[Vanadium and experimental caries. VI. Spectrochemical study on the effect of vanadium on teeth in golden hamsters treated with escalated doses of vanadium in drinking water].
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Glutathione transferases with vanadium-binding activity isolated from the vanadium-rich ascidian Ascidia sydneiensis samea.
Some ascidians accumulate vanadium in vanadocytes, which are vanadium-containing blood cells, at high levels and with high selectivity. However, the mechanism and physiological significance of vanadium accumulation remain unknown. In this study, we isolated novel proteins with a striking homology to glutathione transferases (GSTs), designated AsGST-I and AsGST-II, from the digestive system of the vanadium-accumulating ascidian Ascidia sydneiensis samea, in which the digestive system is thought to be involved in vanadium uptake. Analysis of recombinant AsGST-I confirmed that AsGST-I has GST activity and forms a dimer, as do other GSTs. In addition, AsGST-I was revealed to have vanadium-binding activity, which has never been reported for GSTs isolated from other organisms. AsGST-I bound about 16 vanadium atoms as either V(IV) or V(V) per dimer, and the apparent dissociation constants for V(IV) and V(V) were 1.8 x 10(-4) M and 1.2 x 10(-4) M, respectively. Western blot analysis revealed that AsGSTs were expressed in the digestive system at exceptionally high levels, although they were localized in almost all organs and tissues examined. Considering these results, we postulate that AsGSTs play important roles in vanadium accumulation in the ascidian digestive system.
Amino Acid Sequence↗
A stochastic exposure assessment model to estimate vanadium intake by beef cattle used as sentinels for the South African vanadium mining industry.
This paper presents an environmental exposure assessment model for estimating chronic intake of vanadium (a transition metal) by cattle farmed extensively in areas contaminated by vanadium pollutants. The exposure model differs from most other models in several ways: (1) it does not rely heavily on extrapolating information from the point source (e.g. stack height, exit velocity, exit diameter) to the point of exposure. (2) It incorporates the physiological constraints of the species exposed. (3) It takes into account oral as well as inhalation exposure. (4) It addresses terrain, by using measurements at the point of exposure. (5) It accounts for existing background concentrations of pollutants and pollutants from multiple sources. (6) It uses a stochastic process with distribution functions to account for variability in the data over time. Environmental inputs into the model included aerial fall-out sample vanadium (n=566), unwashed grass sample vanadium (n=342) and soluble soil sample vanadium (n=342). Physiological cattle inputs were derived from two cohorts of Brahman-cross sentinel cattle (n=30). The model provided an estimate of the chronic external exposure dose of vanadium for two separate groups of cattle grazing over a 5-year period (1999-2004) immediately adjacent (median dose=2.14mg vanadium/kg body weight/day) and 2km away (median dose=1.07mg/kg/day) from a South African vanadium-processing plant, respectively. The final output of the model is a distribution curve of the probable vanadium intake based on the variability within the inputs over the 5-year period of the study. The model is adaptable enough for application to other transition metals and species (including man), and could be used as an alternative to plume-dispersion modelling.
Air Pollutants↗
Vanadium chemistry and biochemistry of relevance for use of vanadium compounds as antidiabetic agents.
The stability of 11 vanadium compounds is tested under physiological conditions and in administration fluids. Several compounds including those currently used as insulin-mimetic agents in animal and human studies are stable upon dissolution in distilled water but lack such stability in distilled water at pH 7. Complex lability may result in decomposition at neutral pH and thus may compromise the effectiveness of these compounds as therapeutic agents; Even well characterized vanadium compounds are surprisingly labile. Sufficiently stable complexes such as the VEDTA complex will only slowly reduce, however, none of the vanadium compounds currently used as insulin-mimetic agents show the high stability of the VEDTA complex. Both the bis(maltolato)oxovanadium(IV) and peroxovanadium complexes extend the insulin-mimetic action of vanadate in reducing cellular environments probably by increased lifetimes under physiological conditions and/or by decomposing to other insulin mimetic compounds. For example, treatment with two equivalents of glutathione or other thiols the (dipicolinato)peroxovanadate(V) forms (dipicolinato)oxovanadate(V) and vanadate, which are both insulin-mimetic vanadium(V) compounds and can continue to act. The reactivity of vanadate under physiological conditions effects a multitude of biological responses. Other vanadium complexes may mimic insulin but not induce similar responses if the vanadate formation is blocked or reduced. We conclude that three properties, stability, lability and redox chemistry are critical to prolong the half-life of the insulin-mimetic form of vanadium compounds under physiological conditions and should all be considered in development of vanadium-based oral insulin-mimetic agents.
