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PubMed2004

Existence of a tungsten-binding protein in Acidithiobacillus ferrooxidans AP19-3.

A tungsten-binding protein was purified from a plasma membrane preparation of the iron-oxidizing bacterium, Acidithiobacillus ferrooxidans AP19-3 in an electrophoretically homogenous state. The protein was composed of two subunits with apparent molecular masses of 12 and 20.7 kDa. The molecular mass of the native protein was estimated to be 26.4 kDa in the presence of 1.5% 1-o-octyl-D -glucopyranoside (OGL), indicating that the native tungsten-binding protein is a heterodimeric protein. The amounts of tungsten bound to 1 mg of plasma membranes of A. ferrooxidans AP19-3 and the purified tungsten-binding protein at pH 3.0 were 191 and 1506 mug, respectively. In contrast, the amounts of tungsten bound to 1 mg of albumin, aldolase, catalase, chymotrypsinogen A, ferritin, and ferredoxin at pH 3.0 were 13.1, 18.6, 12.8, 16.6, 11.4, and 6.1 mug, respectively. Incubation of the tungsten-binding protein for 1 h with 10 mM Na(2)WO(4) plus 10 mM metal ion, such as NaVO(3), Na(2)MoO(4), CuSO(4), NiSO(4), MnSO(4), CoSO(4), or CdCl(2), did not markedly affect the amount of tungsten bound to the tungsten-binding protein, suggesting that the protein specifically binds tungsten.

Journal Article↗
PubMed2001

Mechanism of growth inhibition by tungsten in Acidithiobacillus ferrooxidans.

Cell growth of three hundred iron-oxidizing bacteria isolated from natural environments was inhibited strongly by 0.05 mM, and completely by 0.2 mM of sodium tungstate (Na2WO4), respectively. Since no great difference in the level of tungsten inhibition was observed among the 300 strains tested, the mechanism of inhibition by Na2WO4 was studied with Acidithiobacillus ferrooxidans strain AP19-3. When resting cells of AP19-3 were incubated in 0.1 M beta-alanine-SO4(2-) buffer (pH 3.0) with 0.1 mM Na2WO4 for 1 h, the amount of tungsten bound to the cells was 12 microg/mg protein. The optimum pH for tungsten binding to the resting cells was 2 to approximately 3. Approximately 2 times more tungsten bound to the cells at pH 3.0 than at pH 6.0. The tungsten binding was specifically inhibited by sodium molybdenum. However, copper, nickel, cadmium, zinc, manganese, cobalt, and vanadate did not disturb tungsten binding to the resting cells. The iron-oxidizing activity of AP19-3 was inhibited 24, 62, and 77% by 1, 5, and 10 mM of Na2WO4, respectively. Among the components of iron oxidation enzyme system, iron:cytochrome c oxidoreductase activity was not inhibited by 10 mM of Na2WO4. In contrast, the activity of cytochrome c oxidase purified highly from the strain was inhibited 50 and 72%, respectively, by 0.05 and 0.1 mM of Na2WO4. The amounts of tungsten bound to plasma membrane, cytosol fraction, and a purified cytochrome c oxidase were 8, 0.5, and 191 microg/mg protein, respectively. From the results, the growth inhibition by Na2WO4 observed in A. ferrooxidans is explained as follows: tungsten binds to cytochrome c oxidase in plasma membranes and inhibits cytochrome c oxidase activity, and as a results, the generation of energy needed for cell growth from the oxidation of Fe2+ is stopped.

Culture Media↗
PubMed2001

Electroanalytical determination of tungsten and molybdenum in proteins.

Recent crystal structure determinations accelerated the progress in the biochemistry of tungsten-containing enzymes. In order to characterize these enzymes, a sensitive determination of this metal in protein-containing samples is necessary. An electroanalytical tungsten determination has successfully been adapted to determine the tungsten and molybdenum content in enzymes. The tungsten and molybdenum content can be measured simultaneously from 1 to 10 microg of purified protein with little or no sample handling. More crude protein samples require precipitation of interfering surface active material with 10% perchloric acid. This method affords the isolation of novel molybdenum- and tungsten-containing proteins via molybdenum and tungsten monitoring of column fractions, without using radioactive isotopes. A screening of soluble proteins from Pyrococcus furiosus for tungsten, using anion-exchange column chromatography to separate the proteins, has been performed. The three known tungsten-containing enzymes from P. furiosus were recovered with this screening.

