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PubMed1971

Growth effects of vanadium in the rat.

Vanadium is necessary for growing rats raised inside trace elementcontrolled, all plastic isolators on a highly purified amino acid diet. Addifion of vanadium to the diet enhances growth by over 40 percent. A nearly optimum effect is obtained with 10 micrograms of vanadium per 100 grams of diet in (0.1 part per million), supplied in the form of sodium orthovanadate, as seen from series of tests with levels ranging from 1 to 5 micrograms per 100 grams of diet. Different vanadium compounds show different potencies: sodium orthovanadate was effective, metavanadate less active, and pyrovanadate without activity. Tetravalent vanadium, supplied as vanadyl sulfate or acetate, was utilized but produced smaller responses. The amounts of vanadium required are those normally found in tissues and nutrients.

Animals↗
PubMed1996

Molybdenum and vanadium do not replace tungsten in the catalytically active forms of the three tungstoenzymes in the hyperthermophilic archaeon Pyrococcus furiosus.

Three different types of tungsten-containing enzyme have been previously purified from Pyrococcus furiosus (optimum growth temperature, 100 degrees C): aldehyde ferredoxin oxidoreductase (AOR), formaldehyde ferredoxin oxidoreductase (FOR), and glyceraldehyde-3-phosphate oxidoreductase (GAPOR). In this study, the organism was grown in media containing added molybdenum (but not tungsten or vanadium) or added vanadium (but not molybdenum or tungsten). In both cell types, there were no dramatic changes compared with cells grown with tungsten, in the specific activities of hydrogenase, ferredoxin:NADP oxidoreductase, or the 2-keto acid ferredoxin oxidoreductases specific for pyruvate, indolepyruvate, 2-ketoglutarate, and 2-ketoisovalerate. Compared with tungsten-grown cells, the specific activities of AOR, FOR, and GAPOR were 40, 74, and 1%, respectively, in molybdenum-grown cells, and 7, 0, and 0%, respectively, in vanadium-grown cells. AOR purified from vanadium-grown cells lacked detectable vanadium, and its tungsten content and specific activity were both ca. 10% of the values for AOR purified from tungsten-grown cells. AOR and FOR purified from molybdenum-grown cells contained no detectable molybdenum, and their tungsten contents and specific activities were > 70% of the values for the enzymes purified from tungsten-grown cells. These results indicate that P. furiosus uses exclusively tungsten to synthesize the catalytically active forms of AOR, FOR, and GAPOR, and active molybdenum- or vanadium-containing isoenzymes are not expressed when the cells are grown in the presence of these other metals.

Aldehyde Oxidoreductases↗
PubMed2006

Insulin signal mimicry as a mechanism for the insulin-like effects of vanadium.

Among several metals, vanadium has emerged as an extremely potent agent with insulin-like properties. These insulin-like properties have been demonstrated in isolated cells, tissues, different animal models of type I and type II diabetes as well as a limited number of human subjects. Vanadium treatment has been found to improve abnormalities of carbohydrate and lipid metabolism and of gene expression in rodent models of diabetes. In isolated cells, it enhances glucose transport, glycogen and lipid synthesis, and inhibits gluconeogenesis and lipolysis. The molecular mechanism responsible for the insulin-like effects of vanadium compounds have been shown to involve the activation of several key components of insulin-signaling pathways that include the mitogen-activated-protein kinases (MAPKs) extracellular signal-regulated kinase 1/2 (ERK1/2) and p38MAPK, and phosphatidylinositol 3-kinase (PI3-K)/protein kinase B (PKB). It is interesting that the vanadium effect on these signaling systems is independent of insulin receptor protein tyrosine kinase activity, but it is associated with enhanced tyrosine phosphorylation of insulin receptor substrate-1. These actions seem to be secondary to vanadium-induced inhibition of protein tyrosine phosphatases. Because MAPK and PI3-K/PKB pathways are implicated in mediating the mitogenic and metabolic effects of insulin, respectively, it is plausible that mimicry of these pathways by vanadium serves as a mechanism for its insulin-like responses.

