Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Vanadium Compounds”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 91 records · Page 5Linked to original sources
PubMed1986

Action of Mn2+ and vanadium compounds on hormone and forskolin induced stimulation of juvenile rat ovarian adenylate cyclase.

The effect of forskolin on the hormonal (LH, FSH) activation and on the stimulation provided by other effectors (Gpp(NH)p,NaF) of the juvenile rat ovarian adenylate cyclase was investigated. Forskolin exhibited a synergistic action with LH, FSH and Gpp(NH)p but not with NaF. Addition of Ca2+ was inhibitory over a concentration range from 10(-5) to 10(-2) M whereas EGTA enhanced the response at 5.10(-5) M and inhibited it at higher concentration. The cAMP production was increased by addition of Mn2+ at low concentration (up to 5 mM) but markedly decreased at higher concentration (30 mM). FSH induced cAMP production was completely abolished at 30 mM Mn2+. The effect of vanadyl ion was very similar to that of Mn2+ Vanadate anion on the contrary was without effect on FSH stimulation.

Adenylyl Cyclases↗
PubMed2000

Chemistry and insulin-like properties of vanadium(IV) and vanadium(V) compounds.

The chemistry of vanadium compounds that can be taken orally is very timely since a vanadium(IV) compound, KP-102, is currently in clinical trials in humans, and the fact that human studies with inorganic salts have recently been reported. VO(acac)2 and VO(Et-acac)2 (where acac is acetylacetonato and Et-acac is 3-ethyl-2,4-pentanedionato) have long-term in vivo insulin mimetic effects in streptozotocin induced diabetic Wistar rats. Structural characterization of VO(acac)2 and two derivatives, VO(Me-acac)2 and VO(Et-acac)2, in the solid state and solution have begun to delineate the size limits of the insulin-like active species. Oral ammonium dipicolinatooxovanadium(V) is a clinically useful hypoglycemic agent in cats with naturally occurring diabetes mellitus. This compound is particularly interesting since it represents the first time that a well-characterized organic vanadium compound with the vanadium in oxidation state five has been found to be an orally effective hypoglycemic agent in animals.

Administration, Oral↗
PubMed1999

Vanadium.

Vanadium is a steel-grey, corrosion-resistant metal, which exists in oxidation states ranging from -1 to +5. Metallic vanadium does not occur in nature, and the most common valence states are +3, +4, and +5. The pentavalent form (VO3-) predominates in extracellular body fluids whereas the quadrivalent form (VO+2) is the most common intracellular form. Because of its hardness and its ability to form alloys, vanadium (i.e., ferrovanadium) is a common component of hard steel alloys used in machines and tools. Although most foods contain low concentrations of vanadium (< 1 ng/g), food is the major source of exposure to vanadium for the general population. High air concentrations of vanadium occur in the occupation setting during boiler-cleaning operations as a result of the presence of vanadium oxides in the dust. The lungs absorb soluble vanadium compounds (V2O5) well, but the absorption of vanadium salts from the gastrointestinal tract is poor. The excretion of vanadium by the kidneys is rapid with a biological half-life of 20-40 hours in the urine. Vanadium is probably an essential trace element, but a vanadium-deficiency disease has not been identified in humans. The estimated daily intake of the US population ranges from 10-60 micrograms V. Vanadyl sulfate is a common supplement used to enhance weight training in athletes at doses up to 60 mg/d. In vitro and animal studies indicate that vanadate and other vanadium compounds increase glucose transport activity and improve glucose metabolism. In general, the toxicity of vanadium compounds is low. Pentavalent compounds are the most toxic and the toxicity of vanadium compounds usually increases as the valence increases. Most of the toxic effects of vanadium compounds result from local irritation of the eyes and upper respiratory tract rather than systemic toxicity. The only clearly documented effect of exposure to vanadium dust is upper respiratory tract irritation characterized by rhinitis, wheezing, nasal hemorrhage, conjunctivitis, cough, sore throat, and chest pain. Case studies have described the onset of asthma after heavy exposure to vanadium compounds, but clinical studies to date have not detected an increased prevalence of asthma in workers exposed to vanadium.

Animals↗
PubMed2005

Development of an automated protein-tyrosine phosphatase 1B inhibition assay and the screening of putative insulin-enhancing vanadium(IV) and zinc(II) complexes.

