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PubMed2001

Lack of in vivo effect of vanadium on GLUT4 translocation in white adipose tissue of streptozotocin-diabetic rats.

Vanadium treatment, in vivo, corrects the severe hyperglycemia observed in streptozotocin (STZ)-diabetic rats. A number of metabolic effects of vanadium have been demonstrated in vitro and might contribute importantly to normalization of glucose homeostasis. However, many in vitro effects of vanadium occur at concentrations substantially higher than those achieved in vivo. Effects of vanadium on white adipose tissue have been particularly well characterized in vitro. To examine the relationship between in vitro and in vivo actions of vanadium, we examined the effects of vanadium treatment on acute glucose tolerance and adipose tissue GLUT4 control in vivo. In agreement with previous studies, vanadium treatment of STZ-diabetic rats restored normoglycemia with no appreciable restoration of insulin secretion. GLUT4 expression in white adipose tissue was reduced by 22% in STZ-diabetic rats compared with controls. Vanadium treatment did not significantly alter GLUT4 expression in controls, but completely restored normal expression levels in STZ-diabetic rats. In overnight-fasted control animals, GLUT4 translocation to the plasma membrane (PM) was maximally elevated (by 50%) in adipose tissue within 5 to 10 minutes after an intravenous (IV) glucose challenge. No glucose-induced translocation of GLUT4 was detected in diabetic rats, and peak PM GLUT4 content was 40% lower than in controls. Vanadium treatment did not increase peak PM GLUT4 content in either control or diabetic animals in response to a glucose load. Finally, the suppression of whole-body acute glucose tolerance in diabetic animals was only partially normalized by vanadium treatment. We conclude: (1) that concentrations of vanadium effective for maintaining normoglycemia in vivo (typically below 30 micromol/L) promote normal GLUT4 expression, but do not influence the subcellular localization of GLUT4 in white adipose tissue and (2) that in vivo effects of vanadium may not necessarily reflect the actions observed in vitro at supraphysiologic concentrations.

Adipose Tissue↗
PubMed1988

Retention of intratracheally instilled and ingested tetravalent and pentavalent vanadium in the rat.

The retention, subcellular distribution in the liver, kidneys and lungs and binding of vanadium in the rat were investigated at 3 h, 1 d and 12 d after intratracheal instillation of 200 ng/kg body weight of 48V-labelled pentavalent and tetravalent vanadium. The metabolic patterns of both chemical forms of vanadium were similar. The lungs, liver, kidneys, bone, testes and spleen are the target tissues at risk, vanadium being removed from them with time at different rates. Pulmonary vanadium clearance was initially rapid - 80-85% of the 48V was removed within 3 h. At 12 d about 2% of the element was still present in the lung. Intracellularly, the major part of liver, kidney and lung vanadium was present in the nuclear fraction (30-40% of the homogenate), followed by cytosol and mitochondrial fractions. Gel filtration chromatography of the lung cytosol showed two biochemical pools of vanadium: the first corresponding to protein bound vanadium, which may be involved in the long-term accumulation of the element in the lung, the second pool representing a diffusible vanadium form. The retention of the tetravalent and pentavalent vanadium forms was also investigated 1 d after oral administration. No obvious differences were observed in the distribution pattern of 48V in the tissues, the retention factor being higher by two orders of magnitude in comparison with the intratracheally instilled animals. These findings suggest that the metabolic pathways of tetravalent and pentavalent vanadium are independent of the route of vanadium exposure.

Administration, Oral↗
PubMed2006

Pentavalent vanadium at concentration of the underground water level enhances the sweet taste sense to glucose in college students.