Chemical Precipitation↗
PubMed1996

Preliminary data on hard metal workers exposure to tungsten oxide fibres.

The first personal exposure data for tungsten oxide fibres, in two hard metal manufacturing industries is presented. Occupational exposure was studied by static and personal measurements during tungsten metal production. Three different initial materials were used, ammonium-paratungstate (APT), blue oxide and tungsten trioxide. In both factories, airborne tungsten oxide fibres were detected both in static and personal samples. Fibre exposure varies for different activities. Charging of raw material, changing the hammer, cleaning-work on the cyclone and the micro-filter were found to be among the most high dusty operations. However, as workers use respirators during cleaning operations, these filters could not be related to personal exposure. The calcination of APT to the blue oxide generates fibrous dust. The raw material imported as blue oxide is also fibrous material and both charging it into the calcination furnace and re-charging it into the reduction furnace generates unnecessarily additional dusty periods. A single reduction-stage is, therefore, preferable. Furthermore, the tungsten trioxide raw material is non-fibrous, therefore, calcination of APT to tungsten trioxide and its reduction to tungsten metal is preferable with respect to minimising workers exposure to tungsten oxide fibres.

Air Pollutants, Occupational↗
PubMed1980

The influence of tungsten on the molybdenum status of poultry.

1. Large doses of tungsten, administered to the chick either by injection or by feeding, increased tissue concentrations of tungsten and decreased tissue concentrations of molybdenum and tissue activities of xanthine dehydrogenase. 2. The rate of loss of large doses of tungsten from the liver occurred in an exponential manner with a half-life of 27 h. 3. When tungsten was administered to chicks fed on a semi-synthetic diet containing abnormally low concentrations of molybdenum, the activity of hepatic xanthine dehydrogenase was reduced to negligible levels. 4. The alterations in molybdenum metabolism resulting from the administration of large doses of tungsten to the chick appears to be the result of tungsten toxicity and not of molybdenum deficiency. 5. Deaths from tungsten toxicity occurred when tissue concentrations of tungsten were increased to approximately 25 micrograms/g liver. At this tissue tungstencon centration the activity of xanthine dehydrogenase was zero.

Animals↗
PubMed1993

Inflammatory response of the lung to tungsten particles: an experimental study in mice submitted to intratracheal instillation of a calcium tungstate powder.

Tungsten has been implicated as a cause of a severe form of pneumoconiosis in humans, the so-called "hard metal" lung disease. We have investigated the effect of intratracheal instillation of a powder of calcium tungstate on the pulmonary tissue of CD-1 mice. The tungsten-induced alterations were studied using 3 microanatomical methods: cytologic study of exudates obtained by bronchoalveolar lavage (BAL); histologic examination of paraffin-embedded sections of the lung; and scanning electron microscopic (SEM) examination of lung samples using x-ray microanalysis to detect tungsten in situ. The animals were sacrificed 1, 3, 7, 14 and 21 days after a single intratracheal instillation of 250 micrograms calcium tungstate particles suspended in 100 microliters of saline. We found that the metal particles induced a marked inflammatory response in the bronchoalveolar space characterized by a biphasic attraction of leukocytes with cellular peaks observed at day 1 and 14. More than 50% of the BAL macrophages showed ingested tungsten. In the lung parenchyma, the inflammatory infiltrates were predominantly located at the periphery of the bronchiolar walls. From 7 days on after the tungsten deposition, large inflammatory exudates were seen invading focal areas of the alveolar domain of the lung. SEM views revealed that the tungsten particles could be inside alveolar macrophages, in cells making up the alveolar wall, or inside periacinar lymphatics. Our data document that tungsten particles cause a marked inflammatory response in the lung tissue and that the leukocyte exudates may invade alveolar areas of the lung.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Comparative study of the acute lung toxicity of pure cobalt powder and cobalt-tungsten carbide mixture in rat.

