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PubMed1987

Persistence of vanadium compounds in lungs after intratracheal instillation in rats.

Translocation and tissue distribution of two different forms of vanadium compounds, orthovanadate (soluble) and vanadium pentoxide (less soluble), were investigated. Groups of randomly selected rats were injected intratracheally with radiolabeled vanadium (48V) compounds and the animals were sacrificed at 1, 7 and 28 days after treatment. Blood, lungs and other major organs and tissues, namely liver, kidney, spleen, heart, testes, brain, muscle, and bone were sampled and the vanadium contents determined by gamma spectrometry. The less soluble form of vanadium (vanadium pentoxide) was eliminated from the lungs at a slow but exponentially linear rate, whereas the soluble form was translocated rapidly from this organ and exhibited a non-linear decline. Compared to the less soluble form, significantly less vanadium was retained in lungs 7 and 28 days after intratracheal instillation of vanadate. One day after treatment significantly higher concentrations (approximately 4 times) of vanadium after orthovanadate were observed in liver, kidney, spleen and bone compared to the pentoxide. However, tissue residues at 7 and 28 days indicated that both forms of vanadium were rapidly eliminated, except from bone and lungs. Results suggest a prolonged retention of less soluble forms of vanadium and possible health effects following repeated occupational exposure.

Animals↗
PubMed1987

Further studies of vanadium in depressive psychosis.

Three studies are reported. In study 1, vanadium concentration was estimated by neutron activation analysis in hair, whole blood, serum and urine from 13 patients suffering from depressive psychosis and then when on recovery. Vanadium concentration of hair, whole blood and serum decreased significantly with recovery, but there was no significant change in 24-h urinary excretion or in renal clearance of vanadium. In study 2, vanadium concentration was estimated by neutron activation analysis in serum and urine of 31 patients with depressive psychosis and of 27 normal controls. Mean renal clearance of vanadium was significantly lower and mean serum vanadium concentration significantly higher in depressed patients than in controls. Mean 24-h excretion of vanadium did not differ between the two groups. Vanadium excretion did not correlate with urine volume, with serum concentration or with age. In study 3, erythrocyte Na-K ATPase activity and serum vanadium concentrations were estimated in 58 patients. There was a strong negative correlation between the two, supporting the suggestion that changes in tissue vanadium concentration may explain the changes in sodium transport which occur in depressive psychosis.

Adult↗
PubMed1981

Effects of diet composition on vanadium toxicity in laying hens.

Vanadium added to laying rations as NH4 VO3, VOCl2 or VOSO4 at levels of 20 to 80 ppm resulted in a rapid and substantial reduction in albumen quality as measured by Haugh units. Dietary vanadium also resulted in reduced egg production, egg weight, body weight, feed consumption, and poorer shell quality as measured by specific gravity. Ascorbic acid at .4 to .5% effectively protected the hen from the reduction in albumen quality, egg production, and body weight for up to 40 ppm vanadium, but not the reduction of egg weight. Replacement of soybean meal by 20% dietary cottonseed meal also protected the hen from the reduction in albumen quality, egg production, and body weight for up to 40 ppm vanadium. Added at levels of 4 to 8 times the molecular concentration of vanadium, EDTA had no consistent effect on vanadium toxicity. Dehydrated grass, at levels of 6 to 12%, maintained egg production but had no effects on the reduction in albumen quality caused by 40 ppm vanadium. Replacement of soybean meal with herring fish meal and part of the grain with sucrose intensified the depression of albumen quality, egg production, and loss of body weight caused by added vanadium. Neither varying dietary protein levels from 12 to 25% using soybean meal nor the addition of 20 ppm chromium had any effect on the toxicity of added vanadium. It appears that vanadium expresses its toxicity in laying hens by several routes since the protective effects of different dietary changes and additives differentially affected the loss of albumen quality, egg production, body weight, and egg weight.

Animal Feed↗
PubMed2001

[Vanadium: threat and hope].

Vanadium is an element classified in the group of heavy metals, very common in the natural environment and widely used in industry. It is mainly used in the production of nonferrous alloys, most resistant carbon steel, as well as in chemical, glass, paint and varnish, ceramic, and photographic industries. In the atmosphere, two second of vanadium originates from anthropogenic sources, sea-born aerosols and volcanic eruptions. Municipal waste is the major source of vanadium in surface water. It is one of the components of live organisms and participates in many biochemical processes essential for their proper functioning, but in higher concentrations it may induce acute or chronic intoxication that damage biological structures and disorder biochemical systems. The mechanism of vanadium toxic effect has not as yet been elucidated, however, it is already known that this mechanism is rooted among others in vanadium properties able to hinder a number of enzymatic systems. For vanadium the most "critical" systems are respiratory, urinary and hemopoietic. Vanadium salts may also be genotoxic and harmful at different phases of reproduction and development. Numerous studies of a possible use of vanadium in treatment of certain diseases, e.g., diabetes, have been carried out. Some findings on a potential antineoplastic or contraceptive effect of vanadium compounds have recently been reported. To sum up, there are numerous hazards associated with the wide industrial use of vanadium, nevertheless, the number of findings highlighting its nutritive and therapeutic properties is growing.

Antineoplastic Agents↗
PubMed1990

Effect of vanadium, iodine and their interaction on growth, blood variables, liver trace elements and thyroid status indices in rats.