Hypoglycemic Agents↗
Effect of vanadium on bone metabolism in weanling rats: zinc prevents the toxic effect of vanadium.
The effect of vanadium on bone metabolism was investigated in the femoral diaphysis of weanling rats. Vanadium pentoxide (1.0-20.0 mumol V/100 g b.wt.) was administered orally for 3 days. The doses of 15.0 and 20.0 mumol V/100 g caused a significant increase in serum calcium concentration. Bone alkaline phosphatase activity was increased significantly by the doses of 1.0-20.0 mumol V/100 g, while bone acid phosphatase activity was not altered significantly. Bone DNA content was increased significantly by the dose of 1.0-10.0 mumol V/100 g. Bone calcium content was not altered significantly by administration of vanadium. The increase in serum calcium concentration caused by administration of vanadium (20.0 mumol/100 g) was prevented completely by simultaneous injection of zinc sulfate (15.3 mumol Zn/100 g) for 3 days, although zinc alone did not have any effect. Administration of zinc (15.3 mumol/100 g) produced an appreciable increase in bone alkaline phosphatase activity, DNA content, and calcium content. These increases were not enhanced significantly by simultaneous injection of vanadium (2.0 and 20.0 mumol V/100 g). The present study indicates that a comparatively low dose of vanadium may play a nutritional role in bone formation of weanling rats, and that zinc can prevent the relevation of the toxic effect of vanadium with higher doses.
Acid Phosphatase↗
Speciation and preconcentration of vanadium(V) and vanadium(IV) in water samples by flow injection-inductively coupled plasma optical emission spectrometry and ultrasonic nebulization.
An on-line separation, preconcentration and determination system for vanadium(IV) and vanadium(V) comprising inductively coupled plasma optical emission spectrometry (ICP-OES) coupled to a flow injection (FI) method with an ultrasonic nebulization (USN) system was studied. The vanadium species were retained on an Amberlite XAD-7 resin as a vanadium-2-(5-bromo-2-pyridylazo)-5-diethylaminophenol (V-5-Br-PADAP) complex at pH 3.7. Enhanced selectivity was obtained with the combined use of the formation on-line of the complexes and 1,2-cyclohexanediaminetetraacetic acid (CDTA) as masking agent. The vanadium complexes were removed from the microcolumn with 25% v/v nitric acid. A sensitivity enhancement factor of 225 was obtained with respect to ICP-OES using pneumatic nebulization (15-fold for USN and 15-fold for the microcolumn). The detection limit for the preconcentration of 10 mL of aqueous solution was 19 ng L-1. The precision for 10 replicate determinations at the 5 micrograms L-1 V level was 2.3% relative standard deviation (RSD), calculated from the peak heights obtained. The calibration graph using the separation and preconcentration system for vanadium species was linear with a correlation coefficient of 0.9992 at levels from near the detection limits up to at least 100 micrograms L-1. The method was successfully applied to the speciation of vanadium in river water samples.
Flow Injection Analysis↗
Organic vanadium chelators potentiate vanadium-evoked glucose metabolism in vitro and in vivo: establishing criteria for optimal chelators.