The inhibition of protein-tyrosine phosphatase 1B (PTP1B) is a potential target for treatment of type 2 diabetes. Vanadium and zinc metal coordinated complexes have insulin-enhancing activities, and while vanadium compounds inhibit PTP1B, little is known on the mode of action of zinc compounds. In this study we developed an automated PTP1B inhibition assay that allows for a rapid assessment of the PTP1B inhibition strength of candidate compounds. Synthetic vanadium(IV) and zinc(II) complexes were evaluated: IC50 values for vanadium complexes ranged from 0.06 to 0.8 microM whereas for zinc compounds, values were above 10 microM. Vanadium sulfate, a non-conjugated inorganic salt, had stronger inhibition activity than any of the conjugated metal complexes.

Dose-Response Relationship, Drug↗
PubMed1999

Effects of vanadium complexes with organic ligands on glucose metabolism: a comparison study in diabetic rats.

1. Vanadium compounds can mimic actions of insulin through alternative signalling pathways. The effects of three organic vanadium compounds were studied in non-ketotic, streptozotocin-diabetic rats: vanadyl acetylacetonate (VAc), vanadyl 3-ethylacetylacetonate (VEt), and bis(maltolato)oxovanadium (VM). A simple inorganic vanadium salt, vanadyl sulphate (VS) was also studied. 2. Oral administration of the three organic vanadium compounds (125 mg vanadium element 1(-1) in drinking fluids) for up to 3 months induced a faster and larger fall in glycemia (VAc being the most potent) than VS. Glucosuria and tolerance to a glucose load were improved accordingly. 3. Activities and mRNA levels of key glycolytic enzymes (glucokinase and L-type pyruvate kinase) which are suppressed in the diabetic liver, were restored by vanadium treatment. The organic forms showed greater efficacy than VS, especially VAc. 4. VAc rats exhibited the highest levels of plasma or tissue vanadium, most likely due to a greater intestinal absorption. However, VAc retained its potency when given as a single i.p. injection to diabetic rats. Moreover, there was no relationship between plasma or tissue vanadium levels and any parameters of glucose homeostasis and hepatic glucose metabolism. Thus, these data suggest that differences in potency between compounds are due to differences in their insulin-like properties. 5. There was no marked toxicity observed on hepatic or renal function. However, diarrhoea occurred in 50% of rats chronically treated with VS, but not in those receiving the organic compounds. 6. In conclusion, organic vanadium compounds, in particular VAc, correct the hyperglycemia and impaired hepatic glycolysis of diabetic rats more safely and potently than VS. This is not simply due to improved intestinal absorption, indicating more potent insulin-like properties.

Administration, Oral↗
PubMed1997

In vitro antibacterial activity of vanadate and vanadyl compounds against Streptococcus pneumoniae.

All of the vanadate and vanadyl compounds tested in this study showed potent antibacterial activity against Streptococcus pneumoniae: the MIC (minimum inhibitory concentration) values of the vanadium compounds were 4-32 micrograms/ml, while the MIC values of tungstates and molybdates were 128-->8000 micrograms/ml. Scanning electron microscopy showed the elongation of S. pneumoniae strains under low concentrations (< MIC) of vanadium compounds such as (tert-BuNH3)4[V4O12] (1), (tert-BuNH3)6[V10O28] (2), Na3VO4 (7) and VOSO4 (8). The vanadium compounds non-selectively inhibited the incorporation of thymidine, uridine, leucine and glucose into the cells of S. pneumoniae and led to an efflux of potassium ions from the cells. It implies that the vanadium compounds interfere in or on the cell membrane with the transport of substrates and ions through the cell membrane, resulting in antibacterial activity against S. pneumoniae cells.

Cell Membrane↗
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↗
PubMed1993

Immunotoxicity of in vitro vanadium exposures: effects on interleukin-1, tumor necrosis factor-alpha, and prostaglandin E2 production by WEHI-3 macrophages.

