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PubMed2006

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↗
PubMed2006

Diabetes-altered gene expression in rat skeletal muscle corrected by oral administration of vanadyl sulfate.

Treatment with vanadium, a representative of a class of antidiabetic compounds, alleviates diabetic hyperglycemia and hyperlipidemia. Oral administration of vanadium compounds in animal models and humans does not cause clinical symptoms of hypoglycemia, a common problem for diabetic patients with insulin treatment. Gene expression, using Affymetrix arrays, was examined in muscle from streptozotocin-induced diabetic and normal rats in the presence or absence of oral vanadyl sulfate treatment. This treatment affected normal rats differently from diabetic rats, as demonstrated by two-way ANOVA of the full array data. Diabetes altered the expression of 133 genes, and the expression of 30% of these genes dysregulated in diabetes was normalized by vanadyl sulfate treatment. For those genes, the ratio of expression in normal animals to the expression in diabetic animals showed a strong negative correlation with the ratio of expression in diabetic animals to the expression in diabetic animals treated with vanadyl sulfate (P = -0.85). The genes identified belong to six major metabolic functional groups: lipid metabolism, oxidative stress, muscle structure, protein breakdown and biosynthesis, the complement system, and signal transduction. The identification of oxidative stress genes, coupled with the known oxidative chemistry of vanadium, implicates reactive oxygen species in the action of this class of compounds. These results imply that early transition metals or compounds formed from their chemical interactions with other metabolites may act as general transcription modulators, a role not usually associated with this class of compounds.

Administration, Oral↗
PubMed2005

A study of the potential of the pig as a model for the vaginal irritancy of benzalkonium chloride in comparison to the nonirritant microbicide PHI-443 and the spermicide vanadocene dithiocarbamate.

A porcine model was established to test the mucosal toxicity potential of a thiophene thiourea (PHI-443)-based anti-HIV microbicide and a vanadocene-based spermicide, vanadocene dithiocarbamate (VDDTC) in comparison to benzalkonium chloride (BZK). Nine domestic pigs (Duroc) in nonestrus stage received a single intravaginal application of 2% BZK, 2% PHI-443, or 0.1% VDDTC-containing gel. At various times after gel application, cell differentials and levels of inflammatory cytokines (IL-1beta, IL-4, IL-6, IL-8, IL-10, IL-18, IFN-gamma, and TNF-alpha) in cervicovaginal lavage (CVL) fluid were monitored by flow cytometry and ELISA, respectively. Eight pigs were exposed intravaginally to a gel with and without BZK or VDDTC for 4 consecutive days and vaginal tissues were scored histologically for inflammation using a new scoring system. Only CVL fluid from pigs exposed to BZK showed a significant increase of IL-1beta, IL-8, and also IL-18 production when compared to the controls, PHI-443 or VDDTC-treated groups. Maximum levels of BZK-induced IL-1beta (100-fold), IL-8 (2,500-fold), IL-18 (80-fold), and IFN-gamma (10-fold) were found at 24 hours. In the in vivo porcine vaginal irritation model, increased levels of vaginal IL-1beta, IL-8, and IL-18 were associated with histological changes consistent with vaginal inflammation. These results demonstrate that key cervicovaginal inflammatory cytokines are useful in vivo biomarkers for predicting the mucosal toxicity potential of vaginal products in the physiologically relevant and sensitive porcine model.

Animals↗
PubMed1983

Vanadium ions stimulate DNA synthesis in Swiss mouse 3T3 and 3T6 cells.

Vanadyl sulfate and sodium orthovanadate in the concentration range between 5 and 50 microM are shown to be mitogenic for quiescent cultures of Swiss mouse 3T3 and 3T6 cells. The compounds caused a striking shift in the dose-response for the effect of serum on [3H]thymidine incorporation and DNA synthesis. In the absence of serum the effect of vanadium was greatly potentiated by insulin. Vanadium ions produced no more than additive increases in [3H]thymidine incorporation when combined with epidermal growth factor, cholera toxin, or phorbol 12-myristate 13-acetate. Both vanadium compounds stimulated ouabain-inhibitable 86Rb+ uptake, indicating that the vanadium ions increase, rather than inhibit, Na+/K+ pump activity in the intact cell. Neither vanadium compound had any effect on cellular cAMP under a variety of different conditions. The mitogenic effect of the vanadium compounds was similar to that of colchicine. Taxol, which stabilizes cytoplasmic microtubules, prevented the stimulation of DNA synthesis by vanadium.

Animals↗
PubMed2002

Role of neutrophil apoptosis in vanadium-induced pulmonary inflammation in mice.