Several ligands, when complexed with vanadium, potentiate its insulinomimetic activity both in vivo and in vitro. We have recently found that L-Glu-gamma-monohydroxamate (HXM) and L-Asp(beta)HXM were especially potent in this regard. In the present study, we used vanadium-enriched adipose cells and cell-free experimental systems to determine the features of L-Glu(gamma)HXM and L-Asp(beta)HXM that turn these ligands into optimal-synergizing vanadium chelators. We found that L-Glu(gamma)HXM and L-Asp(beta)(HXM) possess the following characteristics: 1) They associate with vanadium(+5) at pH 7.2 within a narrow range of an apparent formation constant of 1.3 to 1.9 x 10(2) M(-1); 2) they have nearly the same binding affinity for the vanadyl(+4) cation and the vanadate(+5) anion at physiological pH values; and 3) they form intense ultraviolet absorbing complexes upon associating with vanadium(+4) at 1 and 3 M stoichiometry, respectively, at pH 3.0. Vanadium ligands lacking any of these three defined criteria synergize less effectively with vanadium to activate glucose metabolism.
Adipocytes↗
Vanadium distribution in rats and DNA cleavage by vanadyl complex: implication for vanadium toxicity and biological effects.
Vanadium ion is toxic to animals. However, vanadium is also an agent used for chemoprotection against cancers in animals. To understand both the toxic and beneficial effects we studied vanadium distribution in rats. Accumulation of vanadium in the liver nuclei of rats given low doses of compounds in the +4 or +5 oxidation state was greater than in the liver nuclei of rats given high doses of vanadium compounds or the vanadate (+5 oxidation state) compound. Vanadium was incorporated exclusively in the vanadyl (+4 oxidation state) form. We also investigated the reactions of vanadyl ion and found that incubation of DNA with vanadyl ion and hydrogen peroxide (H2O2) led to intense DNA cleavage. ESR spin trapping demonstrated that hydroxyl radicals are generated during the reactions of vanadyl ion and H2O2. Thus, we propose that the mechanism for vanadium-dependent toxicity and antineoplastic action is due to DNA cleavage by hydroxyl radicals generated in living systems.
Animals↗
Accumulation of vanadium during embryogenesis in the vanadium-rich ascidian, Ascidia gemmata.
It is a remarkable and previously unrecognized fact that ascidians, which are known to contain high levels of vanadium in their blood cells, begin to accumulate vanadium during embryogenesis. This study revealed that the accumulation starts quite dramatically 2 wk after fertilization, and 2 mo later, the amount of vanadium in larvae is 600,000 times higher than that in the unfertilized egg. These results were obtained by neutron activation analysis, a highly sensitive method for determining levels of vanadium, in the Ascidia gemmata, the ascidian that contains the highest known levels of vanadium and accumulates vanadium at 150 mM in its blood cells, a concentration that corresponds to 4,000,000 times the concentration in seawater.
Animals↗
Reaction of vanadium(V) with thiols generates vanadium (IV) and thiyl radicals.
The in vivo toxicity of vanadium(V) has been found to correlate with the depletion of cellular glutathione and related non-protein thiols. With a view to understanding the mechanism for this observation, we have investigated the oxidation of glutathione, cysteine N-acetylcysteine and penicillamine by vanadium(V), using electron spin resonance (ESR) and ESR spin trapping methodology. The spin trap used was 5,5-dimethyl-1-pyrroline 1-oxide (DMPO). It is found that the oxidation of these thiols by vanadium(V) generates the corresponding thiyl radicals and vanadium- (IV) complexes. The results suggest that free radical reactions play a significant role in the depletion of cellular thiols by vanadium(V) and hence in vanadium(V) toxicity.
Electron Spin Resonance Spectroscopy↗
Distribution of vanadium(V) species between soil and plants in the vicinity of vanadium mine.
