming growth factor-beta and that CTGF is a cell adhesion factor for activated HSCs. Low density lipoprotein receptor-associated protein (LRP) is a receptor for CTGF(1-4) or CTGF(3-4), but not CTGF(4), whereas cell surface heparan sulfate proteoglycans (HSPGs) are binding sites for all CTGF isoforms. Prior occupancy of LRP with other LRP ligands, receptor associated protein, anti-LRP, or a thrombospondin type I peptide (TEWSACSKTCG) resulted in a 50% decrease in the adhesion of activated HSCs to CTGF(1-4) or CTGF(3-4) whereas there was no effect on CTGF(4)-mediated adhesion. Co-incubation of CTGF with heparin or perturbation of cell surface HSPGs with heparinase or sodium chlorate completely blocked adhesion of activated HSCs to all CTGF isoforms. Freshly isolated HSCs demonstrated only weak binding to CTGF but strong binding to fibronectin. Thus HSC adhesion is at least partially promoted by CTGF through its binding to LRP, a process that is heparin-dependent. CTGF-LRP interactions are likely mediated by module 3 and CTGF-heparin interactions occur principally in module 4, although additional motifs may account for the heparin-dependency of LRP binding. These data show that LRP and HSPGs are utilized by HSCs for binding to CTGF and suggest that these cell surface molecules may be involved in mediating CTGF activity or adhesive signaling during the activation process.

Journal Article↗
PubMed2004

Attenuated total reflectance FTIR detection and quantification of low concentrations of aqueous polyatomic anions.

Development of a new quantitative method for determining low concentrations of aqueous polyatomic anions using attenuated total reflectance (ATR) FTIR spectroscopy is described. Evaporated thin-film coatings of anion-selective tetraalkylated ferrocenium salts were applied to the surface of ATR crystals, which enabled anion detection limits to be lowered up to 23 000-fold below those achieved using the commercially available spectrometer with identical uncoated ATR crystals. Linear calibration curves based on d(absorbance)/dt, which is related to the rate of anion exchange in the thin film, were established in the 0.04-30 microM range. Limits of detection (10-min analyses) for perchlorate, chlorate, trifluoromethanesulfonate, perfluoro-n-butanesulfonate, perfluoro-n-octanesulfonate, tetrafluoroborate, hexafluorophosphate, and pinacolylmethylphosphonate in aqueous solution were 0.03, 0.2, 0.05, 0.07, 0.06, 0.06, 0.6, and 0.7 microM, respectively, using the thin-film coatings. This simple detection/quantification method afforded good reproducibility with relatively fast detection times.

Calibration↗
PubMed1994

Tyrosine sulfation of the glycoprotein Ib-IX complex: identification of sulfated residues and effect on ligand binding.

Here, we present evidence that glycoprotein (GP) Ib alpha, one of three polypeptides that make up the GP Ib--IX complex--the receptor for von Willebrand factor (vWf) on the surface of unactivated platelets--is modified by sulfation of tyrosine residues. Only GP Ib alpha was found to incorporate 35S when the GP Ib--IX complex was immunoprecipitated from [35S]sulfate metabolically labeled L and CHO cells that express the recombinant complex. The occurrence of sulfation on tyrosine residues of the polypeptide backbone was determined by removing O- and N-linked oligosaccharides. Limited proteolytic digestion of metabolically labeled GP Ib alpha revealed that sulfated tyrosine residues are located in the 45-kDa globular region containing the vWf binding site. By mutating potentially sulfated tyrosine residues to phenylalanine and comparing the stoichiometry of sulfate incorporation of these mutants to the incorporation in wild-type GP Ib alpha, three clustered tyrosine residues--Tyr-276, Tyr-278, and Tyr-279-were identified that undergo the modification. Culturing cells in sulfate-depleted medium containing sodium chlorate and guaiacol completely inhibited GP Ib alpha sulfation but did not decrease GP Ib-IX expression on the cell surface. Similarly, transiently transfected CHO cells expressed the mutant GP Ib alpha polypeptide on their surfaces at the same levels as they expressed wild-type GP Ib alpha. These results suggest that tyrosine sulfation of GP Ib alpha has little or no effect on the synthesis, assembly, and surface expression of the GP Ib-IX complex. Nevertheless, inhibiting sulfation of GP Ib alpha reduced the binding of 125I-labeled vWf in the presence of ristocetin by up to 37%.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2001

