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PubMed1986

Kinetic model of whole-body vanadium metabolism: studies in sheep.

A compartmental model for vanadium metabolism in sheep has been proposed. The model is consistent with data obtained from sheep fed a control diet (2.6 ppm vanadium) containing 0 or 200 ppm supplemental vanadium. Sheep were administered 48V dioxovanadium either orally or intravenously. Blood, feces, and urine radioactivity were monitored for 6 days postdosing. Several new insights regarding vanadium metabolism are suggested and tested against the data using the model. Some of these include significant absorption of 48V occurs from the upper gastrointestinal tract; an in vivo process is necessary in order for 48V dioxovanadium to be converted into a more biologically reactive species; at steady state the upper and lower gastrointestinal tracts contain at least 10- and 100-fold more mass of vanadium, respectively, than does blood. No statistically significant differences in transport rate constants were found between animals receiving 0 and 200 ppm supplemental dietary vanadium. The availability of a model will enable the refinement of future studies regarding vanadium metabolism in the ruminant.

Administration, Oral↗
PubMed1998

Oxidative stress of vanadium-mediated oxygen free radical generation stimulated by aluminium on human erythrocytes.

It has been suggested that aluminium stimulates vanadium-mediated superoxide radical generation. The oxidative stress of generated superoxide radicals on antioxidant enzyme activity, oxidation of NADH and NADPH, membrane lipid peroxidation and osmotic fragility in human red blood cells (RBC) was investigated. RBC were incubated with varying concentrations of vanadium and aluminium ions at 37 degrees C for 2 h. RBC incubated with vanadium ions showed significantly increased superoxide dismutase and catalase activities, and oxidized NADH and NADPH concentrations compared with control RBC preparations. Erythrocyte lipid peroxidation was assessed by measuring thiobarbituric acid reactivity. RBC incubated with elevated levels of vanadium showed significantly increased membrane lipid peroxidation when compared with control RBC; it increased further on addition of aluminium. A significant positive correlation was observed between the extent of vanadium induced membrane lipid peroxidation and the osmotic fragility of treated RBC. In the presence of vanadium, aluminium stimulates superoxide dismutase and catalase activities. NADH and NADPH oxidation and membrane lipid peroxidation, as well as increasing osmotic fragility of human erythrocytes. The stimulatory effect of aluminium was dependent on concentration. These results may have implications for the mechanism of toxicity of aluminium and vanadium in haemodialysis patients.

Aluminum↗
PubMed1998

Effect of selenium on vanadium toxicity in different regions of rat brain.

The protective effect of selenium on the neurotoxicity of vanadium in different brain regions of rats was investigated. The lipid peroxidation was significantly accentuated after intraperitoneal (i.p.) administration of vanadium (1.5 mg kg-1 b.wt) for a period of 12 consecutive days to rats. The increase in lipid peroxidation was inhibited by selenium treatment (0.02 mg kg-1 b.wt., i.p.) for 12 consecutive days. Vanadium exposure produced a decrease in nonprotein sulfhydryl group. Selenium treatment prevented the depression in nonprotein sulfhydryl group in all the brain regions of the vanadium exposed rats. The concentration of ascorbic acid was decreased after co-administration of selenium and vanadium. These results suggest that selenium protects neuronal cells against neurotoxic effects of vanadium by maintaining the availability of antioxidant nonprotein sulfhydryl groups. The decrease in ascorbic acid levels may have been due to its consumption in forming complexes with vanadium.

Animals↗
PubMed2005

Vanadium, a versatile biochemical effector in chemical rat mammary carcinogenesis.

