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PubMed2001

Effect of vanadium(IV) compounds in the treatment of diabetes: in vivo and in vitro studies with vanadyl sulfate and bis(maltolato)oxovandium(IV).

Vanadyl sulfate (VOSO(4)) was given orally to 16 subjects with type 2 diabetes mellitus for 6 weeks at a dose of 25, 50, or 100 mg vanadium (V) daily [Goldfine et al., Metabolism 49 (2000) 1-12]. Elemental V was determined by graphite furnace atomic absorption spectrometry (GFAAS). There was no correlation of V in serum with clinical response, determined by reduction of mean fasting blood glucose or increased insulin sensitivity during euglycemic clamp. To investigate the effect of administering a coordinated V, plasma glucose levels were determined in streptozotocin (STZ)-induced diabetic rats treated with the salt (VOSO(4)) or the coordinated V compound bis(maltolato)oxovandium(IV) (abbreviated as VO(malto)(2)) administered by intraperitoneal (i.p.) injection. There was no relationship of blood V concentration with plasma glucose levels in the animals treated with VOSO(4), similar to our human diabetic patients. However, with VO(malto)(2) treatment, animals with low plasma glucose tended to have high blood V. To determine if V binding to serum proteins could diminish biologically active serum V, binding of both VOSO(4) and VO(malto)(2) to human serum albumin (HSA), human apoTransferrin (apoHTf) and pig immunoglobulin (IgG) was studied with EPR spectroscopy. Both VOSO(4) and VO(malto)(2) bound to HSA and apoHTf forming different V-protein complexes, while neither V compound bound to the IgG. VOSO(4) and VO(malto)(2) showed differences when levels of plasma glucose and blood V in diabetic rodents were compared, and in the formation of V-protein complexes with abundant serum proteins. These data suggest that binding of V compounds to ligands in blood, such as proteins, may affect the available pool of V for biological effects.

Animals↗
PubMed1986

Vanadium inhibits ACTH-mediated but not cyclic AMP-dependent adrenal steroidogenesis.

We have studied the effect of vanadium on steroidogenesis using dispersed cells from rat adrenals. It was found that when the cells were stimulated by ACTH both vanadate and vanadyl sulfate inhibited adrenal steroidogenesis. In contrast, when steroidogenesis was supported by cAMP analogues, no inhibition was observed. The inhibitory action of vanadium compounds was also seen when cholera toxin or forskolin was used as a stimulant instead of ACTH, indicating that vanadate does not act on the ACTH-receptor protein. When adrenal cells were stimulated by ACTH, cholera toxin- or forskolin-supported cAMP levels were diminished equally by vanadate. In addition, the mitochondrial steroid hydroxylation per se was not inhibited by vanadium compounds using either endogenous or exogenous steroid substrates. Based on these results, it is concluded that the site of inhibition by vanadium is located in the vicinity of the guanine nucleotide-binding protein and the catalytic unit of adenylate cyclase.

Adrenal Cortex Hormones↗
PubMed2002

Control and STZ-diabetic rat liver Golgi complexes under the influence of bis(2,2'-bipyridine)oxovanadium(IV) sulphate. The morphological investigation.

Identification of a vanadium compound with the highest efficacy and least toxicity is the main scientific problem in diabetes treatment. All vanadium complexes, both inorganic and organic, apart from improving physiological and biochemical diabetic parameters, show more or less toxic effects in living organisms. For this reason we decided to test a new vanadium compound: bis(2,2'-bipyridine)oxovanadium(IV), [VO(bpy)2], not used or described so far. This paper stressed morphological alterations of rat liver Golgi apparatus originated from control or streptozotocin (STZ)-diabetic rats treated with 1.8 mmol VO(bpy)2 solution in 0.5% NaCl as drinking liquid for 7 days and compared them with a parallel biochemical study. There was a correlation between the activity of Golgi marker enzyme i.e. galactosyl transferase and morphology of this organelle. In control rats treatment with VO(bpy)2 caused drastic changes, in many cases leading to a complete destruction of liver Golgi apparatus. In STZ-diabetic liver of rats treated with VO(bpy)2 the Golgi apparatus showed characteristic of untreated diabetes arching or even twisting of stack cisternae but improvement of the secretory activity (dilatation of cisternae edges, some secretory vacuoles and vesicles). In our opinion, the parallel action of two drugs: STZ combined with VO(bpy)2, relieves or even eliminate harmful effects of each compound alone.