Alveolitis progressing to lung fibrosis has been reported in workers exposed to cobalt containing dust (e.g., tungsten carbide-cobalt mixture as produced by the hard metal industry) but rarely following exposure to pure cobalt dust (e.g., in cobalt-producing factories). We have previously demonstrated that tungsten carbide-cobalt mixture is more toxic toward rat alveolar macrophages in vitro than pure cobalt metal powder. The present study was undertaken to compare in female rats the acute pulmonary response (lung weight, lung histology, cellular and biochemical analyses of bronchoalveolar lavage fluid, and mortality) following the intratracheal instillation of pure cobalt (Co) particles (median particle size, d50:4 microns), pure tungsten carbide (WC) particles (d50:2 microns), tungsten carbide-cobalt (WC-Co) powder (d50:2 microns; cobalt 6.3%, tungsten 84%, carbon 5.4%) and crystalline silica (d50 less than 5 micron) used as pneumotoxic reference material. WC alone (15.67 mg/100 g body wt) behaves as an inert dust producing only a mild accumulation of macrophages in the alveolar duct walls. Co alone (1.0 mg/100 g) only causes a moderate inflammatory response. An identical amount of Co given as WC-Co mixture (16.67 mg/100 g; corresponding to 1.0 mg Co/100 g) produces a severe alveolitis and fatal pulmonary edema. Cellular and biochemical characteristics of bronchoalveolar lavage fluid collected 24 hr after the intratracheal instillation of WC (1.0 mg/100 g) or Co (0.06 mg/100 g) are not significantly different from those of control animals instilled with sterile saline. On the contrary, bronchoalveolar lavage fluid changes following administration of the WC-Co mixture (1.0 mg/100 g; corresponding to 0.06 mg Co/100 g) are very similar to those induced by crystalline silica (1.0 mg/100 g). The amount of cobalt excreted in urine is significantly higher when the animals are exposed to WC-Co powder as compared to an equivalent amount of pure cobalt particles, suggesting an increased bioavailability of cobalt metal when combined with tungsten carbide. This study demonstrates that the acute lung toxicity of tungsten carbide-cobalt mixture is much higher than that of each individual component and may explain why lung fibrosis is rarely if ever induced by exposure to pure cobalt dust.

Animals↗
PubMed1991

A tungsten-supplemented diet delivered by transplacental and breast-feeding routes lowers intestinal xanthine oxidase activity and affords cytoprotection in ischemia-reperfusion injury to the small intestine.

Ischemia-reperfusion injury has been implicated as playing a major role in the development of necrotizing enterocolitis, a major cause of morbidity and mortality in the newborn. A tungsten-supplemented molybdenum-free diet can reduce xanthine oxidase (XO) enzyme activity in the intestine, which in turn reduces the generation of oxygen radicals after an ischemia-reperfusion insult. This study evaluated the ability of this diet to be effective by indirect means, ie, transplacental and breast-feeding routes. XO activity of the intestine was measured in three groups of CD-1 white rats: I, weanlings fed the tungsten diet or standard chow for 1 week; II, 1-day-old rat pups whose mothers were maintained on the tungsten or standard chow for 7 to 10 days prior to term; and III, rat pups at 1 and 3 weeks after birth whose lactating mothers were maintained on the tungsten or standard chow. Some animals from group III also underwent either a 30- or 60-minute episode of occlusion of the superior mesenteric artery (SMA) to evaluate the protective effects of the diet. XO activity was significantly reduced in all groups receiving the tungsten diet (P less than .0001). Blinded histopathologic studies of the entire small bowel showed significantly less villar necrosis (P less than .05) and fibrosis (P less than .0001) in the tungsten-treated group than in the controls. In the 60-minute occlusion study all tungsten-group animals survived, whereas 7 of 12 in the control group died of intestinal infarction within 24 hours (P less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2006

Conical tungsten tips as substrates for the preparation of ultramicroelectrodes.

Here we describe a simple method to prepare voltammetric microelectrodes using tungsten wires as a substrate. Tungsten wires have a high tensile modulus and enable the fabrication of electrodes that have small dimensions overall while retaining rigidity. In this work, 125 microm tungsten wires with a conical tip were employed. For the preparation of gold or platinum ultramicroelectrodes, commercial tungsten microelectrodes, completely insulated except at the tip, were used as substrates. Following removal of oxides from the exposed tungsten, platinum or gold was electroplated, yielding surfaces with an electroactive area of between 1 x 10-6 and 2 x 10-6 cm2. Carbon surfaces on the etched tip of tungsten microwires were prepared by coating with photoresist followed by pyrolysis. The entire electrode was then insulated with Epoxylite except the tip, yielding an exposed carbon surface with an area of around 4 x 10-6 to 6 x 10-6 cm2. All three types of ultramicroelectrodes fabricated on the tungsten wire had similar electrochemical behavior to electrodes fabricated from wires or fibers insulated with glass tubes.

Carbon↗
PubMed2002

Tungsten-containing enzymes.