Recent studies indicate the role of the micronutrient vanadium in chemoprevention in many animal models, human cancer cell lines, and also in xenografted human carcinomas of the lung, breast, and gastrointestinal tract. The present studies were undertaken to ascertain the antineoplastic potential of vanadium in a defined model of mammary carcinogenesis. Female Sprague-Dawley rats, at 50 days of age, were treated with 7,12-dimethylbenz(alpha) anthracene (DMBA) (0.5 mg/100 g body weight) by a tail vein injection in oil emulsion. Vanadium (ammonium metavanadate) at a concentration of 0.5 ppm (4.27 micromol/l) was supplemented in drinking water and given ad libitum to the experimental group after the carcinogen treatment, and it continued until the termination of the study. In vivo studies of DNA chain breaks demonstrated that vanadium offered significant (61%, P<0.005) protection against generation of single-strand breaks when compared with the DMBA control group. Supplementation of vanadium normalizes the level of zinc, iron, and copper as revealed by proton-induced X-ray emission analysis to a substantial extent (P<0.01). In vitro study of chromosomal aberrations (CAs) revealed that vanadium triggered a protective effect (62.9%) on induction of CAs, which was maximum on structural aberrations followed by numerical and physiological types. Histopathological and morphological analyses were done as end-point biomarkers. We conclude herein that vanadium has the potential to reduce genomic instability in mammary carcinoma in rats.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1999

Distinct glucose lowering and beta cell protective effects of vanadium and food restriction in streptozotocin-diabetes.

Vanadium is an oral insulin-mimetic agent that diminishes hyperglycemia, improves beta-cell insulin store and secretory function, and can reverse the diabetic state chronically after withdrawal from treatment. As food restriction has been reported to enhance insulin sensitivity and reduce insulin demand, we assessed the contribution of a reduced food intake to the glucose lowering and beta-cell protective effects of vanadium. Streptozotocin (STZ)-diabetic rats were untreated (D) or administered vanadyl sulfate in the drinking water (DT) at one week prior to and for 5 weeks following the administration of STZ. An additional group was pair-fed (DP) with an equal amount of food as that consumed by the DT group. Shortly after the induction of diabetes, hyperglycemic D rats demonstrated a significant rise in plasma insulin to levels that initially exceeded that of the controls. This was followed by a steady reduction over several weeks, suggesting a gradual depletion of functional beta-cells. Both vanadium treatment and pair-feeding abolished the insulin hypersecretory response following STZ administration. Glucose lowering was enhanced in DT animals when administered higher concentrations of vanadium, despite no further reduction in food intake, and all DT animals (10/10) were normoglycemic by 5 weeks. Mean pancreatic insulin content in DT rats was improved fourfold and was associated with a greater number of granulated beta-cells. Conversely, food restriction only modestly improved glycemia and the pancreatic insulin store and, unlike DT, DP rats remained highly glucose-intolerant. At 5 weeks of diabetes, fed circulating glucose and insulin levels were strongly correlated (P=0.0002) in the D and DP groups, supporting the notion that glucose lowering with food restriction is dependent on improved plasma insulin levels. A separate correlation was observed in DT animals within a lower range of plasma insulin, suggesting that vanadium, unlike food restriction, reduced plasma glucose by enhancing insulin sensitivity. Thus, vanadium preserves beta-cells in STZ-diabetes at least partially by abolishing the insulin hypersecretory response and the eventual exhaustion of residual insulin stores following a moderate dose of STZ. This property of vanadium would appear to be useful in the treatment of prediabetic and newly diagnosed insulin-dependent diabetes mellitus.

Animals↗
PubMed2002

Scanning x-ray microscopy of living and freeze-dried blood cells in two vanadium-rich ascidian species, Phallusia mammillata and Ascidia sydneiensis samea.

Some ascidians (sea squirts) accumulate the transitional metal vanadium in their blood cells at concentrations of up to 350 mM, about 10(7) times its concentration found in seawater. There are approximately 10 different types of blood cell in ascidians. The identity of the true vanadium-containing blood cell (vanadocyte) is controversial and little is known about the subcellular distribution of vanadium. A scanning x-ray microscope installed at the ID21 beamline of the European Synchroton Radiation Facility to visualize vanadium in ascidian blood cells. Without fixation, freezing or staining realized the visualization of vanadium localized in living signet ring cells and vacuolated amoebocytes of two vanadium-rich ascidian species, Phallusia mammillata and Ascidia sydneiensis samea. A combination of transmission and fluorescence images of signet ring cells suggested that in both species the vacuoles contain vanadium.

Animals↗
PubMed2002

Direct effect of vanadium on citrate uptake by rat renal brush border membrane vesicles (BBMV).