The distribution of vanadium(V) species between soil and plants around the vanadium mine have been studied. The mine dam spilled water around this area after collapsing some time ago. V(V) species were determined by electrothermal atomic absorption spectrometry (ETAAS) after leaching of vanadium(V) compounds with 0.1M of Na2CO3, with a limit of detection 0.2 microg g(-1). The validity of V(V) determination had been confirmed by the spike recovery and of the total amount of vanadium by the analysis of CRM's with good correspondence of found to certified values. The concentration of V(V) species were found to be in the range of 620-1680 microg g(-1) in soil and 4-6 microg g(-1) in grass samples, respectively. The total amount of vanadium in soil varied from 1570 to 3600 microg g(-1) and from 8 to 13 microg g(-1) in grass. The results indicate that considerable amount of vanadium (about 50%) in soils and plants is present as V(V) species.
Carbonates↗
pH-dependent investigations of vanadium(V)-peroxo-malate complexes from aqueous solutions. In search of biologically relevant vanadium(V)-peroxo species.
The established biochemical potential of vanadium has spurred considerable research interest in our lab, with specific focus on pertinent synthetic studies of vanadium(III) with a biologically relevant, organic, dicarboxylic acid, malic acid, in aqueous solutions. Simple reactions between VCl3 and malic acid in water, at different pH values, in the presence of H2O2, led to the crystalline dimeric complexes (Cat)4[VO(O2)(C4H3O5)]2*nH2O (Cat = K+, n = 4, 1; Cat = NH4+, n = 3, 2) and K2[VO(O2)(C4H4O5)]2*2H2O (3). All three complexes were characterized by elemental analysis, FT-IR, and UV/visible spectroscopies. Compound 1 crystallizes in the monoclinic space group P2(1)/c, with a = 8.380(5) A, b = 9.252(5) A, c = 13.714(8) A, beta = 93.60(2) degrees, V = 1061(1) A3, and Z = 4. Compound 2 crystallizes in the triclinic space group P1, with a = 9.158(4) A, b = 9.669(4) A, c = 14.185(6) A, alpha = 104.81(1) degrees, beta = 90.31(1) degrees, gamma = 115.643(13) degrees, V = 1085.0(7) A(3), and Z = 2. Compound 3 crystallizes in the monoclinic space group P2(1)/c, with a = 9.123(8) A, b = 9.439(8) A, c = 10.640(9) A, beta = 104.58(3) degrees, V = 887(1) A3, and Z = 2. The X-ray structures showed that, in 1 and 2, the dimers consist of two (V(V)=O)2O2 rhombic units to which two malate ligands are attached. The ligands are triply deprotonated and, as such, they coordinate to vanadium(V), promoting a pentagonal bipyramidal geometry. In 3, the dimeric (V(V)=O)2O2 rhombic unit persists, with the two doubly deprotonated malate ligands coordinated to the vanadium(V) ions. UV/vis and EPR spectroscopic studies on the intermediate blue solutions of the synthesis reactions of 1-3 support the existence of vanadyl-containing dimeric species. These species further react with H2O2 to yield oxidation of V(IV)2O2 to V(V)2O2 and coordination of the peroxide to vanadium(V). From the collective data on 1-3, it appears that pH acts as a decisive factor in dictating the structural features of the isolated complexes. The details of the introduced structural differentiation in the reported complexes, and their potential relevance to vanadium(V) dicarboxylate systems in biological media are dwelled on.
Crystallography, X-Ray↗
Vanadium levels in French and Californian wines: influence on vanadium dietary intake.
An accurate and reproducible method for direct determination of vanadium (V) in wine using graphite furnace atomic absorption spectrometry (GFAAS) is described. This method gave results insignificantly different from those obtained using dry mineralization of wine samples, with a detection limit of 42 pg. A total of 68 wine samples from different regions of France and California were analysed. Vanadium levels ranged from 7.0 to 90.0 micrograms/l in red and from 6.6 to 43.9 micrograms/l in white wines. The method was also adapted to the determination of vanadium levels in 12 grape samples from different varieties after acid mineralization. Vanadium content varied from 2 to 17 micrograms/kg for white and from 5 to 11 micrograms/kg for red varieties. Our data indicate that wine storage conditions may increase vanadium content. The contribution of wine consumption to daily vanadium dietary intake of the French population was estimated to be 11 micrograms/day per individual.
