Disease relevance of vanadium

• Structural genes for the vanadium nitrogenase from Azotobacter chroococcum [1].
• Vanadium stimulates the (Na+,K+) pump in friend erythroleukemia cells and blocks erythropoiesis [2].
• In general, significantly large increases (p less than 0.001) in calcium, vanadium, copper, zinc, selenium, and rubidium were found in breast tumors, with a less significant increase (p less than 0.05) for nickel [3].
• The trace element vanadium exerts insulinlike effects in vitro and decreases hyperglycemia in insulin-deficient animals [4].
• The present study was undertaken to test the hypothesis that the toxicity and carcinogenicity of vanadium might arise from elevation of reactive oxygen species leading to activation of the transcription factor activator protein-1 (AP-1) [5].

Psychiatry related information on vanadium

• Vanadium and affective disorders [6].
• Tissue vanadium levels in manic-depressive psychosis [7].
• There was a significant reduction in incidence (P < 0.05), total number, multiplicity (P < 0.01) and size of palpable mammary tumors and delay in mean latency period of tumor appearance (P < 0.001) following vanadium supplementation compared to DMBA control [8].
• The recent findings suggest vanadium excess may aggravate the affective symptoms in bipolar affective disorder; selenium may inhibit certain carcinogenesis such as oesophageal cancer; and silicon may inhibit atheromatous formation in the aorta [9].
• Although there are individual differences in diabetic animals given vanadium, some reduction of degenerative changes were observed [10].

High impact information on vanadium

• Vanadium, an inhibitor of the Ca/Mg ATPase of heart sarcolemma, inhibited Ca pump activity by 50% at 1 microM [11].
• Vanadium in blood plasma or serum [12].
• EB-NSAP shares a conserved sequence motif not only with several lipid phosphatases and the mammalian glucose-6-phosphatases, but also with the vanadium-containing chloroperoxidase (CPO) of Curvularia inaequalis [13].
• From Vanadis to Atropos: vanadium compounds as pharmacological tools in cell death signalling [14].
• Recent short-term clinical trials with vanadium salts also seem promising in type II (non-insulin-dependent) diabetic patients in whom liver and peripheral insulin resistance was attenuated, indicating the therapeutic potential of vanadium salts, pending demonstration of their long-term innocuity [15].

Chemical compound and disease context of vanadium

• Vanadyl sulfate (VOSO(4)) is an oxidative form of vanadium that in vitro and in animal models of diabetes has been shown to reduce hyperglycemia and insulin resistance [16].
• Nitrogenase-3 of Azotobacter vinelandii is synthesized under conditions of molybdenum and vanadium deficiency [17].
• Vanadium K-edge X-ray-absorption spectroscopy of the functioning and thionine-oxidized forms of the VFe-protein of the vanadium nitrogenase from Azotobacter chroococcum [18].
• The vanadium nitrogenase of Azotobacter chroococcum. Reduction of acetylene and ethylene to ethane [19].
• N-Methylformamide extracts of acid-treated precipitated VFe protein of the V-nitrogenase of Azotobacter chroococcum are yellow-brown in colour and contain vanadium, iron and acid-labile sulphur in the approximate proportions 1:6:5 [20].

Biological context of vanadium

• From phosphatases to vanadium peroxidases: a similar architecture of the active site [21].
• 3) Vanadium reacts with hydrogen peroxide to form a pervanadate that is required to catalyze the oxidation of halide ions and/or stimulate the phosphorylation of receptor proteins [22].
• Nutritional requirements for boron, silicon, vanadium, nickel, and arsenic: current knowledge and speculation [22].
• The role of intracellular oxidative stress in the mechanism of action of phosphotyrosine phosphatase (PTP) inhibitors was studied using three vanadium-based compounds [23].
• Exposure of cells to vanadium led to the transactivation of NFAT in a time- and dose-dependent manner [24].