Pulmonary exposure to airborne vanadium and vanadium-containing compounds is associated with acute pulmonary inflammation, characterized by a rapid influx of neutrophilic polymorphonuclear leukocytes with a peak response at 6 hours and resolution by 3 days. We hypothesized that neutrophil apoptosis is involved in the resolution of vanadium-induced lung inflammation. To test this hypothesis, mice were exposed to inspired vanadium or saline control and the bronchoalveolar lavage (BAL) cells were examined at various times for apoptosis using terminal deoxyribonucleotidyl transferase-mediated nick end labeling (TUNEL). Control mice showed only resident alveolar macrophages in the BAL with no evidence of apoptosis. In contrast, vanadium-treated mice showed clear apoptosis of BAL cells, which were predominantly neutrophils. The number of apoptotic cells gradually increased and reached a maximal level by 24 hours with subsequent decline. After 24 hours, when the vanadium-induced lung inflammation was in the resolution phase, we observed an increased number of alveolar macrophages in BAL and the engulfment of apoptotic bodies by these macrophages. At 72 hours, the total number of neutrophils in BAL fell to the baseline level, and the number of apoptotic cells was reduced. Clearance of the apoptotic product was demonstrated by the presence of apoptotic bodies in the cytoplasm of alveolar macrophages. We conclude that apoptosis of neutrophils and clearance by alveolar macrophages are important mechanisms in the resolution of vanadium-induced lung inflammation.

Animals↗
PubMed2004

51V magic angle spinning NMR spectroscopy of Keggin anions [PVnW12-nO40](3+n)-: effect of countercation and vanadium substitution on fine structure constants.

Vanadium environments in Keggin oxopolytungstates were characterized by (51)V solid-state MAS NMR spectroscopy. (C(4)H(9))(4)N(+)-, K(+)-, Cs(+)-, as well as mixed Na(+)/Cs(+)- salts of the mono-, di-, and trivanadium substituted oxotungstates, [VW(11)O(40)](4-), [V(2)W(10)O(40)](5-), and [V(3)W(9)O(40)](6-), have been prepared as microcrystalline and crystalline solids. Solid-state NMR spectra report on the local environment of the vanadium site in these Keggin ions via their anisotropic quadrupolar and chemical-shielding interactions. These (51)V fine structure constants in the solid state are determined by the number of vanadium atoms present in the oxoanion core. Surprisingly, the quadrupolar anisotropy tensors do not depend to any significant extent on the nature of the countercations. On the other hand, the chemical-shielding anisotropy tensors, as well as the isotropic chemical shifts, display large variations as a function of the cationic environment. This information can be used as a probe of the local cationic environment in the vanadium-substituted Keggin solids.

Anions↗
PubMed2004

Biphenyl derived Schiff-base vanadium(V) complexes with pendant OH-groups--structure, characterization and hydrogen peroxide mediated sulfide oxygenation.

A series of mononuclear oxovanadium(v) complexes of tridentate Schiff bases HL(1)-HL(4) and H(2)L(5)-H(2)L(8) derived from 6-phenylsalicylaldehyde and 6-(2-hydroxyphenyl)salicylaldehyde and four different amines was synthesized. The systematically selected ligands contain aliphatic or aromatic nitrogen, or alkoxy- and phenoxy-oxygen as third donor atom. The complexes were characterised by spectroscopic methods in solution and the solid state. Single-crystal X-ray analyses were performed with VO(2)L(1)(), VO(2)L(3)x1/2EtOH (), VO(2)L(4)(), VO(OiPr)L(7)xiPrOH, VO(OiPr)L(8) and H(2)L(8). For all compounds the vanadium(v) cores contain distorted tetragonal pyramidal geometry around the dioxo- and oxovanadium site at which the N(2)O- and NO(2)-donor ligands bind equatorially. Complexes and display intramolecular hydrogen bonding of the pendant hydroxyphenyl group to a coordinated oxygen trans to a nitrogen atom and therefore serve as suitable models for the native site of vanadium dependent haloperoxidases. Variable-temperature (1)H NMR spectra revealed significant hydrogen bond interaction in acetonitrile solution. In situ prepared catalysts are active for hydrogen peroxide mediated oxygenation of ethyl phenyl sulfide and showed complete conversion of the substrate to ethyl phenyl sulfoxide, together with small amounts of the corresponding sulfone, as detected by GC/MS after 10 min. The complex of H(2)L(7) turned out to be most efficient while HL(1) and HL(2) were completely inactive. Catalysis is supported by the pendant OH group in the complex of HL(3), the catalyst is twice as active as the complex of HL(4).

Biphenyl Compounds↗
PubMed1993

Multiple reactions in vanadyl-V(IV) oxidation by H2O2.