Animals↗
PubMedDate not supplied

Implications for the catalytic mechanism of the vanadium-containing enzyme chloroperoxidase from the fungus Curvularia inaequalis by X-ray structures of the native and peroxide form.

Implications for the catalytic mechanism of the vanadium-containing chloroperoxidase from the fungus Curvularia inaequalis have been obtained from the crystal structures of the native and peroxide forms of the enzyme. The X-ray structures have been solved by difference Fourier techniques using the atomic model of the azide chloroperoxidase complex. The 2.03 A crystal structure (R = 19.7%) of the native enzyme reveals the geometry of the intact catalytic vanadium center. The vanadium is coordinated by four non-protein oxygen atoms and one nitrogen (NE2) atom from histidine 496 in a trigonal bipyramidal fashion. Three oxygens are in the equatorial plane and the fourth oxygen and the nitrogen are at the apexes of the bipyramid. In the 2.24 A crystal structure (R = 17.7%) of the peroxide derivate the peroxide is bound to the vanadium in an eta2-fashion after the release of the apical oxygen ligand. The vanadium is coordinated also by 4 non-protein oxygen atoms and one nitrogen (NE2) from histidine 496. The coordination geometry around the vanadium is that of a distorted tetragonal pyramid with the two peroxide oxygens, one oxygen and the nitrogen in the basal plane and one oxygen in the apical position. A mechanism for the catalytic cycle has been proposed based on these X-ray structures and kinetic data.

Binding Sites↗
PubMed1976

The effect of pharmacological levels of dietary vanadium on the egg production, shell thickness and egg yolk cholesterol in laying hens and coturnix.

The addition of 100 p.p.m. of vanadium to a ration for White Leghorn laying hens caused a significant increase (p less than 0.01) in the egg shell thickness, but did not cause any significant change in the production, egg weight or egg ypok cholesterol content. The addition of 300 p.p.m. of vanadium caused a severe depression in the egg production which was the only symptom of vanadium toxicity to be observed. The addition of 50, 100, 200 or 300 p.p.m. vanadium to the ration of laying coturnix did not cause any significant change in egg production, egg weight, or egg yolk cholesterol content. The addition of the same levels of vanadium to one-day old male coturnix chicks did not cause any significant growth depression or mortality. We suggest that coturnix may be more resistant to vanadium toxicity than chickens.

Animals↗
PubMed2000

Differential modulation of xenobiotic metabolizing enzymes by vanadium during diethylnitrosamine-induced hepatocarcinogenesis in Sprague-Dawley rats.

Effect of vanadium on hepatic xenobiotic biotransformation in rats exposed to diethylnitrosamine (DENA, 200 mg/kg body weight, intraperitoneally) was investigated to elucidate a possible mechanism of vanadium mediated prevention of chemical carcinogenesis. Vanadium supplementation (0.5 ppm ad libitum with drinking water), at different phases before and after DENA treatment, significantly modulated the decrease in contents of total cytochrome P-450, cytochrome b5, activity of nicotinamide adenine dinucleotide phosphate (NADPH), (reduced form) cytochrome reductase, and uridine diphospho-glucuronyl transferase (UDPGT) in microsomal fractions of whole liver, hyperplastic nodules (HNs) and non nodular surrounding parenchyma (NNSP) as induced by DENA, 20 weeks following its administration. Supplementary vanadium had also substantial influence on the activities of cytosolic enzymes, like, uridine diphospho (UDP)-glucose dehydrogenase and NAD(P)H: quinone oxidoreductase (DT-diaphorase) in the concerned tissue which were observed to be remarkably decreased as a result of DENA treatment in comparison to that of the control counterparts. However, vanadium was found to have little or no effect on the lowering ofaryl hydrocarbon hydroxylase (AHH) activity by DENA administration. On the basis of significant modulation of DENA induced alterations in cytosolic and microsomal enzyme activity it can be presumed that the chemoprotective effect of vanadium might be mediated through elevation of phase II conjugating enzymes which in turn, lead to a move and shift of metabolic profile that reduces the intracellular concentration of carcinogen derived reactive intermediates.