The biological importance of tungsten has been fully proved in the last decade due to isolation of a number of tungsten-containing enzymes (W-enzymes) from hyperthermophilic archaea. Tungsten was previously considered only as an antagonist of molybdenum, because the replacement of molybdenum by tungsten (due to their chemical similarity) leads to inactivation of molybdenum-containing enzymes (Mo-enzymes). In addition to the "true W-enzymes" in which tungsten cannot be replaced by molybdenum, recently some enzymes have been isolated which can use either molybdenum or tungsten in the catalytic process. This review briefly summarizes data on the participation of tungsten in catalysis by some enzymes and the structure of the active sites of W-enzymes.

Bacteria↗
PubMed2005

Modified ion exchange separation for tungsten isotopic measurements from kimberlite samples using multi-collector inductively coupled plasma mass spectrometry.

Tungsten isotope composition of a sample of deep-seated rock can record the influence of core-mantle interaction of the parent magma. Samples of kimberlite, which is known as a carrier of diamond, from the deep mantle might exhibit effects of core-mantle interaction. Although tungsten isotope anomaly was reported for kimberlites from South Africa, a subsequent investigation did not verify the anomaly. The magnesium-rich and calcium-rich chemical composition of kimberlite might engender difficulty during chemical separation of tungsten for isotope analyses. This paper presents a simple, one-step anion exchange technique for precise and accurate determination of tungsten isotopes in kimberlites using multi-collector inductively coupled plasma mass spectrometry (MC-ICP-MS). Large quantities of Ca and Mg in kimberlite samples were precipitated and removed with aqueous H(2)SO(4). Highly pure fractions of tungsten for isotopic measurements were obtained following an anion exchange chromatographic procedure involving mixed acids. That procedure enabled efficient removal of high field strength elements (HFSE), such as Hf, Zr and Ti, which are small ions that carry strong charges and develop intense electrostatic fields. The tungsten yields were 85%-95%. Advantages of this system include less time and less use of reagents. Precise and accurate isotopic measurements are possible using fractions of tungsten that are obtained using this method. The accuracy and precision of these measurements were confirmed using various silicate standard rock samples, JB-2, JB-3 and AGV-1.

Chromatography, Ion Exchange↗
PubMed2001

Inhibition of Ca2+-induced relaxation by oxidized tungsten wires and paratungstate.

Recent studies of rat mesenteric arteries using a wire myograph detected decreased Ca2+ and acetylcholine-induced relaxation responses. Preliminary experiments indicated the reduced responses were associated with the tungsten wire used in the myograph system. Compared with earlier observations, arteries mounted on aged 28-microm tungsten wire showed decreased maximal Ca2+-induced relaxation responses of arteries precontracted with phenylephrine (91.9 +/- 1.5 versus 54.8 +/- 4.5%, p < 0.001) and reduced sensitivity to Ca2+ (ED50 = 1.65 +/- 0.07 versus 4.58 +/- 0.16 mM, p < 0.001). Similar shifts were seen for acetylcholine. When the surface of the wire was cleaned by abrasion with fine sandpaper, both the ED50 for Ca2+ and maximal relaxation significantly improved. An enhanced sensitivity to Ca2+ was also seen when arteries were mounted on newly purchased 14-microm tungsten or 14-microm 24K gold wire with the rank order: 14-microm gold > 14-microm tungsten >> 28-microm aged tungsten wire. Laser Raman spectral analysis of the aged 28-microm tungsten wire showed that the surface was in an oxidized state that shared spectral characteristics with the paratungstate [W12O42](-12) anion. The effect of the paratungstate anion on arterial relaxation was therefore tested. Paratungstate, but not the structurally dissimilar tungstate and metatungstate anions, significantly reduced the sensitivity and magnitude of relaxation induced by Ca2+ and to a lesser extent, relaxation induced by acetylcholine. To learn whether paratungstate inhibits relaxation through the generation of oxygen radicals, the effect of the superoxide dismutase mimetic 4-hydroxy-2,2,6,6-tetramethylpiperidine 1-oxyl (1 mM) was assessed and found to have no effect. Since Ca2+-induced relaxation is inhibited by iberiotoxin, the effect of paratungstate on K+ channel activity was assessed. Paratungstate had no effect on currents through large conductance, Ca2+-activated K+ channels in whole-cell recordings from vascular smooth muscle cells, ruling out an action at the BK(Ca) channel. We conclude that: 1) surface oxidation of tungsten wire commonly used in wire myography significantly and adversely affects vascular responses to vasodilator compounds, 2) the effect is likely mediated by the paratungstate anion, and 3) the effects of the anion are not associated with free radical generation or K+ channel inhibition.