2,2'-Dipyridyl↗
PubMed2004

Influence of vanadyl sulphate [VOSO4] on biochemical activity and morphology of control and streptozotocin-diabetic rat liver Golgi complexes.

The authors describe the influence of vanadyl sulphate on liver Golgi complexes in control and streptozotocin (STZ)-diabetic rats. VOSO4, one of inorganic vanadium compounds widely used in animal models and human diabetes, acts as an insulin-mimetic drug and is relatively well known as a complex activated or inhibited on many enzymes involved in carbohydrate or lipid metabolic pathways. A relatively small in scope investigation was performed on subcellular levels, while changes of Golgi complexes under vanadium influence have not been described with the exception of our previous investigations with four organic derivatives. This paper presents the action of vanadyl sulphate used in 3mM in 0.5% NaCl as a drinking solution for 7 days on control and STZ-diabetic rat liver Golgi complexes. Changes induced by this vanadium compound were greater in the controls as compared to the diabetic rats, what was true for both biochemical and morphological data. Physiological and biochemical analyses showed a partial normalization of the investigated parameters in diabetic animals after short time treatment with vanadyl ions, although STZ-diabetic, vanadium treated rats were affected by two types of adverse effects exterted by these compounds. The controls manifested more numerous and advanced subcellular changes. The moderately developed Golgi apparatus showed no major changes. In the control group, subcellular changes were seen sporadically. More extended Golgi complexes showed certain anomalies.

Animals↗
PubMed2000

Vanadate induces calcium signaling, Ca2+ release-activated Ca2+ channel activation, and gene expression in T lymphocytes and RBL-2H3 mast cells via thiol oxidation.

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. In the presence of external Ca2+, vanadium compounds produced sustained or oscillatory Ca2+ elevations; in nominally Ca2+-free medium, a transient Ca2+ rise was generated. Vanadate-induced Ca2+ signaling was blocked by heparin, a competitive inhibitor of the 1,4, 5-inositol trisphosphate (IP3) receptor, suggesting that Ca2+ influx is secondary to depletion of IP3-sensitive Ca2+ stores. In Jurkat T cells, vanadate also activated the Ca2+-dependent transcription factor, NF-AT. Intracellular dialysis with vanadate activated Ca2+ influx through Ca2+ release-activated Ca2+ (CRAC) channels with kinetics comparable to those of dialysis with IP3. Neither phosphatase inhibitors nor nonhydrolyzable nucleotide analogues modified CRAC channel activation. The action of vanadate, but not IP3, was prevented by the thiol-reducing agent DTT. In addition, the activation of CRAC channels by vanadate was mimicked by the thiol-oxidizing agent chloramine T. These results suggest that vanadate enhances Ca2+ signaling via thiol oxidation of a proximal element in the signal transduction cascade.

Adenosine Triphosphate↗
PubMed2003

Effects of ammonium metavanadate on fertility and reproductive performance of adult male and female rats.