Oxidation of vanadyl sulfate by H2O2 involves multiple reactions at neutral pH conditions. The primary reaction was found to be oxidation of V(IV) to V(V) using 0.5 equivalent of H2O2, based on the loss of blue color and the visible spectrum. The loss of V(IV) and formation V(V) compounds were confirmed by ESR and 51V-NMR spectra, respectively. In the presence of excess H2O2 (more than two equivalents), the V(V) was converted into diperoxovanadate, the major end-product of these reactions, identified by changes in absorbance in ultraviolet region and by the specific chemical shift in NMR spectrum. The stoichiometric studies on the H2O2 consumed in this reaction support the occurrence of reactions of two-electron oxidation followed by complexing two molecules of H2O2. Addition of a variety of compounds--Tris, ethanol, mannitol, benzoate, formate (hydroxyl radical quenching), histidine, imidazole (singlet oxygen-consumption that also used V(IV) as the reducing source. This reaction requires concomitant oxidation of vanadyl by H2O2, favoured at low H2O2:V(IV) ratio. Another secondary reaction of oxygen release was found to occur during vanadyl oxidation by H2O2 in acidic medium in which the end-product was not diperoxovanadate but appears to be a mixture of VO3+ (-546 ppm), VO3+ (-531 ppm) and VO2+ (-512 ppm), as shown by the 51V-NMR spectrum. This reaction also occurred in phosphate-buffered medium but only on second addition of vanadyl. The compounds that stimulated the oxygen-consumption reaction were found to inhibit the oxygen-release reaction. A combination of these reactions occur depending on the proportion of the reactants (vanadyl and H2O2), the pH of the medium and the presence of some compounds that affect the secondary reactions.

Citrates↗
PubMed1985

Effective DNA cleavage by bleomycin-vanadium(IV) complex plus hydrogen peroxide.

It has been firstly found that the bleomycin-vanadyl(IV) complex is effectively capable of cleaving DNA in the presence of hydrogen peroxide. The 1:1 bleomycin-VO(IV) complex has been characterized by ESR and electronic absorption spectra, and its ESR parameters (go = 1.982 and Ao = 93.5 G) are indicative of VO(N5) coordination type for the metal-binding environment. The mode of nucleotide sequence cleavage induced by the present bleomycin-VO(IV)-H2O2 complex system was appreciably different from the corresponding Fe(III) complex system. Of special interest is the fact that the bleomycin-vanadium complex system more preferentially attacked G-A(5'----3') sequences than the bleomycin-iron complex system.

Base Sequence↗
PubMed2002

A fluorescent compound for glucose uptake measurements in isolated rat cardiomyocytes.

A focus of current diabetes research is the development of insulinomimetic compounds for oral treatment of diabetes and its associated cardiac complications. Screening compounds for their potential insulinomimetic effects usually involves the use of radioactive isotopes. The focus of this study was to investigate a nonradioactive fluorescent compound for its use in screening insulinomimetic compounds. The indicator 2-(N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino)-2-deoxyglucose (2-NBDG) has been used by some workers to measure glucose uptake in Escherichia coli and Candida albicans. We propose that 2-NBDG will also be a suitable indicator for mammalian cell lines, in particular rat cardiomyocytes. We found that the indicator could give a reliable reproducible standard curve following appropriate dilution and is taken up by isolated cardiomyocytes. The insulinomimetic compounds vanadyl sulfate and sodium molybdate showed rates of glucose uptake similar to that of insulin. Furthermore, the rate of uptake measured for insulin using this technique (0.04 +/- 0.003 nmol x min(-1) x 10(6) cells(-1) is comparable with previous literature using 2-deoxyglucose uptake measurements on isolated myocytes (0.040 nmol x min(-1) x 10(6) cells(-1), demonstrating the validity of this fluorescent compound for glucose uptake studies.

4-Chloro-7-nitrobenzofurazan↗
PubMed1993

Phosphatase inhibitors, gap junctional intercellular communication and [125I]-EGF binding in hamster fibroblasts.

A number of phosphatase inhibitors (okadaic acid, calyculin A, aluminium fluoride, sodium molybdate, sodium orthovanadate, pervanadate and vanadyl sulphate) were investigated for their effects on gap junctional intercellular communication (GJIC) and [125I]-epidermal growth factor (EGF) binding in early passage Syrian hamster embryo cells (mainly fibroblast-like cells) and in V79 Chinese hamster lung fibroblasts. Only pervanadate decreased GJIC significantly. After the initial pervanadate-induced decrease the GJIC recovered rapidly. Only pervanadate was able to change the band pattern of the gap junction protein connexin43 (cx43) in Western blots. Together this may indicate either that there is a low turnover of phosphate groups in cx43 under basal conditions or that the putative phosphatases are not sensitive to most of the phosphatase inhibitors applied. In contrast, pervanadate, orthovanadate and molybdate decreased [125I]-EGF binding. 12-O-Tetradecanoylphorbol-13-acetate (TPA) is able to induce the phosphorylation of both cx43 and the EGF receptor, concomitantly with a decrease in GJIC and [125I]-EGF binding. These effects are reversible after removal of TPA. It could be imagined that other phosphatases would act on cx43 and the EGF receptor after the forced phosphorylation of the two molecules. Thus TPA was used to downregulate GJIC and [125I]-EGF binding and phosphatase inhibitors were applied in the upregulation phase. Only pervanadate affected the upregulation of GJIC, and pervanadate, orthovanadate and molybdate affected the upregulation of [125I]-EGF binding. Thus it is not an identical complement of phosphatases that act on cx43 and the EGF receptor. All the downregulating agents are assumed to be phosphotyrosine phosphatase inhibitors.

Aluminum Compounds↗