Catalytic protein film voltammetry from a respiratory nitrate reductase provides evidence for complex electrochemical modulation of enzyme activity.

The first step in the respiratory reduction of nitrate to dinitrogen in Paracoccus pantotrophus is catalyzed by the quinol-nitrate oxidoreductase NarGHI. This membrane-anchored protein directs electrons from quinol oxidation at the membrane anchor, NarI, to the site of nitrate reduction in the membrane extrinsic [Fe-S] cluster and Mo-bis-MGD containing dimer, NarGH. Liberated from the membrane, NarGH retains its nitrate reductase activity and forms films on graphite and gold electrodes within which direct and facile exchange of electrons between the electrode and the enzyme occurs. Protein film voltammetry has been used to define the catalytic behavior of NarGH in the potential domain and a complex pattern of reversible, nitrate concentration dependent modulation of activity has been resolved. At low nitrate concentrations the local maximum observed in the catalytic current-potential profile reveals how NarGH can catalyze nitrate reduction via two pathways having distinct specificity constants, k(obs)(cat)/K(obs)(M). Catalysis is directed to occur via one of the pathways by an electrochemical event within NarGH. On increasing the nitrate concentration, the local maximum in the catalytic current becomes less distinct, and the catalytic waveform adopts an increasingly sigmoidal form. A pattern of voltammetry similar to that observed during nitrate reduction is observed during reduction of the stereochemically distinct substrate chlorate. Centers whose change of oxidation state may define the novel catalytic voltammetry of NarGH have been identified by EPR-monitored potentiometric titrations and mechanisms by which the electrochemistry of Mo-bis-MGD or [Fe-S] clusters can account for the observed behavior are discussed.

Catalysis↗
PubMed1985

Kinetic analysis of respiratory nitrate reductase from Escherichia coli K12.

Purified respiratory nitrate reductase from Escherichia coli is able to use either reduced viologen dyes or quinols as the electron donor and nitrate, chlorate, or bromate as the electron acceptor. When reduced viologen dyes act as the electron donor, the enzyme follows a compulsory-order, "Theorell-Chance" mechanism, in which it is an enzyme-nitrate complex that is reduced rather than the free enzyme. In contrast, if quinols are used as the electron donor, then the enzyme operates by a two-site, enzyme-substitution mechanism. Partial proteolysis of the cytochrome b containing holoenzyme by trypsin results in loss of cytochrome b and in cleavage of one of the enzyme's subunits. The cytochrome-free derivative exhibits a viologen dye dependent activity that is indistinguishable from that of the holoenzyme, but it is incapable of catalyzing the quinol-dependent reaction. The quinol-dependent, but not the viologen dye dependent, activity is inhibited irreversibly by exposure to diethyl pyrocarbonate and reversibly by treatment with 2-n-heptyl-4-hydroxyquinoline N-oxide. We conclude that the holoenzyme has two independent and spatially distinct active sites, one for quinol oxidation and the other for nitrate reduction.

Cytochrome b Group↗
PubMed1998

P-selectin mediates adhesion of the human melanoma cell line NKI-4: identification of glycoprotein ligands.