Underground water in volcanic areas contains vanadium when the basalt layer exists among igneous rocks. The concentration of vanadium in drinking water sometimes exceeds 0.8 microM in these areas, however, the physiological effects of vanadium, especially non-toxic effects, at concentrations lower than 1 microM are unknown. In the present experiments, we examined the effect of pentavalent vanadium and tetravalent vanadium at 0.8 and 8.0 microM concentrations on the recognition threshold to taste substances in healthy college students. Pentavalent vanadium, ammonium vanadate, lowered the sweet taste threshold to glucose at 0.8 and 8.0 microM as well. Tetravalent vanadium, vanadium sulfate, did not alter the threshold to glucose either at 8.0 microM or at 0.8 microM. Ammonium vanadate also decreased the sweet taste threshold to L-proline at 8.0 microM. Ammonium vanadate did not influence the sour taste threshold to hydrogen chloride. Neither ammonium sulfate nor ammonium bicarbonate altered the sweet taste threshold to glucose. Therefore, the effect of ammonium vanadate on the sweet taste threshold is attained by vanadium but not by ammonium. It was concluded that pentavalent vanadium at 0.8 microM intensifies the sweet taste sense to glucose rather specifically. We have first shown the physiological effect of vanadium at the concentration of the underground water level.

Adolescent↗
PubMed2005

ERKs activation and calcium signaling are both required for VEGF induction by vanadium in mouse epidermal Cl41 cells.

The previous studies have demonstrated that vanadium exposure can cause a variety of biological effects. However, the mechanisms involved in the biological effects caused by vanadium are not well understood. Our previous studies have shown that exposure of mouse epidermal Cl 41 cells to vanadate stimulated the phosphorylation of both ERKs and p38K, and calcium signaling leading NFAT activation. In view of the evidence that ERKs and p38 kinase contribute to VEGF induction, we investigated in the present study the potential roles of ERKs, p38K, and calcium signaling in VEGF induction caused by vanadium exposure. Exposure of Cl 41 cells to vanadium led to VEGF induction in both time- and dose-dependent manners. Pre-treatment of Cl 41 cells with PD98059, an inhibitor of MEK1/2-ERKs pathway, but not SB202190, an inhibitor for p38K pathway, resulted in a dramatic inhibition of VEGF induction by vanadium. More interesting, pre-treatment of Cl 41 cells with intracellular calcium chelator, but not calcium channel blocker, resulted in a dramatic decrease in VEGF induction by vanadium. However, both PI-3K inhibitors and overexpression of Deltap85, a dominant negative PI-3K mutant, resulted in only a marginal decrease in VEGF induction by vanadium. Moreover, mTOR, as a downstream molecule of PI-3K, did not attribute to VEGF induction by vanadium because rapamycin pre-treatment did not show any inhibitory effect on VEGF induction. These results indicate that ERKs and intracellular stored calcium release play a critical role in VEGF induction by vanadium. PI-3K is partially involved in VEGF induction by vanadium, while p38K and mTOR are not involved. Those results will help us to understand the molecular mechanisms involved in vanadium-induced biological effects.

Animals↗
PubMed2006

Chronic vanadium poisoning in calves and its treatment with calcium disodium ethylenediaminetetraacetate.

Sixteen Friesland heifer calves aged between 96 and 157 days were removed from a dairy farm that had been polluted with vanadium and randomly allocated into two equal groups (n = 8). The objective of the trial was to determine whether calcium disodium ethylenediaminetetraacetate (CaNa(2)EDTA) could be used as a treatment for cattle running in environments high in background vanadium. The treatment group received 80 mg CaNa(2)EDTA per kg body weight intraperitonealy (i.p.) twice a week over a 10-week period. The control group received normal saline i.p. over the same period. During the trial calves were exposed to a daily intake of vanadium in the form of contaminated tef hay derived from the farm of origin. In addition, the total mixed ration was spiked with a further 20 mg V(2)O(5)/kg feed to compensate for possible on-farm inhalation exposure. A stochastic model was used to estimate daily intake of vanadium as a distribution function. The model estimated that the daily intake of vanadium varied between an absolute minimum of 33 mg/day to an absolute maximum of 124 mg/day. The average intake of vanadium was 71.8 mg per day per calf. Various chemical pathology parameters were measured throughout the trial as well as urine excretion rates of vanadium and lymphocyte stimulation counts. All calves were slaughtered and necropsied in cohorts of 4-6 animals at monthly intervals after completion of the trial and withdrawal of vanadium from the ration. Tissue concentrations of vanadium were determined and necropsy findings were noted. The study found that CaNa(2)EDTA appears to enhance the excretion of vanadium in calves, but could not prove that the treatment had a protective effect against vanadium exposure. Calves were able to tolerate the prolonged treatment with CaNa(2)EDTA without side-effects.