Animals↗
PubMed1991

[Distribution of vanadium in tissues of nonpregnant and pregnant Wistar rats].

This paper reports tissue distribution of vanadium in nonpregnant and pregnant Wistar rats. The experimental results showed that vanadium concentrations in nonpregnant rats were respectively from high to low: I. no treatment: ovary greater than uterus greater than kidney greater than lung greater than heart muscle greater than spleen greater than brain greater than liver greater than blood; II. 4h after single i.p. injection of V2O5 (5 mg/kg): kidney greater than ovary greater than liver greater than bone greater than uterus greater than lung greater than heart muscle greater than spleen greater than brain greater than blood. The results suggest that female genital organs are important organs in distribution of vanadium. The kidney is a main excretory organ. After 24h of treatment, a larger amount of vanadium in body has been excreted. Vanadium can pass through blood-brain barrier. Distribution of vanadium on gestation days 12 after 4h single i.p. injection of V2O5 (5 mg/kg) is: kidney greater than ovary greater than uterus greater than placenta greater than liver greater than fetus greater than bone greater than heart muscle greater than lung greater than brain greater than spleen greater than blood; on gestation days 16-18 after 4h single i.p. injection of V2O5 (5 mg/kg) is: kidney ovary greater than placenta greater than lung greater than bone greater than uterus greater than heart muscle greater than spleen greater than fetus greater than liver greater than brain greater than blood; after 24h (on gestation days 16-18) is: kidney greater than ovary greater than placenta greater than spleen greater than bone greater than lung greater than liver greater than fetus heart muscle greater than brain blood.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

[Quantitation of manganese and vanadium levels in the lung of "normal" and occupationally exposed persons].

Manganese and vanadium concentrations were measured in the lung and in hilus tissue of 30 non-exposed and 10 occupationally exposed patients. The analyses were performed by electrothermal atomic absorption spectrometry with Zeeman background compensation after wet oxidative digestion. The pulmonary tissue sampling of 30 non-exposed persons was carried out in terms of topographic anatomical criteria from different lung segments and lobes, resp. The manganese concentrations vary between 70 and 360 ng/g, and for vanadium between 9 and 40 ng/g in relation to wet weight. On the average manganese concentrations are 3 to 5 times higher compared to vanadium concentrations, 2 to 4 times higher values were detected in hilus tissue compared to the lung parenchyme. With regard to the topographic anatomy 1.1 to 1.5 higher manganese and vanadium concentrations have been found in the upper lung areas. In 10 of the occupationally exposed persons the sampling was taken from various segments as far as available. In some cases only one lung tissue sample could be analysed. Two former high-grade steel welders and eight former workers from a Norwegian nickel refinery have been investigated. Esp. the manganese concentrations in lung tissue of the welders raised by the factor 100. The manganese content in other occupationally exposed persons has also been increased in comparison to the normal group whereas the vanadium concentrations were - with one exception - in the normal range. Synoptically these results demonstrate that the determination of manganese and vanadium concentrations in the lung tissue might give additional information especially concerning a former occupational exposure. Such investigations can also be of interest when giving medical expertise opinion.

Humans↗
PubMed1989

Improved determination of vanadium in biological fluids by electrothermal atomic absorption spectrometry.