Anatomical context of vanadium

• Lithium carbonate treatment did not alter the ATPase activities, and the quantity of vanadium present in the membranes could not account for the variations in the enzyme activities observed [25].
• Nuclear magnetic resonance spectrum of living tunicate blood cells and the structure of the native vanadium chromogen [26].
• Taxol, which stabilizes cytoplasmic microtubules, prevented the stimulation of DNA synthesis by vanadium [27].
• This effect was approximately 9-fold higher (140 +/- 15% of maximal insulin response) in adipocytes derived from rats that had been treated with vanadium for several days [28].
• Using ratiometric Ca2+ imaging and patch-clamp measurement of Ca2+ channel activity, we investigated Ca2+ signaling induced by vanadium compounds in Jurkat T lymphocytes and rat basophilic leukemia cells [29].

Associations of vanadium with other chemical compounds

• Although their activity is often inferior to that of other systems, the use of vanadium-based catalysts in homogeneous Ziegler-Natta polymerizations allows the preparation of high-molecular-weight polymers with narrow molecular-weight distributions, ethene/alpha-olefin copolymers with high alpha-olefin incorporation, and syndiotactic polypropene [30].
• These studies confirm that the inhibitory form of vanadium usually observed in in vitro experiments is vanadate, in one or more of its hydrated forms [31].
• Highly purified peroxovanadium (pV) compounds, each containing an oxo ligand, one or two peroxo anions, and an ancillary ligand in the inner coordination sphere of vanadium, were shown to decrease plasma glucose markedly in both normal Sprague-Dawley and insulin-deprived diabetic BB rats [32].
• The in vitro metal uptake is nonspecific, and manganese, iron, and vanadium all bind, but only manganese restores catalytic activity [33].
• The steady state kinetic mechanism of the bromide-assisted disproportionation of hydrogen peroxide, forming dioxygen, catalyzed by vanadium bromoperoxidase has been investigated and compared to the mechanism of monochlorodimedone (MCD) bromination under conditions of 0.0125-6 mM H2O2, 1-500 mM Br-, and pH 4.55-6.52 [34].

Gene context of vanadium

• In this study, the lung fibrotic responses were investigated in COX-1 or COX-2-deficient (-/-) mice following vanadium pentoxide (V(2)O(5)) exposure [35].
• The present studies investigated the signaling pathways of vanadate, a vanadium ion with +5 oxidation state, to activate NF-kappaB transcription factor, a pivotal regulator of inflammatory responses [36].
• Mechanism of extracellular signal-regulated kinase (ERK)-1 and ERK-2 activation by vanadium pentoxide in rat pulmonary myofibroblasts [37].
• Immunohistochemical analysis in vivo indicated a decrease in cell proliferation (24.68% p < 0.05) and an increase among the TUNEL-positive apoptotic cells along with strong expressions of p53 and Bax, and downregulation of Bcl2 proteins in the mammary tissue of vanadium-treated animals [38].
• Importantly, overexpression of a dominant negative mutant PKClambda blocked Akt phosphorylation at Ser473 and Thr308, whereas it did not inhibit p70S6k phosphorylation at Thr389 and Thr421/Ser424, suggesting that aPKC activation is specifically involved in vanadium-induced activation of Akt, but not in activation of p70S6k [39].

Analytical, diagnostic and therapeutic context of vanadium

• The detection of these variant forms of pp60v-src depended on the prior treatment of the transformed cell cultures with vanadium ions or the inclusion in the cell disruption buffer of Mg2+ or ATP-Mg2+ [40].
• The presence of vanadium in this enzyme could be established with atomic absorption spectrophotometry and electron paramagnetic resonance [41].
• Heterologous expression of the vanadium-containing chloroperoxidase from Curvularia inaequalis in Saccharomyces cerevisiae and site-directed mutagenesis of the active site residues His(496), Lys(353), Arg(360), and Arg(490) [42].
• Sequence alignment suggests that mammalian G6Pases, lipid phosphatases, acid phosphatases, and a vanadium-containing chloroperoxidase (whose tertiary structure is known) share a conserved phosphatase motif [43].
• A potent (Na,K)-ATPase inhibitor purified from "Sigma Grade* ATP has been identified as vanadium using electron probe microanalysis and confirmed by microwave-induced emission spectroscopy and electron paramagnetic resonance spectroscopy [44].

References