Animals↗
PubMed1996

Vanadium(IV)-mediated free radical generation and related 2'-deoxyguanosine hydroxylation and DNA damage.

Free radical generation, 2'-deoxyguanosine (dG) hydroxylation and DNA damage by vanadium(IV) reactions were investigated. Vanadium(IV) caused molecular oxygen dependent dG hydroxylation to form 8-hydroxyl-2'-deoxyguanosine (8-OHdG). During a 15 min incubation of 1.0 mM dG and 1.0 mM VOSO4 in phosphate buffer solution (pH 7.4) at room temperature under ambient air, dG was converted to 8-OHdG with a yield of about 0.31%. Catalase and formate inhibited the 8-OHdG formation while superoxide dismutase enhanced it. Metal ion chelators, DTPA and deferoxamine, blocked the 8-OHdG formation. Incubation of vanadium(IV) with dG in argon did not generate any significant amount of 8-OHdG, indicating the role of molecular oxygen in the mechanism of vanadium(IV)-induced dG hydroxylation. Vanadium(IV) also caused molecular oxygen-dependent DNA strand breaks in a pattern similar to that observed for dG hydroxylation. ESR spin trapping measurements demonstrated that the reaction of vanadium(IV) with H2O2 generated OH radicals, which were inhibited by DTPA and deferoxamine. Incubation of vanadium(IV) with dG or with DNA in the presence of H2O2 resulted in an enhanced 8-OHdG formation and substantial DNA double strand breaks. Sodium formate inhibited 8-OHdG formation while DTPA had no significant effect. Deferoxamine enhanced the 8-OHdG generation by 2.5-fold. ESR and UV measurements provided evidence for the complex formation between vanadium(IV) and deferoxamine. UV-visible measurements indicate that dG, vanadium(IV) and deferoxamine are able to form a complex, thereby, facilitating site-specific 8-OHdG formation. Reaction of vanadium(IV) with t-butyl hydroperoxide generated hydroperoxide-derived free radicals, which caused 8-OHdG formation from dG and DNA strand breaks. DTPA and deferoxamine attenuated vanadium(IV)/t-butyl-OOH-induced DNA strand breaks.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed2004

Reduction of vanadium(V) with Acidithiobacillus ferrooxidans and Acidithiobacillus thiooxidans.

Biotechnological leaching has been proposed as a suitable method for extraction of vanadium from spent catalysts and oil ash. In the biological leaching process, the vanadium(V) can be reduced to vanadium(IV), which is a less toxic and more soluble form of the vanadium. The present investigation showed that Acidithiobacillus ferrooxidans efficiently reduced vanadium(V) in the form of vanadium pentaoxide, to vanadyl(IV) ions, and tolerated high concentrations of vanadium(IV) and vanadium(V). A. ferrooxidans was compared with Acidithiobacillus thiooxidans, which has previously been utilized for vanadium leaching and reduction. Vanadium pentaoxide and sodium vanadate were used as model compounds. The results of this study indicate possibilities to develop an economical and technically feasible process for biotechnological vanadium recovery.

Acidithiobacillus↗
PubMed2006

The permeability and cytotoxicity of insulin-mimetic vanadium (III,IV,V)-dipicolinate complexes.