Vanadium is a ubiquitous trace metal present in most plant and animal tissues. Environmental exposure to trivalent and pentavalent inorganic vanadium compounds has been related to impaired different phases of reproduction. Therefore, the effects of a pentavalent inorganic vanadium compound on general reproductive performance and fertility were investigated in male and female rats. Sexually mature male and female rats were exposed to 200 ppm ammonium metavanadate in drinking water. Male rats were exposed for 70 days, while the female rats exposed for 14 days premating, during mating, and throughout the whole length of gestation and lactation periods till weaning. The effects on male sex organ weights and fertility were evaluated at the end of exposure period. However, the effects on female fertility as well as developmental and postnatal effects were evaluated throughout the exposure period. The fertility was significantly reduced in both treated groups, with more pronounced suppressive effects in the male treated group. The number of implantation sites and the number of viable fetuses were significantly reduced in pregnant females of both treated groups. However, the number of resorptions, dead fetuses, and pre- and postimplantation losses were significantly increased. The incidence of resorptions was significantly increased in treated female group compared with untreated female group. The behavioral responses as well as fetal survival and viability indices were decreased in both treated groups during the lactation period. The incidence of these effects was more pronounced in the treated female group. The morphological, visceral, and skeletal anomalies were recorded significantly increased in fetuses of both treated groups, with more pronounced effects on fetuses of treated females. In conclusion, the exposure of adult male and female rats to ammonium metavanadate would cause adverse effects on fertility and reproduction.

Animals↗
PubMed2002

Vanadium in cancer treatment.

Vanadium compounds exert preventive effects against chemical carcinogenesis on animals, by modifying, mainly, various xenobiotic enzymes, inhibiting, thus, carcinogen-derived active metabolites. Studies on various cell lines reveal that vanadium exerts its antitumor effects through inhibition of cellular tyrosine phosphatases and/or activation of tyrosine phosphorylases. Both effects activate signal transduction pathways leading either to apoptosis and/or to activation of tumor suppressor genes. Furthermore, vanadium compounds may induce cell-cycle arrest and/or cytotoxic effects through DNA cleavage and fragmentation and plasma membrane lipoperoxidation. Reactive oxygen species generated by Fenton-like reactions and/or during the intracellular reduction of V(V) to V(IV) by, mainly, NADPH, participate to the majority of the vanadium-induced intracellular events. Vanadium may also exert inhibitory effects on cancer cell metastatic potential through modulation of cellular adhesive molecules, and reverse antineoplastic drug resistance. It also possesses low toxicity that, in combination with the synthesis of new, more potent and better tolerated complexes, may establish vanadium as an effective non-platinum, metal antitumor agent.

Animals↗
PubMed1998

[Determination of vanadium concentration in foods produced on the Eastern Coast of Lake Maracaibo].

In the northeastern coast of Lake Maracaibo it has been reported some years ago a high incidence of congenital malformations of the Central Nervous Systems (Neural Tube Defects Type). This epidemiological problem is present in other countries too (Ireland and New Zealand) and has been associated with oil activities. In fact, some experimental works inform about the vanadium compounds cellular toxic effects mainly in the Central Nervous System of mammals. The main goal of this work is to measure the vanadium content in foods produced in the northeastern coast of Lake Maracaibo. Lagunillas, Valmore Rodriguez, and Baralt were the districts selected for the work. The digestion of the samples achieved by the methodology reported by Myron et al., with Graphite Furnace Atomic Absorption. The amounts of vanadium in the different foods analized were higher than the controls in the bibliographic reports. At this moment, there is not definitive proofs that vanadium compounds are the etiological agents of the Neural Tube Defects, but, these compounds are presents in foods produced in the northeastern coast of Lake Maracaibo.

Food Analysis↗
PubMed1994

Amelioration of diabetes and cataract by Na3VO4 plus U-83836E in streptozotocin treated rats.