Activated endothelial cells and stimulated platelets express the cell adhesion molecule P-selectin (CD62P), which mediates adhesion to various leukocytes and certain types of cancer cells. In this study, we show Ca2+-dependent binding of P-selectin to NKI-4 cells, a cell line derived from a human melanoma. The binding is inhibited by P7 (a leukocyte adhesion blocking mAb against P-selectin), but not by PL5 (a leukocyte adhesion blocking mAb against P-selectin glycoprotein ligand-1; PSGL-1). Further, expression of PSGL-1 could not be detected on NKI-4 cells by either PL5 mAb or an Ab against a synthetic peptide corresponding to a portion of the PSGL-1 sequence. P-selectin affinity chromatography of lysates from in vivo [3H]-glucosamine-labeled NKI-4 cells resulted in the isolation of three glycoproteins, with apparent molecular masses of approximately 250, approximately 110, and approximately 100 kDa under reducing conditions and approximately 230, approximately 105, and approximately 85 kDa under nonreducing conditions. These molecules could be precipitated by P-selectin, but not by E-selectin. EDTA and the P7 mAb, but not the PL5 mAb, inhibited the binding of P-selectin to the purified ligands. Surprisingly, we found that sodium chlorate, a sulfation inhibitor, did not inhibit the binding of P-selectin to NKI-4 cells and that [35S]-sulfate did not label the NKI-4 cell ligands. We conclude that P-selectin-dependent adhesion of the human melanoma cell line NKI-4 is mediated by a novel class of glycoprotein ligands.

Animals↗
PubMed2000

Mechanisms of fibroblast growth factor 2 intracellular processing: a kinetic analysis of the role of heparan sulfate proteoglycans.

The interaction of fibroblast growth factor 2 (FGF-2) with heparan sulfate proteoglycans (HSPG) has been demonstrated to enhance receptor binding and alter the intracellular distribution of internalized FGF-2. In the present study, the intracellular fate of FGF-2 was analyzed in vascular smooth muscle cells (VSMC) under native and HSPG-deficient conditions. HSPG-deficient cells were generated by treatment with sodium chlorate. Cells were incubated with FGF-2 at 37 degrees C for prolonged periods (0-48 h) to allow for FGF-2 uptake and processing. Processing of FGF-2 occurred in stages. Initially a family of low molecular weight (LMW) fragments (4-10 kDa) were detected that accumulated to much higher ( approximately 10-fold) levels in native compared to heparan sulfate-deficient cells. Pulse-chase experiments revealed that the half-life of these LMW intermediates was significantly greater in native ( approximately 18 h) compared to HSPG-deficient cells ( approximately 4 h). Rate constants for FGF-2 processing were derived by modeling the uptake and processing of FGF-2 as a set of first-order differential equations. The kinetic analysis indicated that the greatest differences between native and HSPG-deficient VSMC was in the formation of LMW and further suggested that these FGF-2 products appear to represent a stable subpool of internal FGF-2 that is favored in cells that contain HSPG. Thus, HSPG might function as a cellular switch between immediate and prolonged signal activation by heparin-binding growth factors such as FGF-2. In the absence of HSPG, FGF-2 can interact with and activate its receptor, yet in the presence of HSPG, FGF-2 might be able to mediate prolonged or unique biological responses through intracellular processes.

Animals↗
PubMedDate not supplied

Novel functional biodegradable polymer II: fibroblast growth factor-2 activities of poly(gamma-glutamic acid)-sulfonate.

Basic fibroblast growth factor (FGF-2) mitogenic activities of sulfonated poly(gamma-glutamic acid) (gamma-PGA-S) were investigated with chlorate-treated L929 fibroblast culture tests. When 72% of the carboxyl groups in gamma-PGA were sulfonated (gamma-PGA-S72), cell numbers reached a maximum. The activity of gamma-PGA-S72 was higher than that of gamma-PGA and synthetic heparinoids and was almost comparable to that of heparin. Cytotoxicity of gamma-PGA-S72 was not observed, regardless of the degree of sulfonation. FGF-2-protective effects of gamma-PGA-S72 against acid and thermal inactivation were also evaluated, and gamma-PGA-S72 showed higher FGF-2-protective effects in comparison to nonsulfonated gamma-PGA. The steric structures of various sulfonated gamma-PGA-Ss were analyzed by molecular modeling (molecular orbital method (MOPAC)) and indicated that gamma-PGA-Ss are helical in vacuo. Results from MOPAC and the molecular mechanics method (MM2) demonstrated that electrostatic interactions can take place between sulfonic and carboxyl groups of gamma-PGA-S and basic amino acid residues in FGF-2. gamma-PGA-S72 can interact with FGF-2 strongly.