We made sensitive and accurate electrothermal atomic absorption spectrometric measurements of vanadium in small volumes of serum. The wet-digested sample was extracted into an organic solvent, with N-benzoyl-N-(o-tolyl)hydroxylamine (BTA) as the chelating reagent. After evaporating the solvent, we dissolved the residue in acetic acid, and injected a 60-microL aliquot into a graphite furnace. In this way we could measure vanadium concentrations as low as 80 ng/L in 4 mL of serum. The within-run CV was 3.3% for serum, 7.7% for urine. Analytical recoveries of vanadium added to serum and urine were 90.3% and 90.8%, respectively. We measured vanadium concentrations in sera from 64 healthy persons (group 1), 15 nondialyzed uremic patients (group 2), and 11 hemodialyzed patients (group 3). The highest concentration of vanadium in group 1 was 240 ng/L; about 60% of the values for this group were less than 80 ng/L. In group 3, the vanadium concentrations were extremely high (15 +/- 14.2 micrograms/L, mean +/- SD), less so (but still above normal) in group 2 (1.58 +/- 3.16 micrograms/L).

Adult↗
PubMed1998

[Genotoxic effects of vanadium compounds].

Vanadium is a metal member of the periodic table VB group, with atomic weight 59.95 and atomic number 23 and it has some oxidizing states from -1 to +5. Vanadium has many industrial uses and its contribution with environmental contamination is growing every day. In the last 10 years research about the vanadium effects on living beings, has been increasing substantially, due to its presence in the environment from different sources. Interest for vanadium and their compounds is because its toxic effects and uses in some biomedical areas: such as antineoplastic, cholesterol and glucose level blood, diuretic, oxygen haemoglobin affinity. Vanadium toxic effects are so due to the fact of its property of inhibiting many enzymatic systems. Vanadate and vanadyl ions make chemical complexes exhibiting the property of inhibiting or increasing the activity of the enzymes participating in the DNA and RNA synthesis. They also induce mutagenic and genotoxic effects. Biochemical assays show cytotoxic effects, increase in the cellular differentiation, gene expression alterations and other biochemical and metabolic alterations. Research has been done with in vitro systems, but few with laboratory animals. It is necessary to carry out more work in the field of genetic toxicology with vanadium compounds. This type of compounds may be considered mutagenic and genotoxic, with cytotoxic and aneuploidogenous effects.

Animals↗
PubMed2002

Vanadium increases GLUT4 in diabetic rat skeletal muscle.

The effect of vanadium in lowering blood glucose in diabetic animals is well established; however, the exact mechanism of action of vanadium still eludes us. There are several reports from in vitro studies indicating that vanadium increases enzyme activity in insulin signalling pathways; however, these findings have not been duplicated in vivo. Glucose transporters (GLUT) have a major role to play in any glucoregulatory effects. Insulin dependent GLUT4 is a major glucose transporter present in skeletal muscle, adipocytes and heart. In the present study we found that the plasma glucose in streptozotocin (STZ) diabetic animals was restored to normal following treatment with a single dose of BMOV, an organic vanadium compound, given by oral gavage (0.6 mmol/kg), similar to the response with chronic BMOV treatment. The response to BMOV by oral gavage was rapid and the animals were normoglycemic within 24 h of treatment and still demonstrated a significant effect even after 72 h. Using a specific antibody against GLUT4 we found an overall reduction in the GLUT4 in the total membrane fraction in skeletal muscle of diabetic animals. However, with a single dose of BMOV the GLUT4 level was restored to normal. This is the first report that establishes a direct effect of vanadium on the regulation of GLUT4 expression in diabetic animals in vivo, and may at least partially explain the glucoregulatory effects of vanadium.

Animals↗
PubMed2006

Laboratory-evolved vanadium chloroperoxidase exhibits 100-fold higher halogenating activity at alkaline pH: catalytic effects from first and second coordination sphere mutations.