Experimental work in our laboratory has confirmed the protective activity of vanadium compounds on hyperglycemia and glycosuria in streptozotocin (STZ) diabetes. Furthermore, diabetic cataract has also been partially prevented. Nevertheless, the combination of a natural antioxidant, vitamin E, with Na3 VO4 has not further enhanced this ameliorating effect. Our experimental approach has been an attempt to block the prooxidant activity of both STZ and vanadate, with the purpose of eliciting the best possible antidiabetic protection. More recently, a lipid soluble synthetic antioxidant U-78517F, a 2-methylaminochroman, has been reported to have a significant protective effect against brain injury and ischemia. This compound inhibits the iron-dependent lipid peroxidation 100 times more effectively than vitamin E. This investigation has introduced a combination of the vanadium compound plus the aforesaid lazaroid, as its (-) enantiomer, U-83836E, in order to improve the insufficient protection when vitamin E was used. For twelve weeks, male Wistar rats, rendered diabetic with STZ, were administered Na3VO4 in drinking water along with the lazaroid carried by the food. Four, eight and twelve weeks after the beginning of the protective treatment, fluid and food intake, diuresis and excreted feces, glycosuria and proteinuria were determined on biological samples obtained in metabolic cages; body weight and glycemia were also recorded. At weeks 6 and 12 of the treatment, the opaqueness of the eye lenses was controlled and registered. At the end of the experiment, circulating glycosylated hemoglobin (HbA1c), fructosamine, N-acetyl-beta-D-glucosaminidase (NAG), and fluorescent peroxides were evaluated. Within the first month of treatment, protection by the combination paralleled that elicited by vanadate alone. At subsequent steps, U-83836E significantly improved the protective effect of vanadate alone on polydipsia and polyuria, but especially on hyperglycemia and glycosuria. The further ameliorating effect of the lazaroid was also observed on HbA1c and NAG, and, most important, on the cataract. In conclusion, these findings demonstrate that the lazaroid U-83836E succeeds in further protecting the most important symptoms of diabetes treated with vanadate, and that this antioxidant acts effectively even when it is administered orally in food, in a non invasive manner.

Acetylglucosaminidase↗
PubMed1981

Vanadium in photosynthesis of Chlorella fusca and higher plants.

The influence of vanadium compounds (vanadate, vanadyl citrate) on photosynthesis in Chlorella fusca and in algal and spinach chloroplasts has been investigated. It was found that: 1. At moderately high concentrations (at least 0.1 mM) both vanadate and vanadyl citrate enhance photosynthetic O2 production in intact C. fusca cells. At lower V concentration (about 2 microM) only vanadate stimulates photosynthesis. The increase is dependent on culture conditions and on light intensity. 2. Up to 1 mM V, neither vanadium compound influences PS II activity, either in intact cells or in algal or spinach chloroplasts. 3. The PS I reaction in algal and spinach chloroplasts is maximally enhanced (3-fold) in presence of vanadium (20 microM). The increase is independent of light intensity. 4. Cr(VI), Mo(VI), and W(VI) (1 mM) stimulate photosynthesis in intact C. fusca cells, but do not influence the photosystems of isolated chloroplasts. Vanadium is suggested to act as a redox catalyst in the electron transport from PS II to PS I.

Chlorella↗
PubMed2006

Pentavalent vanadium induces hepatic metallothionein through interleukin-6-dependent and -independent mechanisms.

Metallothionein (MT) is a low-molecular-weight cysteine-rich protein which has a high affinity for metals. The synthesis of MT is induced by heavy metals such as cadmium and zinc. However, little is known about the induction of MT by tetravalent or pentavalent metals. We investigated the induction of MT synthesis by a pentavalent vanadium compound in mice. Hepatic MT concentrations were increased by subcutaneous injection of ammonium metavanadate (AMV) dose-dependently, and to the similar levels as those induced by zinc chloride. However, accumulation of vanadium in the liver was very low, while high concentrations of vanadium were detected in the kidney. High performance liquid chromatography/inductively coupled argon plasma-mass spectrometry (HPLC/ICP-MS) chromatogram of the liver cytosol of AMV-treated mice revealed that the major metal bound to MT was not vanadium, but zinc. The chromatogram of the liver cytosol of MT null mice demonstrated the existence of a low-molecular-weight vanadium-binding protein that is different from MT. A time-course study showed that concentrations of serum interleukin-6 (IL-6) and serum amyloid A (SAA), an acute-phase protein, increased after the AMV injection. To confirm the involvement of IL-6 in MT induction by AMV administration, IL-6 null and wild-type mice were injected with AMV. In IL-6 null mice, hepatic MT induction by AMV administration decreased significantly to about a half of wild-type mice. These data suggest that both IL-6-dependent and -independent mechanisms are involved in MT induction by vanadium compounds in mice.