Animals↗
PubMed2002

Evidence of perchlorate (ClO4-) reduction in plant tissues (poplar tree) using radio-labeled 36ClO4-.

Phytoremediation of perchlorate (ClO4) by poplar trees Populus deltoidex nigrawas investigated using small cuttings growing in hydroponic Hoagland solution and plant tissue cultures, consisting of spherical photosynthetic cell aggregates (i.e. nodules) developing in Murashige and Skoog culture medium. Both plants and nodules were grown under a 16 h/8 h photoperiod cycle and under sterile conditions. Degradation experiments, performed by the incubation of pregrown plants and nodules in the presence of 36Cl radio-labeled ClO4- (25 mg L(-1)), showed a reduction of the initial ClO4- concentration in the solution of about 50% after 30 d of incubation. Analysis of the distribution of radioactivity in different plant fractions indicated that 27.4% of the total was translocated to the leaves, while 66.9% remained in the solution. Very little radioactivity (less than 3.0%) was detected in the other parts of the plants. 32.0% of the radioactivity recovered in the solution was shown to consist of 36Cl- and 68.0% of nontransformed 36ClO4-. The radioactivity recovered in the leaf extracts was distributed as chloride (36Cl-) (1.6% of the total), chlorite (36ClO2-) (2.4%), chlorate (36ClO3-) (4.8%), nontransformed 36ClO4- (21.6%), and an unidentified organic compound (1.4%). The radioactivity recovered in the solution containing submerged nodules consisted of 36Cl- (6.4% of the total), 36ClO3- (1.3%), and nontransformed 36ClO4- (51.5%). Radioactivity detected in the nodule extracts was distributed as 36Cl- (2.0% of the total), 36ClO2- (5.2%), 36ClO3- (6.4%), 36ClO4- (22.7%), and an unidentified organic compound (0.5%). These results provide evidence of perchlorate reduction inside poplar tree tissues. 36ClO4- is partially reduced to 36ClO3-, 36ClO2-, and 36Cl-.

Biodegradation, Environmental↗
PubMed2003

Bromate in chlorinated drinking waters: occurrence and implications for future regulation.

Bromate is a contaminant of commercially produced solutions of sodium hypochlorite used for disinfection of drinking water. However, no methodical approach has been carried out in U.S. drinking waters to determine the impact of such contamination on drinking water quality. This study utilized a recently developed method for quantitation of bromate down to 0.05 microg/L to determine the concentration of bromate present in finished waters that had been chlorinated using hypochlorite. Forty treatment plants throughout the United States using hypochlorite in the disinfection step were selected and the levels of bromate in the water both prior to and following the addition of hypochlorite were measured. The levels of bromate in the hypochlorite feedstock were also measured and together with the dosage information provided by the plants and the amount of free chlorine in the feedstock, it was possible to calculate the theoretical level of bromate that would be imparted to the water. A mass balance was performed to compare the level of bromate in finished drinking water samples to that found in the corresponding hypochlorite solution used for treatment. Additional confirmation of the source of elevated bromate levels was provided by monitoring for an increase in the level of chlorate, a co-contaminant of hypochlorite, atthe same point in the treatment plant where bromate was elevated. This study showed that bromate in hypochlorite-treated finished waters varies across the United States based on the source of the chemical feedstock, which can add as much as 3 microg/L bromate into drinking water. Although this is within the current negotiated industry standard that allows up to 50% of the maximum contaminant level (MCL) for bromate in drinking water to be contributed by hypochlorite, it would be a challenge to meet a tighter standard. Given that distribution costs encourage utilities to purchase chemical feedstocks from local suppliers, utilities in certain regions of the United States may be put at a distinct disadvantage if future lower regulations on bromate levels in finished drinking water are put into place. Moreover, with these contaminant levels it would be almost impossible to lower the maximum permissible contribution to bromate in finished water from hypochlorite to 10% of the MCL, which is the norm for other treatment chemicals. Until this issue is resolved, it will be difficult to justify a lowering of the bromate MCL from its current level of 10 to 5 microg/L or lower.