Canada↗
Localization of vanabins, vanadium-binding proteins, in the blood cells of the vanadium-rich ascidian, Ascidia sydneiensis samea.
Some species of the family Ascidiidae accumulate vanadium in concentrations in excess of 350 mM, which is about 10 (7)-fold higher than the concentration of vanadium in seawater. In these species, signet ring cells with a single large vacuole in which vanadium ions are contained function as vanadium-accumulating cells. These have been termed vanadocytes. We recently isolated five vanadium-binding proteins, which we named Vanabin1, Vanabin2, Vanabin3, Vanabin4, and VanabinP, from vanadocytes of the vanadium-rich ascidian Ascidia sydneiensis samea. In this study, we analyzed localization of the Vanabins in the blood cells of A. sydneiensis samea using monoclonal antibodies and confocal microscopy. The Vanabin1 and Vanabin2 proteins were found in the cytoplasm and/or in some organelles of vanadocytes. Vanabin3 was also detected in the cytoplasm, while Vanabin4 was found exclusively in the cytoplasmic membrane.
Amino Acid Sequence↗
[Transplacental passage of vanadium after treatment with vanadium pentoxide in Wistar rat].
The passage of vanadium pentoxide across the placenta into the embryo/fetus was investigated by analyzing the vanadium content in embryo/fetus at various intervals between 1 h and 48 h after treatment of pregnant Wistar rats with single dose of the V2O5 (5mg/kg) on days 16-18 of gestation, at 4h after treatment of pregnant rats with single dose of V2O5 (5mg/kg) on day 12, and at 120 h after treatment of pregnant rats with dose of V2O5 0.33, 1.0, 3.0 mg/kg on days 6 through 15. The V concentration was determined by catalytic polarography. At after treatment on day 12, the V concentrations in maternal blood, placenta and embryos were elevated in comparison with those of the untreated group. At 4-48 h after treatment on days 16-18, the V concentrations in placenta and fetuses were elevated in comparison with those of the untreated group. The V concentration at 4 h after treatment in various tissues is the highest one among different time points. On days 16-18, 4 h after treatment, the V concentration in placenta was elevated in comparison with that on day 12 of gestation, but the V concentration in embryo/fetus was decreased. At 120 h after treatment on days 6-15, the V concentration in fetus is still high in comparison with that of the untreated group. The V content of fetus varied according to doses, suggesting that embryo/fetus accumulates vanadium. The results showed that vanadium can pass through the placental barrier and enter the embryo/fetus during the embryonal organogenesis in rat, but placenta accumulates vanadium, and the barrier action increases with placental maturity.
Animals↗
Model investigations for vanadium-protein interactions: vanadium(III) compounds with dipeptides and their oxovanadium(IV) analogues.
The reaction of VCl(3) with 1,10-phenanthroline and a series of dipeptides (H(2)dip), having aliphatic as well as aromatic side chains, in methyl alcohol and in the presence of triethylamine affords vanadium(III) compounds of the general formula [V(III)(dip)(MeOH)(phen)]Cl. Aerial oxidation/hydrolysis of the vanadium(III) species gives their oxovanadium(IV) analogues of the general formula [V(IV)O(dip)(phen)]. X-ray crystallographic characterization of the [V(IV)O(dip)(phen)] compounds (where dip(2-)=Gly- L-Ala, Gly- L-Val and Gly- L-Phe) revealed that the vanadium atom possesses a severely distorted octahedral coordination and is ligated to a tridentate dip(2-) ligand at the N(amine) atom, the deprotonated N(peptide) atom and one of the O(carboxylate) atoms, as well as an oxo group and two phenanthroline nitrogen atoms. Circular dichroism characterization of the V(III)/V(IV)O(2+)-dipeptide compounds revealed a strong signal for the V(IV)O(2+) species in the visible range of the spectrum, with a characteristic pattern which may be exploited to identify the N(am), N(pep) and O(car) ligation of a peptide or a protein to V(IV)O(2+) center, and a weak Cotton effect of opposite sign to their vanadium(III) analogues. The visible spectra of the V(III)-dipeptide compounds revealed two d-d bands with high intensity, thus indicating that the covalency of the metal-donor atoms is significant, i.e. the vanadium d orbitals are significantly mixed with the ligand orbitals, and this is confirmed by the low values of their Racah B parameters. The high-intensity band of the V(IV)O(2+)-dipeptide compounds at approximately 460 nm implies also a strong covalency of the metal with the equatorial donor atoms and this was supported by the EPR spectra of these compounds. Moreover, the V(III)/V(IV)O(2+)-dipeptide complexes were characterized by EPR and IR spectroscopies as well as conductivity and magnetic susceptibility measurements.