Directed evolution was performed on vanadium chloroperoxidase from the fungus Curvularia inaequalis to increase its brominating activity at a mildly alkaline pH for industrial and synthetic applications and to further understand its mechanism. After successful expression of the enzyme in Escherichia coli, two rounds of screening and selection, saturation mutagenesis of a "hot spot," and rational recombination, a triple mutant (P395D/L241V/T343A) was obtained that showed a 100-fold increase in activity at pH 8 (k(cat) = 100 s(-1)). The increased K(m) values for Br(-) (3.1 mm) and H(2)O(2) (16 microm) are smaller than those found for vanadium bromoperoxidases that are reasonably active at this pH. In addition the brominating activity at pH 5 was increased by a factor of 6 (k(cat) = 575 s(-1)), and the chlorinating activity at pH 5 was increased by a factor of 2 (k(cat) = 36 s(-1)), yielding the "best" vanadium haloperoxidase known thus far. The mutations are in the first and second coordination sphere of the vanadate cofactor, and the catalytic effects suggest that fine tuning of residues Lys-353 and Phe-397, along with addition of negative charge or removal of positive charge near one of the vanadate oxygens, is very important. Lys-353 and Phe-397 were previously assigned to be essential in peroxide activation and halide binding. Analysis of the catalytic parameters of the mutant vanadium bromoperoxidase from the seaweed Ascophyllum nodosum also adds fuel to the discussion regarding factors governing the halide specificity of vanadium haloperoxidases. This study presents the first example of directed evolution of a vanadium enzyme.

Ascomycota↗
PubMed2005

Ferromagnetism and Curie temperature of Vanadium-doped nitrides.

Electronic structures, exchange interaction mechanism between magnetic ions and Curie temperature of Vanadium-doped nitrides (AlN, GaN, and InN) are studied within KKR-LSDA-CPA. It is found that the ferromagnetic super-exchange interaction mechanism is dominant at low concentrations of Vanadium, but the anti-ferromagnetic super-exchange interaction appears and reduces the stabilization of ferromagnetism at sufficiently high concentrations (x > 0.10), especially for Vanadium-doped AlN and Vanadium-doped GaN. The estimation of the Curie temperature within the mean field approximation shows the Curie temperature of Vanadium-doped nitrides exceeding room temperature with a few constituents of Vanadium.

Journal Article↗
PubMed1999

Structural chemistry of vanadium oxides with open frameworks.

The present work is dedicated to a crystal-chemical and topographical analysis of vanadium oxides with open structures. The review covers, apart from a few exceptions, only pure vanadium oxide structures with vanadium in oxidation states greater than +3. Purely tetrahedral frameworks are not discussed because of their traditional, well known crystal chemistry and only a few examples of cluster compounds are provided. Structural classification and notation of vanadium oxide frameworks are proposed based on the following scheme: polyhedra --> chain --> layer --> three-dimensional framework. Thus, approximately 60 types of vanadium oxide frameworks are divided into five classes by type of coordination polyhedra present and into 14 subclasses by a more complex structural formation. Details are also given of the analysis of vanadium-oxygen coordination polyhedra and their metamorphosis: tetrahedron-trigonal bipyramid-square pyramid-octahedron, as well as the combinatorial deduction of possible structures for the most common framework types.

Journal Article↗
PubMedDate not supplied

Glucose-lowering effects of a new organic vanadium complex, bis(maltolato)oxovanadium(IV).

Inorganic vanadium has been shown, both in vivo and in vitro, to have insulin-mimetic properties. A new organic vanadium complex, bis(maltolato)oxovanadium(IV) (BMOV), was developed to increase the absorption of vanadium from the gastrointestinal tract, thereby reducing the dose of vanadium necessary to produce glucose-lowering effects. BMOV was administered in the drinking water for 25 weeks to control and streptozotocin-induced diabetic, male Wistar rats. BMOV treatment produced a stable euglycemic state in 70% of diabetic treated animals. The other 30% of the diabetic treated animals demonstrated fluctuations in glucose control over the entire study period. The initial effective dose of BMOV was 0.45 mmol/kg, which decreased to an effective maintenance dose of 0.18 mmol/kg, significantly lower than the dose of inorganic vanadium salts used in previous studies. BMOV treatment did significantly reduce fluid consumption levels in control treated animals after 10 weeks of therapy; however, the food consumption for control treated animals was only intermittently lower than that for controls. Plasma cholesterol and triglyceride levels were normalized with BMOV treatment for all diabetic treated animals, without a concomitant increase in plasma insulin levels. An oral glucose tolerance test demonstrated that glucose homeostasis in control-treated animals occurred at significantly lower plasma insulin levels than in control animals. BMOV effectively produced the glucose-lowering effects at significantly lower dose than previously used for inorganic vanadium salts, without any overt signs of toxicity.