Vanadium pentoxide is used as a catalyst and a ferrovanadium alloy ingredient in automotive steels and in jet engines and airframes. In addition, vanadium is found in fuel oils. Thus, occupational exposures to vanadium pentoxide and trioxide may occur during the cleaning of oil-fired ship boilers, and from oil-fired power station boilers. Occupational exposure to vanadium pentoxide induces green tongue, asthmatic symptoms and albuminuria with cast. Urinary citrate is freely filtered at the glomerulus, and its reabsorption in the proximal tubule is the major determinant of the rate of renal excretion. In this study, we exposed rat renal brush border membrane vesicles (BBMV) to vanadium pentoxide and examined their citrate uptake characteristics. The preincubation of BBMV with 1 mM V2O5 for 8 hours significantly inhibited citrate uptake compared with that of BBMV without V2O5, preincubation. These findings indicate that the preincubation of BBMV with vanadium pentoxide results in a time-dependent inhibition of citrate uptake by BBMV. These findings might contribute to nephrotoxicity in vanadium exposure.

Animals↗
PubMed1976

The effect of diet on the toxicity of vanadium.

Five experiments were conducted with growing chicks to determine the effectiveness of various materials in modifying the toxicity of vanadium. The toxicity of vanadium (as it is measured by growth depression and mortality) was much greater when vanadium was added to a semipurified diet than when it was added to a practical diet containing natural ingredients. When EDTA was added to diets containing 50 to 200 p.p.m. vanadium, the growth depression was reduced from 22.1% and 75.9% to 8.4% and 36.7% respectively, and the mortality was reduced from 80% to 20% among chicks fed 200 p.p.m. vanadium. The addition of 10% lactose to a diet containing 100 p.p.m. vanadium increased the growth depression from 41% to 76.2% and caused 80% mortality. Chromium added to diets containing 100 and 200 p.p.m. vanadium improved the growth and reduced the mortality.

Animal Feed↗
PubMed1983

Toxicity of vanadium in female Leghorn chickens.

A study was conducted to determine the influence of dietary vanadium, fed after the onset of production, on hen day egg production, body weight changes, and mortality in laying breed chickens. Calcium orthovanadate was fed to 29-week-old female laying breed chickens at calculated levels of 0, 12.5, 25, 50, and 100 ppm dietary vanadium for five consecutive 28-day laying periods. Hen-day egg production and hen body weights were not influenced by the addition of 12.5 or 25 ppm dietary vanadium. Overall hen body weights and the hen day egg production were decreased in hens fed diets to which 50 ppm vanadium was added with a severe reduction in both parameters at 100 ppm. There were no mortalities during the experiment in the groups fed the 0, 12.5, 25, or 50 ppm vanadium diets. Mortality in the group fed the 100 ppm vanadium diet was 11, 39, and 56% at the end of the 28-day Periods 3, 4, and 5, respectively. There were no significant differences in egg weights, although a trend existed for lower egg weights with increasing levels of dietary 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↗
PubMedDate not supplied

Elimination of the interferences of anions in the kinetic spectrophotometric determination of vanadium (V) solution.

Accurate determination of vanadium (V) in industrial waste water is of great importance in environmental, biological and toxicological studies. Most of kinetic spectrophotometric methods based on the catalytic effect of vanadium (V), when applied to real samples for determination of trace levels of vanadium (V) lack the satisfactory sensitivity and selectivity. This may be attributed to the serious interferences of various anions which are common pollutants in industrial waste water. The oxidation of gallic acid by ammonium persulphate, catalysed by vanadium (V) was chosen for our study. The effect of the serious interferences of various anions such as chloride, bromate, bromide, chromate, iodide, iodate, molybdate, carbonate and sulphate on the net absorbance given by 4 microg l(-1) of vanadium (V) solution were studied. The minimum concentrations of citric acid, EDTA, ascorbic acid and oxalic acid as leveling off agents required to level off interfering effects due to the aforementioned anions in the kinetic determination of vanadium (V) were 50, 70, 80 and 120 microg ml(-1), respectively. In the presence of optimum concentrations of effective leveling off agents, the dynamic range can be extended and sensitivity increased as compared with the proposed method without levelling off agents. The proposed method is a rapid, sensitive and selective method for the determination of ultra trace amounts of vanadium (V) in real samples with satisfactory results.