Alanine Transaminase↗
PubMed1996

Vanadium-induced chemokine mRNA expression and pulmonary inflammation.

Occupational exposure to vanadium is common in petrochemical, mining, steel, and utilities industries and results in toxic effects largely confined to the respiratory system. Vanadium exposure has been associated with inflammatory changes in the upper and lower respiratory tracts in addition to changes in pulmonary function. We investigated the abilities of several vanadium compounds to increase mRNA levels for selected cytokines in bronchoalveolar lavage (BAL) cells and also to induce pulmonary inflammation. Rats (200-250 g) were intratracheally instilled with either sodium metavanadate (NaVO3), vanadyl sulfate (VOSO4), vanadium pentoxide (V2O5) at several concentrations, or vehicle alone. Pulmonary inflammation was assessed by cytologic analysis of cells recovered from the respiratory tract (1 hr to 10 days postexposure). All three vanadium compounds were capable of inducing pulmonary inflammation in a dose-dependent manner. Neutrophil influx was greatest following exposure to VOSO4 (peaked at approximately 40% of cell population) and lowest following exposure to V2O5 (peaked at approximately 20 %). Significant neutrophil influx was detected as early as 4 hr following the instillation of NaVO3 and VOSO4 but not until 24 hr upon exposure to V2O5. The VOSO4-induced inflammatory response persisted longer (5 days) than that induced by NaVO3 and V2O5. Analysis of inflammatory cytokine mRNA expression closely followed these cytologic observations. Levels of mRNA for macrophage inflammatory protein-2 (MIP-2) and KC, considered the principal neutrophil chemotactic factors expressed in the rat, were rapidly induced as early as 1 hr following exposure, continued to be expressed throughout 48 hr, and were low but detectable at 5 and 10 days. NaVO3 and VOSO4, both very soluble forms of vanadium, tended to induce pulmonary inflammation and inflammatory cytokine mRNA expression more rapidly and more intensely than the less soluble form, V2O5. Analysis of KC mRNA expression in BAL cells 24 hr after instillation of NaVO3 by PCR in situ hybridization confirmed the increase in KC mRNA levels and indicated that alveolar macrophages have the highest expression level observed. Vanadium content of lavage fluid, BAL cells, and lung indicated rapid clearance of the metal from the lung surface and substantial accumulation by BAL cells and lung tissue. The rapid expression of MIP-2 and KC mRNA in BAL cells prior to the observed neutrophilia implicate them as important in the initiation of inflammation.

Animals↗
PubMed1998

Vanadium and diabetes.

We demonstrated in 1985 that vanadium administered in the drinking water to streptozotocin (STZ) diabetic rats restored elevated blood glucose to normal. Subsequent studies have shown that vanadyl sulfate can lower elevated blood glucose, cholesterol and triglycerides in a variety of diabetic models including the STZ diabetic rat, the Zucker fatty rat and the Zucker diabetic fatty rat. Long-term studies of up to one year did not show toxicity in control or STZ rats administered vanadyl sulfate in doses that lowered elevated blood glucose. In the BB diabetic rat, a model of insulin-dependent diabetes, vanadyl sulfate lowered the insulin requirement by up to 75%. Vanadyl sulfate is effective orally when administered by either single dose or chronic doses. It is also effective by the intraperitoneal route. We have also been able to demonstrate marked long-term effects of vanadyl sulfate in diabetic animals following treatment and withdrawal of vanadyl sulfate. Because vanadyl sulfate is not well absorbed we have synthesized and tested a number of organic vanadium compounds. One of these, bismaltolato-oxovanadium IV (BMOV), has shown promise as a therapeutic agent. BMOV is 2-3x more potent than vanadyl sulfate and has shown less toxicity. Recent studies from our laboratory have shown that the effects of vanadium are not due to a decrease in food intake and that while vanadium is deposited in bone it does not appear to affect bone strength or architecture. The mechanism of action of vanadium is currently under investigation. Several studies indicate that vanadium is a phosphatase inhibitor and that vanadium can activate serine/threonine kinases distal to the insulin receptor presumably by preventing dephosphorylation due to inhibition of phosphatases Short-term clinical trials using inorganic vanadium compounds in diabetic patients have been promising.