Animals↗
PubMed2000

Biochemical and morphological study on liver Golgi complex in streptozotocin-diabetic and control rats treated with bis(kojato)oxovanadium(IV) [VO(ka)2]x2H2O. Part II. Prolonged treatmentwith vanadium compound.

In this study oral treatment with bis(kojato)oxovanadium(IV) solution was administered twice. The first, short vanadium treatment (so called pretreatment) was used to accustom animals to the flavour of this liquid. After 2-2.5 weeks the second treatment, in high concentration and for a longer time served as a "drug". The physiological parameters such as weights of animals and their livers, reduction of liquid and food intake were lower than in control. Activity of Golgi marker enzyme GalT was significantly lower in both vanadium treated groups (p < 0.01), but in diabetic vanadium treated group it was higher, albeit not significantly, than in control vanadium treated rats. The morphology of Golgi complexes in diabetic rats on prolonged vanadium treatment was similar to that in the one week treated rats (see Part I). Rounded stacks of cisternae characteristic of untreated streptozotocin (STZ)-diabetes were also seen in vanadium treated diabetic rats, but in comparison with untreated diabetic livers, the secretory activities of Golgi complexes were preserved or even stimulated.

Administration, Oral↗
PubMed1990

Peripheral erythrocyte levels, hemolysis and three vanadium compounds.

Three vanadium compounds of different valence states were administered to adult mice. Two, four, and eight days following treatment of vanadium, cardiac blood was collected. The blood sample was used to ascertain the peripheral erythrocyte count (cell/mm3) and to determine the in vitro hemolytic index of erythrocytes obtained from mice treated in vivo with either the tri-, tetra-, or pentavalent vanadium compound. Data indicate that the tetravalent form was the most effective test substance in 1) promoting rupture of isolated erythrocytes compared to red cells retrieved from control mice and 2) depressing the erythrocyte count obtained from heart blood; maximum effects were manifest four days post-treatment. For all treatments there appeared to be a good correlation between the degree of vanadium-induced hemolysis and the peripheral erythrocyte count reduction following exposure to the vanadium.

Analysis of Variance↗
PubMed2002

Influence of chelation and oxidation state on vanadium bioavailability, and their effects on tissue concentrations of zinc, copper, and iron.

Today, vanadium compounds are frequently included in nutritional supplements and are also being developed for therapeutic use in diabetes mellitus. Previously, tissue uptake of vanadium from bis(maltolato)oxovanadium(IV) (BMOV) was shown to be increased compared to its uptake from vanadyl sulfate (VS). Our primary objective was to test the hypothesis that complexation increases vanadium uptake and that this effect is independent of oxidation state. A secondary objective was to compare the effects of vanadium complexation and oxidation state on tissue iron, copper, and zinc. Wistar rats were fed either ammonium metavanadate (AMV), VS, or BMOV (1.2 mM each in the drinking water). Tissue uptake of V following 12 wk of BMOV or AMV was higher than that from VS (p < 0.05). BMOV led to decreased tissue Zn and increased bone Fe content. The same three compounds were compared in a cellular model of absorption (Caco-2 cells). Vanadium uptake from VS was higher than that from BMOV or AMV at 10 min, but from BMOV (250 microM only, 60 min), uptake was far greater than from AMV or VS. These results show that neither complexation nor oxidation state alone are adequate predictors of relative absorption, tissue accumulation, or trace element interactions.

Animals↗