Anions↗
PubMed2005

Effects of vanadium complexes on cell growth of human leukemia cells and protein-DNA interactions.

Vanadium complexes are known to possess potent insulin-mimetic effects, high affinity for several enzymes and anticancer activity, which deserve increasing attention for application to biomedical sciences. Different vanadium complexes have been found to be more effective than the simple vanadium-(IV) and -(V) salts in experiments performed both in vitro and in vivo. Application of polyoxometalates as potential drugs against Herpes Simplex Virus and AIDS have also increased the interest to study the association between vanadium containing species and proteins. The aim of our research was to investigate the in vitro antiproliferative activity of a variety of vanadium-containing compounds, and study their ability to interfere with the molecular interactions between GATA-1 and NF-kappaB transcription factors and target DNA elements, employing electrophoretic mobility shift assays. All of the used vanadium compounds were found to exhibit antiproliferative activity, despite with differences in efficacy. Inhibition of K562 cell growth was not associated with differentiation, but with activation of apoptosis. Vanadium complexes with a +5 oxidation state and their discrete anionic units appear essential for the respective effects on K562 cells; a +4 oxidation state appears to be important in inhibiting transcription factors/DNA interactions.

Apoptosis↗
PubMed1982

More sensitive flameless atomic absorption analysis of vanadium in tissue and serum.

We describe a sensitive method for the determination of vanadium in biological substances by atomic absorption spectroscopy. By using background correction and pyrolytically coated graphite tubes with flameless apparatus, this vanadium assay has a sensitivity of 65 pg and a detection limit of 30 pg, approximately sixfold more sensitive than previously reported assays involving this technique. The vanadium concentrations have been determined in several biological materials, including bovine liver and human serum. To investigate signal interferences, we have determined vanadium concentrations in matrix solutions containing several elements at physiologically relevant concentrations. Evaluated by the method of standard additions, the vanadium signals are linear with concentration over a range of 3 to 100 micrograms/L. Tissue vanadium concentrations are similar to those previously reported. Serum vanadium concentrations can be determined directly, and we found values ranging from 2.22 to 3.94 micrograms/L in human serum. The improved sensitivity permits the use of sample sizes substantially smaller than previously required.

Animals↗
PubMed2005

The effects of vanadium treatment on bone in diabetic and non-diabetic rats.

Vanadium-based drugs lower glucose by enhancing the effects of insulin. Oral vanadium drugs are being tested for the treatment of diabetes. Vanadium accumulates in bone, though it is not known if incorporated vanadium affects bone quality. Nine- to 12-month-old control and streptozotocin-induced diabetic female Wistar rats were given bis(ethylmaltolato)oxovanadium(IV) (BEOV), a vanadium-based anti-diabetic drug, in drinking water for 12 weeks. Non-diabetic rats received 0, 0.25 or 0.75 mg/ml BEOV. Groups of diabetic rats were either untreated or treated with 0.25-0.75 mg/ml BEOV as necessary to lower blood glucose in each rat. In diabetic rats, this resulted in a Controlled Glucose group, simulating relatively well-managed diabetes, and an Uncontrolled Glucose group, simulating poorly managed diabetes. Plasma insulin, glucose and triglyceride assays assessed the diabetic state. Bone mineral density (BMD), mechanical testing, mineral assessment and histomorphometry measured the effects of diabetes on bone and the effects of BEOV on non-diabetic and diabetic bone. Diabetes decreased plasma insulin and increased plasma glucose and triglycerides. In bone, diabetes decreased BMD, strength, mineralization, bone crystal length, and bone volume and connectivity. Treatment was effective in incorporating vanadium into bone. In all treated groups, BEOV increased osteoid volume. In non-diabetic bone, BEOV increased cortical bone toughness, mineralization and bone formation. In controlled glucose rats, BEOV lowered plasma glucose and improved BMD, mechanical strength, mineralization, bone crystal length and bone formation rate. In poorly controlled rats, BEOV treatment slightly lowered plasma glucose but did not improve bone properties. These results suggest that BEOV improves diabetes-related bone dysfunction primarily by improving the diabetic state. BEOV also appeared to increase bone formation. Our study found no negative effects of vanadium accumulation in bone in either diabetic or non-diabetic rats at the dose given.