Bromates↗
PubMed2003

Tribromopyrrole, brominated acids, and other disinfection byproducts produced by disinfection of drinking water rich in bromide.

Using gas chromatography/mass spectrometry (GC/MS), we investigated the formation of disinfection byproducts (DBPs) from high bromide waters (2 mg/L) treated with chlorine or chlorine dioxide used in combination with chlorine and chloramines. This study represents the first comprehensive investigation of DBPs formed by chlorine dioxide under high bromide conditions. Drinking water from full-scale treatment plants in Israel was studied, along with source water (Sea of Galilee) treated under carefully controlled laboratory conditions. Select DBPs (trihalomethanes, haloacetic acids, aldehydes, chlorite, chlorate, and bromate) were quantified. Many of the DBPs identified have not been previously reported, and several of the identifications were confirmed through the analysis of authentic standards. Elevated bromide levels in the source water caused a significant shift in speciation to bromine-containing DBPs; bromoform and dibromoacetic acid were the dominant DBPs observed, with very few chlorine-containing compounds found. Iodo-trihalomethanes were also identified, as well as a number of new brominated carboxylic acids and 2,3,5-tribromopyrrole, which represents the first time a halogenated pyrrole has been reported as a DBP. Most of the bromine-containing DBPs were formed during pre-chlorination at the initial reservoir, and were not formed by chlorine dioxide itself. An exception wasthe iodo-THMs, which appeared to be formed by a combination of chlorine dioxide with chloramines or chlorine (either added deliberately or as an impurity in the chlorine dioxide). A separate laboratory study was also conducted to quantitatively determine the contribution of fulvic acids and humic acids (from isolated natural organic matter in the Sea of Galilee) as precursor material to several of the DBPs identified. Results showed that fulvic acid plays a greater role in the formation of THMs, haloacetic acids, and aldehydes, but 2,3,5-tribromopyrrole was produced primarily from humic acid. Because this was the first time a halopyrrole has been identified as a DBP, 2,3,5-tribromopyrrole was tested for mammalian cell cytotoxicity and genotoxicity. In comparison to other DBPs, 2,3,5-tribromopyrrole was 8x, 4.5x, and 16x more cytotoxic than dibromoacetic acid, 3-chloro-4-(dichloromethyl)-5-hydroxy-2-[5H]-furanone [MX], and potassium bromate, respectively. 2,3,5-Tribromopyrrole also induced acute genomic damage, with a genotoxic potency (299 microM) similar to that of MX.

Bromides↗
PubMed2001

Kinetics and mechanism of catalytic decomposition and oxidation of chlorine dioxide by the hypochlorite ion.

The oxidation of ClO(2) by OCl(-)is first order with respect to both reactants in the neutral to alkaline pH range: -d[ClO(2)]/dt = 2k(OCl)[ClO(2)][OCl(-)]. The rate constant (T = 298 K, mu = 1.0 M NaClO(4)) and activation parameters are k(OCl) = 0.91 +/- 0.02 M(-1) s(-1), DeltaH = 66.5 +/- 0.9 kJ/mol, and DeltaS(++) = -22.3 +/- 2.9 J/(mol K). In alkaline solution, pH > 9, the primary products of the reaction are the chlorite and chlorate ions and consumption of the hypochlorite ion is not observed. The hypochlorite ion is consumed in increasing amounts, and the production of the chlorite ion ceases when the pH is decreased. The stoichiometry is kinetically controlled, and the reactants/products ratios are determined by the relative rates of the production and consumption of the chlorite ion in the ClO(2)/OCl(-) and HOCl/ClO(2)(-) reactions, respectively.