Treatment of cultured mouse macrophages with either of two different vanadium compounds was shown to affect the production/release of two major immunoregulatory cytokines. The pentavalent vanadium compound ammonium metavanadate was shown previously to disrupt cell-mediated immunity at the earliest stages of an in vivo anti-Listerial response, in that mice treated with vanadium displayed decreased accessory cell recruitment and numbers of activated macrophages at infection sites. To determine whether these effects were due to vanadium-induced alterations in the production of biologically-active mediators, mouse macrophage-like WEHI-3 cells were treated in vitro with ammonium metavanadate or vanadium pentoxide prior to stimulation with lipopolysaccharide endotoxin (LPS). After stimulation, monokine (tumor necrosis factor-alpha and interleukin-1) and prostaglandin E2 (PGE2) activities were assessed. Both vanadium compounds decreased recovered monokine activities; measured TNF alpha concentrations were also reduced. Spontaneous release of the IL-1/TNF-regulating prostanoid PGE2 was significantly increased by the highest concentration of vanadate tested, although LPS-stimulated PGE2 production was unaffected by either compound. These results indicate that, in vitro, pentavalent vanadium can interfere with immunoregulatory mediators critical for maintaining host immunocompetence.

Animals↗
PubMed2001

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↗
PubMed2005

A nonspecific phosphotyrosine phosphatase inhibitor, bis(maltolato)oxovanadium(IV), improves glucose tolerance and prevents diabetes in Zucker diabetic fatty rats.

The molecular basis of insulin resistance, a major risk factor for development of Type II diabetes, involves defective insulin signaling. Insulin-mediated signal transduction is negatively regulated by the phosphotyrosine phosphatase, PTP1B, and numerous studies have demonstrated that organo-vanadium compounds, which are nonselective phosphotyrosine phosphatase inhibitors, have insulin-mimetic properties. However, whether or not vanadium compounds can prevent the transition from insulin resistance to overt diabetes is unknown. We compared the ability of bis(maltolato)oxovanadium(IV) (BMOV), an orally bioavailable organo-vanadium compound, and rosiglitazone maleate (RSG), a known insulin sensitizer, to prevent development of diabetes in Zucker diabetic fatty (ZDF) rats. Treatment began at 6 weeks of age when animals are insulin resistant and hyperinsulinemic, but not yet hyperglycemic, and ended at 12 weeks of age, which is 4 weeks after ZDF rats typically develop overt diabetes. BMOV-treated ZDF rats did not develop hyperglycemia, showed significant improvement in insulin sensitivity, and retained normal pancreatic islet morphology and endocrine cell distribution, similar to RSG-treated animals. BMOV and RSG treatment also prevented the hyper-phagia and polydipsia present in untreated ZDF rats; however, BMOV-treated ZDF rats gained much less weight than did RSG-treated animals. Circulating levels of adiponectin decreased in untreated ZDF rats compared to lean controls, but these levels remained normal in BMOV-treated ZDF rats. In contrast, in RSG-treated ZDF rats, plasma adiponectin levels were nearly 4-fold higher than in lean control rats, primarily as a result of a large increase in the amount of low-molecular weight forms of adiponectin in circulation. These data demonstrate that phosphatase inhibition offers a new approach to diabetes prevention, one that may have advantages over current approaches.

Animals↗
PubMed2005

Synthesis of vanadium(IV,V) hydroxamic acid complexes and in vivo assessment of their insulin-like activity.

We synthesized vanadyl (oxidation state +IV) and vanadate (oxidation state +V) complexes with the same hydroxamic acid derivative ligand, and assessed their glucose-lowering activities in relation to the vanadium biodistribution behavior in streptozotocin-induced diabetic mice. When the mice received an intraperitoneal injection of the complexes, the vanadate complex more effectively lowered the elevated glucose levels compared with the vanadyl one. The glucose-lowering effect of the vanadate complex was linearly related to its dose within the range from 2.5 to 7.5 mg V/kg. In addition, pretreatment of the vanadate complex induced a larger insulin-enhancing effect than the vanadyl complex. Both complexes were more effective than the corresponding inorganic vanadium compounds. The vanadyl and vanadate complexes, but not the inorganic vanadium compounds, resulted in almost the same organ vanadium distribution. Consequently, the observed differences in the insulin-like activity between the complexes would reflect the potency of the two compounds in the +IV and +V oxidation states in the subcellular region.

Animals↗
PubMed1997

Maltol complexes of vanadium (IV) and (V) regulate in vitro alkaline phosphatase activity and osteoblast-like cell growth.