Absorptiometry, Photon↗
PubMed1999

Solution Characterization of Vanadium(V) and -(IV) N-(Phosphonomethyl)iminodiacetate Complexes: Direct Observation of One Enantiomer Converting to the Other in an Equilibrium Mixture(1).

The vanadium(V) and -(IV) complexes formed with N-(phosphonomethyl)iminodiacetate (pida(4)(-)) complexes in water and in aqueous mixed-solvent systems were characterized by employing potentiometry, multinuclear NMR, EPR, and visible spectroscopy. The vanadium(V) complexes in water had a 1:1 metal to ligand stoichiometry. The diprotonated vanadium(V)-pida complex with a charge of -1 existed below pH 2. After the first deprotonation, the dianionic species was stable from pH 1 to 6. The trianionic species was stable at neutral pH. Observations are most consistent with the protonation sites of these complexes on the organic ligand. Intra- and intermolecular exchange processes were identified using (13)C homonuclear EXSY spectroscopy. Given the asymmetric vanadium atom in the VO(2)pida(3)(-) complex, one of the exchange processes observed was the conversion of one enantiomer to the other in an equilibrium mixture. Studies of the corresponding vanadium(IV)-pida system in dioxane-water mixtures showed the presence of not only mononuclear species but also a dinuclear species (which was recently characterized by X-ray crystallography). In 80:20 (v/v) dioxane-water mixtures, the dinuclear species became the major species in solution, as evidenced by absorption spectroscopy and EPR spectroscopy. Potentiometric measurements in mixed solvents failed to conclusively favor any stoichiometry. In conclusion, the mononuclear vanadium(IV) and -(V) complexes with the H(4)pida ligand appear to be structurally related and could readily be distinguished from the dinuclear vanadium(IV)-pida complex that was characterized both in the solid state and in mixed-solvent solutions.

Journal Article↗
PubMed2005

Chiral self-dimerization of vanadium complexes on a SiO2 surface for asymmetric catalytic coupling of 2-naphthol: structure, performance, and mechanism.

Vanadium monomers with chiral tridentate Schiff-base ligands were supported on SiO(2) through a chemical reaction with surface silanols, where we found a new chirality creation by the self-dimerization of the vanadyl complexes on the surface. The chiral self-dimerization and the role of surface silanols in the self-assembly were investigated by means of X-ray absorption near-edge structure (XANES), extended X-ray absorption fine structure (EXAFS), diffuse-reflectance ultraviolet/visible (DR-UV/VIS), X-ray photoelectron spectroscopy (XPS), Fourier transform infrared (FT-IR), electron spin resonance (ESR), and density functional theory (DFT) calculations. The surface vanadyl complexes had a distorted square-pyramidal conformation with a V=O bond. FT-IR spectra revealed that the Ph-O moiety of Schiff-base ligands was converted to Ph-OH by a surface-concerted reaction between the vanadium precursors and surface SiOH groups. The Ph-OH in an attached vanadyl complex interacted with a COO moiety of another vanadyl complex by hydrogen bonding to form a self-dimerized structure at the surface. The interatomic distance of V-V in the surface self-assembly was evaluated to be 0.40 +/- 0.05 nm by ESR after O(2) adsorption. The self-dimerized V structure on SiO(2) was modeled by DFT calculations, which demonstrated that two vanadium monomers with Ph-OH linked together by two hydrogen bonds and their V=O groups were directed opposite to each other. The surface self-dimerization of the vanadium precursors fixes the direction of the V=O bond and the plane of the Schiff-base ligand. Thus, a new chiral reaction field was created by two types of chirality: the chiral Schiff-base ligand and the chiral V center. We have also found that the chiral self-dimerized vanadyl complexes exhibit remarkable catalytic performance for the asymmetric oxidative coupling of 2-naphthol: 96% conversion, 100% selectivity to 1,1'-binaphthol (BINOL), and 90% enantiomeric excess (ee). Increasing the vanadium loading on SiO(2) caused a dramatic swell of enantioselectivity, and the maximum 90% ee was observed on the supported catalyst with the full coverage of the vanadyl complex (3.4 wt % vanadium). This value is equivalent to the maximum ee reported in homogeneous catalysis for the coupling reaction. Furthermore, the supported vanadium dimers were reusable without loss of the catalytic performance. To our knowledge, this is the first heterogeneous catalyst for the asymmetric oxidative coupling of 2-naphthol.