Animals↗
PubMed2002

Cholesterol depletion blocks redistribution of lipid raft components and insulin-mimetic signaling by glimepiride and phosphoinositolglycans in rat adipocytes.

UNLABELLED: Glycosylphosphatidylinositol-anchored plasma membrane (GPI) proteins, such as Gce1, the dually acylated nonreceptor tyrosine kinases (NRTKs), such as pp59(Lyn), and the membrane protein, caveolin, together with cholesterol are typical components of detergent/carbonate-insoluble glycolipid-enriched raft domains (DIGs) in the plasma membrane of most eucaryotes. Previous studies demonstrated the dissociation from caveolin and concomitant redistribution from DIGs of Gce1 and pp59(Lyn) in rat adipocytes in response to four different insulin-mimetic stimuli, glimepiride, phosphoinositolglycans, caveolin-binding domain peptide, and trypsin/NaCl-treatment. We now characterized the structural basis for this dynamic of DIG components. MATERIALS AND METHODS: Carbonate extracts from purified plasma membranes of basal and stimulated adipocytes were analyzed by high-resolution sucrose gradient centrifugation. RESULTS: This process revealed the existence of two distinct species of detergent/carbonate-insoluble complexes floating at higher buoyant density and harboring lower amounts of cholesterol, caveolin, GPI proteins, and NRTKs (lcDIGs) compared to typical DIGs of high cholesterol content (hcDIGs). The four insulin-mimetic stimuli decreased by 40-70% and increased by 2.5- to 5-fold the amounts of GPI proteins and NRTKs at hcDIGs and lcDIGs, respectively. Cholesterol depletion of adipocytes per se by incubation with methyl-beta-cyclodextrin or cholesterol oxidase also caused translocation of GPI proteins and NRTKs from hcDIGs to lcDIGs and their release from caveolin in reversible fashion without concomitant induction of insulin-mimetic signaling. Cholesterol depletion, however, reduced by 50-60% the stimulus-induced translocation as well as dissociation from hcDIGs-associated caveolin of GPI proteins and NRTKs, activation of NRTKs as well as insulin-mimetic signaling and metabolic action. In contrast, insulin-mimetic signaling induced by vanadium compounds was not significantly diminished by cholesterol depletion. CONCLUSIONS: The data provide evidence that insulin-mimetic signaling in rat adipocytes provoked by glimepiride, phosphoinositolglycans, caveolin-binding domain peptide, and trypsin/NaCl-treatment, but not vanadium compounds, relies on the dynamics of DIGs-the translocation of certain GPI proteins and NRTKs from hcDIGs to lcDIGs mediated by a trypsin/NaCl-sensitive cell surface component. The resultant stimulation of pp59(Lyn) in course of its dissociation from caveolin and incorporation into lcDIGs in combination with an lcDIGs-independent signal seems to substitute for activation of the insulin receptor tyrosine kinase.

Adipocytes↗
PubMed2000

A possible role of oxidative stress in the vanadium-induced cytotoxicity in the MC3T3E1 osteoblast and UMR106 osteosarcoma cell lines.