Vanadium (III,IV,V)-dipicolinate complexes with different redox properties were selected to investigate the structure-property relationship of insulin-mimetic vanadium complexes for membrane permeability and gastrointestinal (GI) stress-related toxicity using the Caco-2 cell monolayer model. The cytotoxicity of the vanadium complexes was assayed with 3-(4,5-dimethylthiazoyl-2-yl) 2,5-diphenyltetrazolium bromide (MTT) assays and the effect on monolayer integrity was measured by the trans-epithelial electric resistance (TEER). The three vanadium complexes exhibited intermediate membrane permeability (P(app) = 1.4-3.6x10(-6) cm/s) with low cellular accumulation level (<1%). The permeability of all compounds was independent of the concentration of vanadium complexes and excess picolinate ligands. Both V(III) and V(V)-dipicolinate complexes induced 3-4-fold greater reactive oxygen and nitrogen species (RONS) production than the V(IV)-dipicolinate complex; while the vanadium (III)-dipicolinate was 3-fold less damaging to tight junction of the Caco-2 cell monolayer. Despite the differences in apparent permeability, cellular accumulation, and capacity to induce reactive oxygen and nitrogen species (RONS) levels, the three vanadium complexes exhibited similar cytotoxicity (IC50 = 1.7-1.9 mM). An ion pair reagent, tetrabutylammonium, increased the membrane apparent permeability by 4-fold for vanadium (III and IV)-dipicolinate complexes and 16-fold for vanadium (V)-dipicolinate as measured by decrease in TEER values. In addition, the ion pair reagent prevented damage to monolayer integrity. The three vanadium (III,IV,V)-dipicolinate complexes may pass through caco-2 monolayer via a passive diffusion mechanism. Our results suggest that formation of ion pairs may influence compound permeation and significantly reduce the required dose, and hence the GI toxicity of vanadium-dipicolinate complexes.

Caco-2 Cells↗
PubMed1981

Concerning the form of biochemically active vanadium.

A survey has been made of the descriptive chemistry of vanadium as it pertains to physiological environments. Taking into account the vanadium concentration, pH, coordinating ligands and chelates, presence of other cations, oxidation-reduction potentials and the kinetics of the various vanadium-containing species, the following suggestions are made. Free vanadium ions will be monomeric. Monomeric vanadium(V) and vanadium(IV) will each exist in a specific hydrated form. Extracellular vanadium will be in the vanadate, Vv, form. Intracellular vanadium will most likely be predominantly in the vanadyl, Viv, form. Both extracellular vanadium(V) and intracellular vanadium(IV) will be bound to bi- or tridentate ligands if at all. If oxidation-reduction processes involving vanadium are fast relative to transmembrane transport, the transmembrane potential will not be coupled to the Vv/Viv Nernstian potential.

Calorimetry↗
PubMed2006

Vanadium and bone development: putative signaling pathways.

Vanadium is a trace element present in practically all cells in plants and animals. It exerts interesting actions in living systems. At pharmacological doses, vanadium compounds display relevant biological actions such as mimicking insulin and growth factors as well as having osteogenic activity. Some vanadium compounds also show antitumoral properties. The importance of vanadium in bone arises from the studies developed to establish the essentiality of this element in animals and humans. Bone tissue, where the element seems to play an important role, accumulates great amounts of vanadium. This paper reviews the physiology of osteoblasts, the involvement of different growth factors on bone development, and the effects of vanadium derivatives on the skeletal system of animal models and bone-related cells. Two cellular lines are discussed in particular; one derived from a rat osteosarcoma (UMR106) and the other is a nontransformed osteoblast cell line (MC3T3-E1). The effects of different growth factors and their mechanisms of action in these cellular lines are reviewed. These models of osteoblasts are especially useful in understanding the intracellular signaling pathways of vanadium derivatives in hard tissues. Vanadium uses an intricate interplay of intracellular mechanisms to exert different biochemical and pharmacological actions. The effects of vanadium derivatives on some cellular signaling pathways related to insulin are compiled in this review. The comprehension of these intracellular signaling pathways may facilitate the design of vanadium compounds with promising therapeutic applications as well as the understanding of secondary side effects derived from the use of vanadium as a therapeutic agent.