Circular Dichroism↗
Vanadium in ascidians: changes in vanadium coordination and oxidation state upon cell lysis.
Changes in vanadium coordination during cell lysis have been followed by EPR spectroscopy of the blood cells of the phleborbranch ascidians Ascidia ceratodes and PHallusia julinea. The spectra obtained for A. ceratodes whole blood samples can be mainly ascribed to aquated oxovanadium(IV) in which the signals are broadened in freshly frozen blood relative to when the cells are lysed by thawing. The sources of this broadening are discussed and it is shown that the oxovanadium(IV) signal has its origin in a small percentage of damaged or lysed cells which release vanadium into a low sulfate, low acid environment in fresh samples. When thawed, the cells lyse releasing acid and sulfate into the environment of the oxovanadium(IV), with consequent narrowing of the EPR spectral linewidth. Freshly frozen P. julinea blood cell samples have EPR spectra with parameters intermediate between aquated oxovanadium(IV) and the "type I" parameters observed in a previous investigation of tissue samples of this species (S. G. Brand, C. J. Hawkins, A. T. Marshall, G. W. Nette, and D. L. Parry, Comp. Biochem. Physiol. 93B, 425 (1989)). A. ceratodes tissue samples also have EPR spectra that differ from that of the blood. It is suggested that EPR studies on tissue samples are more indicative of the resting state of vanadium in the cells as there is more physiological material to provide a pH buffering effect to stabilize the cells. Schemes are presented which incorporate all of the EPR observations in ascidian literature, where cellular lysis is proposed to be accompanied by vanadium undergoing oxidation and a series of chelate exchanges from a "type I" complex to aquated oxovanadium(IV). Protons released during these exchanges are suggested to provide the acidity characteristic of blood cell lysates. The biological implications of the concomitant release of vanadium and tunichrome (S. W. Taylor, D. L. Parry, C. J. Hawkins, and J. H. Swinehart, Comp. Biochem. Physiol. 106A, 531 (1993)) from the blood cells, to the process of wound repair are discussed.
Animals↗
Relationships between iron and vanadium metabolism: the exchange of vanadium between transferrin and ferritin.
The study of possible relationships between iron and vanadium metabolism (E. Sabbioni and E. Marafante, Proc. XIth Int. Conf. Biochem., 13-5-R122, Toronto, Canada) was extended to the vanadium in the biochemical mechanisms which involve the exchange of iron between transferrin and ferritin. The transfer of vanadium between transferrin and ferritin was investigated using 48V radiotracer and gel filtration technique. 48V labeled human transferrin and horse spleen ferritin, 48V plasma from rats injected with 48VO2+, unlabelled rat liver cytosol, and plasma were used as sources of the two proteins for their incubation under different conditions. The results show that the equilibrium: V - transferrin in equilibrium V - ferritin occurs in vitro at physiological pH under the conditions of this experiment. No transfer of vanadium between the two proteins, however, occurs when they are incubated simply in a buffer at pH = 7.4. The maximum transfer was observed when transferrin and ferritin were mixed in their natural environments such as plasma and liver cytosol. This suggests that the exchange of the vanadium between the two proteins is affected by biochemical factors which are present in the body. A brief evaluation of the significance on the very low amounts of the element exchanged between the two proteins is also presented.
Animals↗