Acetylcholine↗
PubMed1997

A model of the distribution and retention of tungsten in the human body.

Expanding industrial and military uses of tungsten could result in substantially increased levels of this metal in the environment in the next few years. Although occupational experiences and available toxicological studies on laboratory animals suggest that tungsten may have a relatively low order of toxicity, the data are weak and inconclusive. There is a need not only for more systematic studies of the behavior and effects of tungsten in different animal species but also for a reliable, biologically realistic biokinetic model for tungsten in man that can be used to relate concentrations of this metal in environmental media to concentrations in tissues of exposed persons and translate results of experimental studies into terms of environmental exposures. This paper is intended as a first step toward development of such a biokinetic model. Information related to the biokinetics of tungsten in mammalian species is examined, a biologically meaningful compartmental model structure is proposed, provisional transfer rates between compartments are selected, areas are identified where additional biokinetic data on tungsten are most needed and suggestions are made for further research into the biokinetics of tungsten.

Environmental Exposure↗
PubMedDate not supplied

Endovascular embolization of varicoceles: resorption of tungsten coils in the spermatic vein.

PURPOSE: To investigate whether resorption of tungsten coils occurs in patients with varicoceles treated by endovascular embolization of the spermatic vein. METHODS: Patients who had previously had varicocele embolization were requested by letter to attend the radiology department. Blood levels of tungsten were compared with a group of controls. Fluoroscopic images of the coils were taken and compared with those obtained during the original procedures. RESULTS: Nineteen patients attended, whose procedure had been done 19-57 months previously (mean 40 months). Blood levels of tungsten were raised in 18 patients compared with the controls. Radiographic evidence of loss of substance of the coils was seen in four patients. CONCLUSION: Tungsten coil resorption occurs in varicocele embolization. In view of the unknown long-term effects of raised blood tungsten levels and the availability of alternative embolization agents, we feel that it is unwise to persist in the use of tungsten coils in this application.

Adult↗
PubMed1996

Tungsten in biological systems.

Tungsten (atomic number 74) and the chemically analogous and very similar metal molybdenum (atomic number 42) are minor yet equally abundant elements on this planet. The essential role of molybdenum in biology has been known for decades and molybdoenzymes are ubiquitous. Yet, it is only recently that a biological role for tungsten has been established in prokaryotes, although not as yet in eukaryotes. The best characterized organisms with regard to their metabolism of tungsten are certain species of hyperthermophilic archaea (Pyrococcus furiosus and Thermococcus litoralis), methanogens (Methanobacterium thermoautotrophicum and Mb. wolfei), Gram-positive bacteria (Clostridium thermoaceticum, C. formicoaceticum and Eubacterium acidaminophilum), Gram-negative anaerobes (Desulfovibrio gigas and Pelobacter acetylenicus) and Gram-negative aerobes (Methylobacterium sp. RXM). Of these, only the hyperthermophilic archaea appear to be obligately tungsten-dependent. Four different types of tungstoenzyme have been purified: formate dehydrogenase, formyl methanufuran dehydrogenase, acetylene hydratase, and a class of phylogenetically related oxidoreductases that catalyze the reversible oxidation of aldehydes. These are carboxylic reductase, and three ferredoxin-dependent oxidoreductases which oxidize various aldehydes, formaldehyde and glyceraldehyde 3-phosphate. All tungstoenzymes catalyze redox tungsten in these enzymes is bound by a pterin moiety similar to that found in molybdoenzymes. The first crystal structure of a tungsten- or pterin-containing enzyme, that of aldehyde ferredoxin oxidoreductase from P. furiosus, has revealed a catalytic site with one W atom coordinated to two pterin molecules which are themselves bridged by a magnesium ion. The geochemical, ecological, biochemical and phylogenetic basis for W- vs. Mo-dependent organisms is discussed.

Aldehyde Oxidoreductases↗
PubMed2004

Liver necrosis and fulminant hepatic failure in rats: protection by oxyanionic form of tungsten.