Animals↗
PubMed1979

[Field tests carried out to determine the occupational exposure to vanadium (author's transl)].

In a metallurgic plant we analysed blood samples, urine and finger-nails of 54 workers exposed to vanadium. On the basis of orientating dust measurements it can be assumed that the results obtained were, as a rule, clearly lower than the MAC values for vanadium pentoxide dust. The median vanadium concentration in whole-blood was 2.9 micrograms/l. This indicates that the exposed persons differ significantly from the control group. The median vanadium concentration measured in urine was 37.8 micrograms/l. This means that there is a significant difference in comparison with the control group (0.8 micrograms/l). In order to obtain values of greater reliability, the vanadium concentration resulting from the analysis of spontaneous urine samples was to be referred to the creatinine content. Conversion yields a medium vanadium concentration of 33.9 and 0.6 micrograms/g creatinine for the exposed workers and normal persons respectively. The cystine content found in the finger-nails of persons occupationally exposed to vanadium was significantly reduced with respect to the comparative group (8.9 against 9.9 mg cystine per 100 mg finger-nails). Within the groups of persons examined no correlation is found to exist between the cystine content of the finger-nails and the age of the persons, nor between the vanadium concentrations in blood and urine. After a weekend without exposure the vanadium concentrations in blood and urine dropped. In general, this drop was the more pronounced the higher the initial value was. Roughly two to four days after the occupational exposure had ceased, the values dropped to the half of the initial value. Based on the test results available, the vanadium concentrations in blood and urine reflect the extent of an occupational vanadium exposure and are suitable indicators for estimating the potential threat caused by this heavy metal.

Age Factors↗
PubMed2002

Vanadocytes, cells hold the key to resolving the highly selective accumulation and reduction of vanadium in ascidians.

Since Henze discovered vanadium in the blood (or coelomic) cells of an ascidian in 1911, this unusual phenomenon has attracted the interest of many investigators. The highest concentration of vanadium (350 mM) in the blood cells of Ascidia gemmata, which belongs to the suborder Phlebobranchia, is 10(7) times higher than that in seawater. Of the approximately 10 types of blood cells, a combination of cell fractionation and neutron-activation analysis revealed that the signet ring cells were the true vanadocytes. In the vanadocytes, 97.6% of the vanadium is in the +3 oxidation state (III). The extremely low pH of 1.9 found in vanadocytes suggests that protons, concentrated by an H(+)-ATPase, might be linked to the accumulation of vanadium energetically. The antigen recognized by a monoclonal antibody, S4D5, prepared to identify vanadocytes, was determined to be 6-PGDH in the pentose phosphate pathway. NADPH produced in the pentose phosphate pathway in vanadocytes is thought to participate in the reduction of vanadium(V) to vanadium(IV). During embryogenesis, a vanadocyte-specific antigen first appears in the body wall at the same time that significant accumulations of vanadium become apparent. Three different vanadium-associated proteins (VAPs) were extracted from the blood cells of vanadium-rich ascidians. These are 12.5, 15, and 16 kDa in size and are associated with vanadium in an approximate ratio of 1:16. The cDNA encoding the 12.5 and 15 kDa VAPs was isolated and the proteins encoded were found to be novel. Further biochemical and biophysical characterization of the VAPs is in progress.

Animals↗
PubMed2001

Salinity dependence of vanadium toxicity against the brackish water hydroid Cordylophora caspia.