Vanadium compounds have been found to possess insulin- and growth factor-mimetic effects. In consequence, these derivatives are potentially useful as effective oral therapeutic agents in diabetic patients. However, their use has been limited by various toxic side-effects and by the low solubility of different derivatives. Recently, vanadium complex with maltol, a sugar used as a common food additive, have been synthesised and investigated in animals, showing possible insulin-mimetic effects with low toxic side-effects. In the present study we have investigated the effect of bis(maltolato)oxovanadium (IV) (BMOV) and bis(maltolato)dioxovanadium (V) (BMV) on bone cells in culture as well as their direct effect on alkaline phosphatase in vitro. A comparison was also made with the action of vanadate and vanadyl cation. Vanadium compounds regulated cell proliferation in a biphasic manner with similar potencies. Osteoblast differentiation, assessed by alkaline phosphatase activity, was found to be dose-dependent, with the inhibitory effect being stronger for vanadate and BMOV than for vanadyl and BMV. All vanadium compounds directly inhibited bovine intestinal ALP with a similar potency. Thus, maltol vanadium derivatives behave in a similar way to vanadate and vanadyl in osteoblast-like UMR 106 cells in culture.

Alkaline Phosphatase↗
PubMed2002

Novel vanadium(V) compounds with a layer structure: synthesis, crystal structures, and solid state NMR spectroscopy of [(VO(2))(2)(4,4'-bpy)(0.5)(4,4'-Hbpy)(XO(4))] x H(2)O (X = P and As).

A novel vanadium(V) phosphate and the arsenate analogue, [(VO(2))(2)(4,4'-bpy)(0.5)(4,4'-Hbpy)(XO(4))].H(2)O (X = P, As; bpy = bipyridine), have been synthesized under hydrothermal conditions and structurally characterized by single-crystal X-ray diffraction. They are the first structurally characterized compounds in the vanadium(V)/4,4'-bpy/phosphate (or arsenate) systems. The two compounds are isostructural and crystallize in the triclinic space group P macro (No. 2) with a = 7.9063(3) A, b = 10.2201(4) A, c = 12.1336(5) A, alpha = 113.4652(7) degrees, beta = 95.7231(7) degrees, gamma = 94.4447(7) degrees, and Z = 2 for the phosphate, and a = 7.8843(6) A, b = 10.3686(7) A, c = 12.2606(9) A, alpha = 113.464(1) degrees, beta = 95.560(1) degrees, gamma = 94.585(1) degrees, and Z = 2 for the arsenate. The structure consists of phosphate-bridged vanadium(V) double chains linked through 4,4'-bpy ligands to form a sheet with the monoprotonated 4,4'-Hbpy(+) ligand being coordinated to the metal atom as a pendent group. The (1)H MAS NMR spectrum exhibits four resonances at 14.2, 9.5, 7.2, and 3.7 ppm with an intensity ratio close to 1:6:6:2, corresponding to three different types of protons in 4,4'-bpy and 4,4'-Hbpy(+) and one type of protons in H(2)O. The peak at 14.2 ppm can be assigned to the proton bonded to the pyridine nitrogen atom, which confirms the presence of 4,4'-Hbpy(+).

Journal Article↗
PubMedDate not supplied

[Comparative characteristics of vanadium-containing compounds, possessing insulin-like effects].

The serum glucose concentration, HbAc1, fructoseamine, the activity of AST, ALT, amylase, glycogen content and glucokinase activity in rat hepatocytes were examined in streptozotocin-diabetic rats during long-term orthovanadate and vanadyl sulphate treatment. The improvement of this parameters were demonstrated after oral orthovanadate and vanadyl sulphate administration. However, insulin-mimetic properties of vanadyl sulphate were more marked in comparison with orthovanadate. LD-50 and cytotoxicity analysis in isolated hepatocytes showed that vanadyl sulphate was less toxic than orthovanadate.

Animals↗
PubMed2005

Efficacy of lower doses of vanadium in restoring altered glucose metabolism and antioxidant status in diabetic rat lenses.