The cytotoxicity and free radical production induced by vanadium compounds were investigated in an osteoblast (MC3T3E1) and an osteosarcoma (UMR106) cell lines in culture. Vanadate induced cell toxicity, reactive oxygen species (ROS) formation and thiobarbituric acid reactive substances (TBARS) increased in a concentration-dependent manner (0.1-10 mM) after 4 h. The concentration-response curve of vanadate-induced cytotoxicity and oxidative stress in MC3T3E1 cells was shifted to the left of the UMR106 curve, suggesting a greater sensitivity of the non-transformed cells in comparison to the osteosarcoma UMR106 cells. Supplementing with vitamin E acetate (80 microM) significantly inhibited ROS and TBARS formation but did not improve the vanadate-dependent decrease in cell number. Other vanadium compounds (vanadyl, pervanadate, and VO/Aspi, a complex of vanadyl(IV) with aspirin) showed different degrees of cell toxicity and induced oxidative stress. Altogether these results suggest that oxidative stress is involved in vanadium induced osteoblastic cytotoxicity, although the mechanism is unknown.

Antioxidants↗
PubMed1991

Oral vanadium administration to streptozotocin-diabetic rats has marked negative side-effects which are independent of the form of vanadium used.

In the present investigation, the effects of oral administration of sodium metavanadate, sodium orthovanadate and vanadyl sulphate to alleviate some signs of diabetes in streptozotocin-treated rats have been evaluated. Streptozotocin-induced diabetic rats drank aqueous solutions (NaCl, 80 mM) containing sodium metavanadate (0.15 mg/ml), sodium orthovanadate (0.23 mg/ml), or vanadyl sulphate pentahydrate (0.31 mg/ml) for 28 days. The vanadium-treated animals were compared to controls, either diabetic or nondiabetic, receiving drinking water containing NaCl (80 mM) only. Daily food and fluid intake were significantly decreased in the vanadium-treated animals relative to diabetic controls. Also, vanadium treatment reduced the level of hyperglycemia in diabetic rats, with sodium metavanadate being the most effective of the vanadium compounds tested. However, daily vanadium intake was significantly lower in the animals receiving sodium metavanadate. Signs of toxicity were observed in all vanadium-treated animals as evidenced by some deaths, decreased weight gain, and increased serum concentrations of urea and creatinine. Moreover, vanadium was detected in all tissues analyzed. Although some signs of diabetes were improved by vanadium treatment, because of the severe toxic side effects noted in all of the vanadium-treated animals, it seems evident that oral vanadium administration is not a suitable therapy of diabetes mellitus in streptozotocin-diabetic rats.

Administration, Oral↗
PubMed2002

Magnetic properties of a homologous series of vanadium jarosite compounds.

Redox-based, hydrothermal synthetic methodologies have enabled the preparation of a new series of stoichiometrically pure jarosites of the formula, AV(3)(OH)(6)(SO(4))(2) with A = Na(+), K(+), Rb(+), Tl(+), and NH(4)(+). These jarosites represent the first instance of strong ferromagnetism within a Kagomé layered framework. The exchange interaction, which is invariant to the nature of the A(+) ion (theta(CW) approximately equal to +53(1) K), propagates along the d(2) magnetic sites of the triangular Kagomé lattice through bridging hydroxyl groups. An analysis of the frontier orbitals suggests this superexchange pathway to possess significant pi-orbital character. Measurements on a diamagnetic host jarosite doped with magnetically dilute spin carriers, KGa(2.96)V(0.04)(OH)(6)(SO(4))(2), reveal significant single-ion anisotropy for V(3+) ion residing in the tetragonal crystal field. This anisotropy confines the exchange-coupled moments to lie within the Kagomé layer. Coupling strengths are sufficiently strong to prevent saturation of the magnetization when an external field is applied orthogonal to the Kagomé layer. Antiferromagnetic ordering of neighboring ferromagnetic Kagomé layers becomes dominant at low temperatures, characteristic of metamagnetic behavior for the AV(3)(OH)(6)(SO(4))(2) jarosites. This interlayer exchange coupling decreases monotonically with increasing layer spacing along the series, A = Na(+), K(+), Rb(+), NH(4)(+), and Tl(+), and it may be overcome by the application of external field strengths in excess of approximately 6 kOe.

Journal Article↗