Vanadium, an abundant metal, enters the environment through natural rock weathering or by combustion of oil products. A third pathway is the leaching of vanadium-rich building materials. Stones made from steel industry residual slags, so-called slag stones, contain rather large amounts of vanadium. The increasing use of these slag stones in riverbank reinforcement has therefore led to increased interest in the toxicity of vanadium to aquatic organisms. The aim of the study was to determine the toxicity of vanadium to the brackish water hydroid Cordylophora caspia and the effect of vanadium on the membrane-bound enzyme Na, K-ATPase at various salinities. EC50 values for population growth inhibition were determined from 1.74 to 7.96 mg x L(-1) vanadium, depending on salinity. The maximum inhibition of population growth by vanadium was observed at low salinities. Correspondingly, maximum Na, K-ATPase inhibition was also measured at low salinities and decreased with increasing salinity. The present study suggests that the observed inhibition of population growth of C. caspia caused by vanadium-contaminated rearing water is due to the vanadium-induced inhibition of phosphatases.

Animals↗
PubMed1991

Flavoenzymes reduce vanadium(V) and molecular oxygen and generate hydroxyl radical.

ESR spectroscopic evidence is presented for the formation of vanadium(IV) in the reduction of vanadium(V) by three typical, NADPH-dependent, flavoenzymes: glutathione reductase, lipoyl dehydrogenase, and ferredoxin-NADP+ oxidoreductase. The vanadium(V)-reduction mechanism appears to be an enzymatic one-electron reduction process. Addition of superoxide dismutase (SOD) showed that the generation of vanadium(IV) does not involve the superoxide (O2-) radical significantly. Measurements under anaerobic atmosphere showed, however, that the enzymes-vanadium-NADPH mixture can cause the reduction of molecular oxygen to generate H2O2. The H2O2 and vanadium(IV) thus formed react to generate hydroxyl (.OH) radical. The .OH formation is inhibited strongly by catalase and to a lesser degree by SOD, but it is enhanced by exogenous H2O2, suggesting the occurrence of a Fenton-like reaction. The inhibition of vanadium(IV) formation by N-ethylmaleimide indicates that the SH group on the flavoenzyme's cystine residue plays an important role in the enzyme's vanadium(V) reductase function. These results thus reveal a new property of the above-mentioned, NADPH-dependent flavoenzymes--their function as vanadium(V) reductases, as well as that as generators of .OH radical in the vanadium(V) reduction mechanism.

Animals↗
PubMedDate not supplied

Vanadium: a review of the reproductive and developmental toxicity.

While the essentiality of vanadium for living organisms has yet to be established with certainty, vanadium has become an increasingly important environmental metal. Moreover, in recent years pharmacological interest in vanadium has also increased because of the hypothetical utilization of oral vanadium as an alternative therapy to parenteral insulin in diabetic patients. Adverse effects of vanadium depend on the circulating levels of this element. Among those effects, it is now well established that vanadate (V+5) and vanadyl (V+4) may be reproductive and developmental toxicants in mammals. Decreased fertility, embryolethality, fetotoxicity, and teratogenicity have been reported to occur in rats, mice, and hamsters following vanadium exposure. The reproductive vanadium toxicity, the maternal and embryo/fetal toxicity of this trace element, the perinatal and postnatal effects of vanadium, as well as the prevention by chelating agents of vanadium-induced developmental toxicity are reviewed here. The developmental effects of vanadium in pregnant diabetic rats are also summarized.

Animals↗
PubMed2005

The public health implications of farming cattle in areas with high background concentrations of vanadium.