Journal Article↗
PubMed2004

Multielectron atom transfer reactions of perchlorate and other substrates catalyzed by rhenium oxazoline and thiazoline complexes: reaction kinetics, mechanisms, and density functional theory calculations.

The title complexes, the Re(O)L(2)(Solv)(+) complexes (L = hoz, 2-(2'-hydroxyphenyl)-2-oxazoline(-) or thoz, 2-(2'-hydroxyphenyl)-2-thiazoline(-); Solv = H(2)O or CH(3)CN), are effective catalysts for the following fundamental oxo transfer reaction between closed shell molecules: XO + Y --> X + YO. Among suitable oxygen acceptors (Y's) are organic thioethers and phosphines, and among suitable oxo donors (XO's) are pyridine N-oxide (PyO), t-BuOOH, and inorganic oxyanions. One of the remarkable features of these catalysts is their high kinetic competency in effecting perchlorate reduction by pure atom transfer. Oxo transfer to rhenium(V) proceeds cleanly to afford the cationic dioxorhenium(VII) complex Re(O)(2)L(2)(+) in a two-step mechanism, rapid substrate (XO) coordination to give the precursor adduct cis-Re(V)(O)(OX)L(2)(+) followed by oxygen atom transfer (OAT) as the rate determining step. Electronic variations with PyO derivatives demonstrated that electron-withdrawing substituents accelerate the rate of Re(VII)(O)(2)L(2)(+) formation from the precursor adduct cis-Re(V)(O)(OX)L(2)(+). The activation parameters for OAT with picoline N-oxide and chlorate have been measured; the entropic barrier to oxo transfer is essentially zero. The potential energy surface for the reaction of Re(O)(hoz)(2)(OH(2))(+) with PyO was defined, and all pertinent intermediates and transition states along the reaction pathway were located by density functional theory (DFT) calculations (B3LYP/6-31G). In the second half of the catalytic cycle, Re(O)(2)L(2)(+) reacts with oxygen acceptors (Y's) in second-order reactions with associative transition states. The rate of OAT to substrates spans a remarkable range of 0.1-10(6) L mol(-)(1) s(-)(1), and the substrate reactivity order is Ph(3)P > dialkyl sulfides > alkyl aryl sulfides > Ph(2)S approximately DMSO, which demonstrates electrophilic oxo transfer. Competing deactivation and inhibitory pathways as well as their relevant kinetics are also reported.

Journal Article↗
PubMed2006

Three autocatalysts and self-inhibition in a single reaction: a detailed mechanism of the chlorite-tetrathionate reaction.

The chlorite-tetrathionate reaction has been studied spectrophotometrically in the pH range of 4.65-5.35 at T = 25.0 +/- 0.2 degrees C with an ionic strength of 0.5 M, adjusted with sodium acetate as a buffer component. The reaction is unique in that it demonstrates autocatalysis with respect to the hydrogen and chloride ion products and the key intermediate, HOCl. The thermodynamically most-favorable stoichiometry, 2S(4)O(6)2- + 7ClO2- + 6H2O --> 8SO(4)2- + 7Cl- + 12H+, is not found. Under our experimental conditions, chlorine dioxide, the chlorate ion, or both are detected in appreciable amounts among the products. Initial rate studies reveal that the formation of chlorine dioxide varies in an unusual way, with the chlorite ion acting as a self-inhibitor. The reaction is supercatalytic (i.e., second order with respect to autocatalyst H+). The autocatalytic behavior with respect to Cl- comes from chloride catalysis of the chlorite-hypochlorous acid and hypochlorous acid-tetrathionate subsystems. A detailed kinetic study and a model that explains this unusual kinetic behavior are presented.

Journal Article↗