The hepatic lesion produced as a result of oxidative stress is of wide occurrence. In the present study, the effect of tungsten on liver necrosis and fulminant hepatic failure (FHF) has been studied in rats treated with various compounds known to produce oxidative stress. Supplementation of animals with sodium tungstate for 7 weeks before the induction of liver injury by chemicals including thioacetamide (TAA), carbon tetrachloride (CCl(4)), or chloroform (CHCl(3)) could protect progression of hepatic injury. Various biochemical changes associated with liver damage and oxidative stress were measured. Hepatic malondialdehyde content, endogenous tripeptide, and reduced glutathione were measured as oxidative stress markers. The activity of xanthine oxidase, which generates reactive oxygen species (ROS) as a by-product, was also determined and found to be perturbed. Tungsten supplementation to rats caused a significant decrease in lipid peroxidation and lowered the levels of the biochemical markers of hepatic lesions produced by TAA, CCl(4) (CCl(4)), or CHCl(3). Tungsten could also cause an increase in the survival rate in rats receiving lethal doses of TAA, CCl(4), or CHCl(3). The protective effect of tungsten, however, is suggested to be limited to the conditions where the hepatic lesion is reported to be due to the generation of ROS. The progression of liver injury produced by the compounds causing oxidative stress without initiating the generation of free radicals such as bromobenzene (BB), or acetaminophen (AAP), could not be inhibited by tungsten. The possible mechanism explaining the role of oxyanionic form of tungsten in free radical-induced hepatic lesions is discussed.

Acetaminophen↗
PubMed2006

Xanthine oxidase inhibitor tungsten prevents the development of atherosclerosis in ApoE knockout mice fed a Western-type diet.

Hyperlipidemia enhances xanthine oxidase (XO) activity. XO is an important source of reactive oxygen species (ROS). Since ROS are thought to promote atherosclerosis, we hypothesized that XO is involved in the development of atherosclerosis. ApoE(-/-) mice were fed a Western-type (WD) or control diet. In subgroups, tungsten (700 mg/L) was administered to inhibit XO. XO is a secreted enzyme which is formed in the liver as xanthine dehydrogenase (XDH) and binds to the vascular endothelium. High expression of XDH was found in the liver and WD increased liver XDH mRNA and XDH protein expression. WD induced the conversion of XDH to the radical-forming XO. Moreover, WD increased the hepatic expression of CD40, demonstrating activation of hepatic cells. Aortic tissue of ApoE(-/-) mice fed a WD for 6 months exhibited marked atherosclerosis, attenuated endothelium-dependent relaxation to acetylcholine, increased vascular oxidative stress, and mRNA expression of the chemokine KC. Tungsten treatment had no effect on plasma lipids but lowered the plasma XO activity. In animals fed a control diet, tungsten had no effect on radical formation, endothelial function, or atherosclerosis development. In mice fed a WD, however tungsten attenuated the vascular superoxide anion formation, prevented endothelial dysfunction, and attenuated KC mRNA expression. Most importantly, tungsten treatment largely prevented the development of atherosclerosis in the aorta of ApoE(-/-) mice on WD. Therefore, tungsten, potentially via the inhibition of XO, prevents the development of endothelial dysfunction and atherosclerosis in ApoE(-/-) mice on WD.

Animals↗
PubMed2005

Temperature dependent electrochemical investigations of molybdenum and tungsten oxobisdithiolene complexes.

To achieve a better understanding why thermophilic and hyperthermophilic organisms use tungsten instead of molybdenum within the active sites of their molybdopterin dependent oxidases, electrochemical investigations of model complexes for the active sites of enzymes belonging to the DMSO reductase (molybdenum) and the aldehyde oxidoreductase (tungsten) family have been undertaken. Cyclic voltammetry and differential pulse voltammetry of four pairs of molybdenum and tungsten oxobisdithiolene compounds show huge differences in the response of their redox potentials to rising or decreasing temperatures, depending on the substituents at the dithiolene group. The mnt2- compounds (1a, 1b) respond with decreasing redox potentials E(1/2) to rising temperatures whereas all other compounds show positive gradients deltaE/deltaT. In every case the values for the gradients for the tungsten compounds are greater than those for the molybdenum compounds. Six of the investigated compounds are known in the literature and two compounds were newly synthesized. These two new compounds include the pyrane subunit of the native molybdopterin ligand and should therefore be even better models for the active site of the molybdopterin containing enzymes. The molybdenum/tungsten pair with these new ligands shows a remarkably small difference for the redox potentials of the transition M(IV) <--> M(V) of only 30 mV at 25 degrees C and the reversion of the usual order with higher potentials for the molybdenum than the tungsten compound at a temperature of 70 degrees C; a temperature that is in the range where usually tungsten containing enzymes instead of molybdenum containing ones are found.

Binding Sites↗