Forty-two adult Brahman-cross cattle farmed extensively in two groups, immediately adjacent to and 2 km from a vanadium processing plant respectively, were slaughtered over a 5 year period at a nearby abattoir. Cattle were being exposed to vanadium at close to no-adverse-effect levels. The dose of vanadium that cattle were taking in prior to slaughter was calculated for each animal from environmental and physiological data using a stochastic risk assessment model. The median exposure doses in the month prior to slaughter ranged from 0.55 to 2.73 mg vanadium/kg body weight/day. A range of tissues was taken from the cattle at slaughter for vanadium determination and tissue levels of vanadium in muscle, liver and kidney are reported. The concentrations of vanadium in the milk of cattle from the same farm sampled over 5 years are also reported. Concentrations were further modelled using a lognormal distribution function to look at possible extreme values that are likely to occur. The concentrations of vanadium in commonly consumed tissues ranged from <0.05 to 11.51 mg/kg (wet-mass basis). The median concentration of vanadium in milk was 0.23 mg vanadium/kg. People drinking milk were at highest risk. The potential oral daily intake of vanadium for people consuming these foodstuffs was modelled using a stochastic model. The model predicted that there is less than a 5% chance that the potential daily intake of vanadium from milk will be >0.44 microg/kg/day for adults. Based on this upper limit it was concluded from current knowledge of toxicity in humans that the tissue and milk residues from cattle should pose no health risk to the consumer.

Agriculture↗
PubMed2001

Vanadium-induced nuclear factor of activated T cells activation through hydrogen peroxide.

The present study investigated the role of reactive oxygen species (ROS) in activation of nuclear factor of activated T cells (NFAT), a pivotal transcription factor responsible for regulation of cytokines, by vanadium in mouse embryo fibroblast PW cells or mouse epidermal Cl 41 cells. Exposure of cells to vanadium led to the transactivation of NFAT in a time- and dose-dependent manner. Scavenging of vanadium-induced H(2)O(2) with N-acety-L-cyteine (a general antioxidant) or catalase (a specific H(2)O(2) inhibitor) or the chelation of vanadate with deferoxamine, resulted in inhibition of NFAT activation. In contrast, an increase in H(2)O(2) generation by the addition of superoxide dismutase or NADPH enhanced vanadium-induced NFAT activation. This vanadate-mediated H(2)O(2) generation was verified by both electron spin resonance and fluorescence staining assay. These results demonstrate that H(2)O(2) plays an important role in vanadium-induced NFAT transactivation in two different cell types. Furthermore, pretreatment of cells with nifedipine, a calcium channel blocker, inhibited vanadium-induced NFAT activation, whereas and ionomycin, two calcium ionophores, had synergistic effects with vanadium for NFAT induction. Incubation of cells with cyclosporin A (CsA), a pharmacological inhibitor of the phosphatase calcineurin, blocked vanadium-induced NFAT activation. All data show that vanadium induces NFAT activation not only through a calcium-dependent and CsA-sensitive pathway but also involved H(2)O(2) generation, suggesting that H(2)O(2) may be involved in activation of calcium-calcineurin pathways for NFAT activation caused by vanadium exposure.

Animals↗
PubMedDate not supplied

Vanadium as a modulator of cellular regulatory cascades and oncogene expression.

Vanadium, a trace metal in the environment and in biological systems, influences the behavior of enzymes, mimics and regulates growth factor activity, is a potential mutagenic and carcinogenic agent, and regulates gene expression. The diverse biological actions of vanadium result from its capacity to function as an oxyanion, oxycation, or prooxidant. Vanadium is found in water, rocks, and soils in low concentration and in relatively high concentrations in coal and oil deposits. Vanadium compounds at much higher concentrations than are typically ingested are being considered in the treatment of diabetes mellitus. The actions of insulin and vanadium on the insulin receptor are similar, but the mechanisms are not identical. Vanadium modulates growth-factor-mediated signal transduction pathways. Vanadium promotes cell transformation and diminishes cell adhesion. Consistent with its mitogenic action and its capacity to mimic mitogenic growth factors, vanadium stimulates expression of protooncogenes. In particular, oxygen-derived active species are involved in the expression of the jun protooncogene in the presence of vanadium. The unique cellular activity of vanadium makes it a tool of unparalleled potential for studying mechanisms of cell growth, differentiation, and metabolism.

Animals↗