Vanadium compounds are potent in controlling elevated blood glucose levels in experimentally induced diabetes. However the toxicity associated with vanadium limits its role as therapeutic agent for diabetic treatment. A vanadium compound sodium orthovanadate (SOV) was given to alloxan-induced diabetic Wistar rats in lower doses in combination with Trigonella foenum graecum, a well-known hypoglycemic agent used in traditional Indian medicines. The effect of this combination was studied on lens morphology and glucose metabolism in diabetic rats. Lens, an insulin-independent tissue, was found severely affected in diabetes showing visual signs of cataract. Alterations in the activities of glucose metabolizing enzymes (hexokinase, aldose reductase, sorbitol dehydrogenase, glucose-6-phosphate dehydrogenase) and antioxidant enzymes (glutathione peroxidase, glutathione reductase) besides the levels of related metabolites, [sorbitol, fructose, glucose, thiobarbituric acid reactive species (TBARS) and reduced glutathione (GSH)] were observed in the lenses from diabetic rats and diabetic rats treated with insulin (2 IU/day), SOV (0.6 mg/ml), T. f. graecum seed powder (TSP, 5%) and TSP (5%) in combination with lowered dose of vanadium SOV (0.2 mg/ml), for a period of 3 weeks. The activity of the enzymes, hexokinase, aldose reductase and sorbitol dehydrogenase was significantly increased whereas the activity of glucose-6-phosphate dehydrogenase, glutathione peroxidase and glutathione reductase decreased significantly in lenses from 3 week diabetic rats. Significant increase in accumulation of metabolites, sorbitol, fructose, glucose was found in diabetic lenses. TBARS measure of peroxidation increased whereas the levels of antioxidant GSH decreased significantly in diabetic condition. Insulin restored the levels of altered enzyme activities and metabolites almost to control levels. Sodium orthovanadate (0.6 mg/ml) and Trigonella administered separately to diabetic animals could partially reverse the diabetic changes, metabolic and morphological, while vanadate in lowered dose in combination with Trigonella was found to be the most effective in restoring the altered lens metabolism and morphological appearance in diabetes. It may be concluded that vanadate at lowered doses administered in combination with Trigonella was the most effective in controlling the altered glucose metabolism and antioxidant status in diabetic lenses, these being significant factors involved in the development of diabetic complications, that reflects in the reduced lens opacity.

Analysis of Variance↗
PubMedDate not supplied

Increased potency of vanadium using organic ligands.

The in vivo glucose lowering effect of orally administered inorganic vanadium compounds in diabetes was first reported in our laboratory in 1985. While both vanadate and vanadyl forms of vanadium are orally active, they are still not well absorbed. We have synthesized several organic vanadium compounds and one compound, bis(maltolato)oxovanadium(lV) or BMOV, has been extensively investigated. BMOV proved effective in lowering plasma glucose and lipids in STZ-diabetic rats when administered in drinking water over a 25 week period. The maintenance dose (0.18 mmol/kg/day) was approximately 50% of that required for vanadyl sulfate (VS). Secondary complications of diabetes were prevented by BMOV and no marked toxicity was noted. Oral gavage of STZ-diabetic rats with BMOV also reduced blood glucose levels. The ED50 for BMOV was 0.5 mmol/kg, while for VS the estimated ED50 was 0.9 mmol/kg. BMOV was also effective by the intraperitoneal route in STZ-diabetic rats. The ED50 was 0.08 mmol/kg compared to 0.22 mmol/kg for VS. Some animals treated p.o. or i.p. remained euglycemic for up to 14 weeks. An i.v. infusion of BMOV of 0.05 mmol/kg over a 30 min period reduced plasma glucose levels by 50% while VS was not effective.

Animals↗
PubMed1984

Cytotoxic effect of vanadium and oil-fired fly ash on hamster tracheal epithelium.

Hamster tracheal organ cultures were used to study the in vitro effects of vanadium and oil-fired fly ash on mucociliary respiratory epithelium. Two vanadium compounds, VOSO4 and V2O5, and fly ash from an oil-fueled power plant were dissolved or suspended in culture medium over a range of concentrations and epithelia were exposed for 1 hr/day, for 9 consecutive days. At intervals during this period, alterations in cilia-beating frequency, cytology, and histology were documented by light microscopy. Explants treated with VOSO4 either decreased ciliary activity or produced ciliostasis depending upon the concentration and length of exposure. Early morphological alterations consisted of vacuolization of both nuclei and cytoplasm. After multiple exposures, cytology of VOSO4-treated respiratory mucosa was markedly affected. Similar changes were observed in cultures exposed to V2O5; however, the cytotoxicity appeared earlier and was more pronounced. Fly ash-treated explants produced similar biological effects when compared to both vanadium compounds. Thus, the data indicate that the extent of vanadium toxicity depends, at least in part, on the vanadium content of the compound tested, and that exposure to this metal and vanadium-rich fly ash can inhibit normal mucociliary function, a vital clearance mechanism in the respiratory tract.

Animals↗