Journal Article↗
PubMedDate not supplied

Inhibition of altered liver cell foci and persistent nodule growth by vanadium during diethylnitrosamine-induced hepatocarcinogenesis in rats.

The effect of vanadium, a recently established trace element, on diethylnitrosamine (DENA)-induced hepatocarcinogenesis was examined in male Sprague-Dawley rats. Rats were divided into four groups (Groups 1-4). While Group 1 served as normal group, initiation of hepatocarcinogenesis was performed in all other groups (Groups 2-4) by a single intraperitoneal injection of DENA (200 mg/kg body weight). Supplementary vanadium at the level of 0.2 and 0.5 ppm (as ammonium monovanadate) added to the drinking water was given to Groups 3 and 4 respectively ad libitum four weeks before DENA administration and continued for 8 or 16 weeks after the carcinogenic insult. Rats were sacrificed at the 12th or 20th week after the experiment began. No significant differences were observed in food and water intakes or in growth rates among the groups. Supplementation with vanadium (in Groups 3 and 4) for 12 or 20 weeks dose-dependently reduced the incidence, total number, multiplicity and altered the size distribution of visible persistent (neoplastic) hepatocyte nodules as compared to DENA control (Group 2). Mean nodular volume and nodular volume as percentage of liver volume were also inhibited upon vanadium supplementations. The morphometric analysis of preneoplastic focal lesions observed in hematoxylin and eosin-stained liver sections revealed the occurrence of a decreased number of altered liver cell foci/cm2 and the average focal area, coupled with a decrement in the percentage area of liver parenchyma occupied by foci in vanadium-supplemented groups (Groups 3 and 4). All these results were found to be more pronounced at the 20th week as compared to the 12th week of the study. However, the results with 0.5 ppm vanadium at the 20th week were mostly at a statistically significant level. The findings of the study suggest that vanadium at a dose of 0.5 ppm may have a potential anticarcinogenic property against chemically induced hepatic neoplasia without any apparent sign of toxicity. This attribute could open new vistas in cancer chemotherapy.

Animals↗
PubMed1985

Biodistribution and pharmacokinetics of vanadium following intraperitoneal administration of vanadocene dichloride to mice.

The biodistribution and pharmacokinetics of vanadium following i.p. administration of vanadocene dichloride (VDC), a representative of a new class of organometallic anticancer agents, is reported for Strain A mice. A convenient flameless atomic absorption spectroscopic assay is described and is used to determine kinetic profiles for vanadium in blood, kidney, liver, small intestine and brain tissue for times up to 24 h after administration. For a VDC dose of 80 mg/kg, vanadium concentration decreases rapidly from both the blood and small intestine, and the data can be fit to a phenomenological exponential function (blood: t1/2 = 118 +/- 43 min; small intestine: t1/2(alpha) = 18.10 +/- 0.14 min, t1/2(beta) = 341 +/- 45 min). In contrast, vanadium accumulates in both the kidney and liver up to a maximal concentration (1.12 +/- 0.06 mM and 0.56 +/- 0.06 mM after 12 and 8 h, respectively), and is then excreted with estimated half-lives of 7.9 +/- 0.7 and 12.1 +/- 0.1 h, respectively. No detectable levels of vanadium are found in the brain tissue over the temporal course of the experiment. These results are compared to previous mammalian studies with cis-dichlorodiammineplatinum(II) (CDDP) and related 'second generation' platinum derivatives; there are both qualitative similarities between the vanadium and platinum systems as well as important quantitative differences.

Animals↗