A two-factor, two-by-three factorially arranged experiment was performed to ascertain whether iodine affects the response of rats to vanadium deprivation. Male weanling Wistar-Kyoto rats were fed a 16% casein 68% acid-washed ground corn diet for 8 weeks. The variables were supplemental vanadium at 0 or 1 microgram/g and supplemental iodine at 0, 0.33 or 25 micrograms/g. Vanadium deprivation increased thyroid weight and thyroid weight/body weight ratio and decreased the concentration of vanadium in liver. Vanadium and iodine interacted such that, as dietary iodine was increased, plasma glucose increased in the vanadium-deficient rats but decreased in the vanadium-supplemented rats. Also, as dietary iodine was increased, thyroid peroxidase activity decreased; the decrease was more marked in the vanadium-supplemented than the vanadium-deprived rats. The findings suggest that vanadium may have a physiological role affecting iodine metabolism and thyroid function.

Animals↗
PubMedDate not supplied

Inhibition by vanadium of sodium and potassium dependent adenosinetriphosphatase derived from animal and human tissues.

Inhibition of adenosinetriphosphatase (ATPase) by vanadium pentoxide (dissolved in water or in sodium hydroxide solution) was studied in microsomal fractions and tissue homogenates of kidney, brain, and heart of several species, including humans (kidney only). In some preparations vanadium was found to be the most potent inhibitor of Na+ + K+ATPase activity so far reported. Concentrations of vanadium causing 50 percent inhibition of Na+ + K+ATPase activity ranged from 6 x 10(-8) to 5 x 10(-7) M in microsomal fractions and from 2 x 10(-7) to 1 x 10(-6) M in tissue homogenates. Renal and cardiac enzymes were more sensitive to vanadium than the brain enzyme, a phenomenon independent of enzyme specific activity. The enzyme in tissue homogenates was more resistant to vanadium than the microsomal enzyme derived from the same tissues, suggesting a presence in tissues of protective agents. Mg2+ ATPase, which contaminated the enzyme preparations to a variable degree, was 1,000-10,000 times more resistant to vanadium than was Na+ + K+ATPase. More detailed studies on the mechanism of inhibition were performed with dog and human kidney enzymes. The reversible nature of the inhibition was suggested by the fact that fractional inactivation of Na+ + K+ATPase by vanadium was independent of enzyme protein concentrations. The inhibitory effect was reduced by Na+ and increased by K+ or Mg2+. ATP alone, but not MgATP, antagonized the inhibition. This could mean that vanadium inhibits the Na+ + K+ATPase at the site activated by Na+, and that ATP protects the enzyme either by binding vanadium or by competing for a mutual receptor on the enzyme. The inhibition was reduced by bovine serum albumin, probably binding vanadium. The inhibition was also diminished by reducing agents, ascorbic acid and citric acid.

Adenosine Triphosphate↗
PubMedDate not supplied

Protective role of vanadium on the early process of rat mammary carcinogenesis by influencing expression of metallothionein, GGT-positive foci and DNA fragmentation.

Vanadium, a dietary micronutrient, is now proving to be a promising anti-tumour agent. The present study was conducted to ascertain its anti-neoplastic potential against an experimental mammary carcinogenesis. Female Sprague-Dawley rats at 50 days of age were treated with 7,12-dimethylbenz(alpha)anthracene (DMBA; 0.5 mg per 100 g body weight) by a single tail vein injection in an oil emulsion. Vanadium (ammonium monovanadate) at a concentration of 0.5 p.p.m. was supplemented in the drinking water and given ad libitum to the experimental group immediately after the carcinogen treatment and it continued until the termination of the study (24 weeks for histological, immunological and biochemical observations and 35 weeks for morphological findings). It was found that vanadium treatment brought about substantial protection against DMBA-induced mammary carcinogenesis. This was evident from histological findings that showed substantial repair of hyperplastic lesions following supplementation of vanadium alone. There was a significant reduction in incidence (P<0.05), total number, multiplicity (P<0.01), size of palpable mammary tumours and delay in mean latency period of tumour appearance (P<0.001) following vanadium supplementation compared to the DMBA control. The immunohistochemical localization of metallothionein (a prognostic marker for breast cancer) showed reduced expression with vanadium treatment. Further, DNA fragmentation in the mammary tissue of the vanadium-treated group indicated apoptosis. In this group, vanadium also caused a significant decrease in the number (P<0.002) and focal area (P<0.05) of gamma-glutaminetranspeptidase-positive hepatic foci. The results clearly show the anti-neoplastic potential of vanadium.

Animals↗
PubMed1995

Time course effects of vanadium supplement on cytosolic reduced glutathione level and glutathione S-transferase activity.

The influence of vanadium, an important dietary micronutrient, was evaluated on the cytosolic reduced glutathione (GSH) content and glutathione S-transferase (GST) activity in several rat target tissues. Supplementation of drinking water with vanadium at the level of 0.2 or 0.5 ppm for 4, 8, or 12 wk was found to increase the GSH level with a concomitant elevation in GST activity in the liver followed by small intestine mucosa, large intestine mucosa, and kidney. The results were almost dose-dependent and mostly pronounced with 0.5 ppm vanadium after 12 wk of its continuous supplementation. Neither the GSH level nor GST activity was significantly altered in forestomach and lung following vanadium supplementation throughout the study. The levels of vanadium that were found to increase the content of GSH and activity of GST in the liver, intestine, and kidney did not exert any toxic manifestation as evidenced from water and food consumption as well as the growth responses of the experimental animals. Moreover, these doses of vanadium did not impair either hepatic or renal functions as they did not alter the serum activities of glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), sorbitol dehydrogenase (SDH), as well as serum urea and creatinine level. All these results clearly indicate that vanadium under the doses employed in our study has a significant inducing role on GSH content with a concurrent elevation in GST activity in the liver and specific extrahepatic tissues without any apparent sign of cytotoxicity. This attribute of vanadium may have a greater importance in terms of biotransformation and detoxification of xenobiotics, including carcinogens. In addition, since the ability to afford an increment in the endogenous GSH-GST pool by anticarcinogenic natural substances has been found to correlate with their activity to inhibit neoplastic transformation, the trace element vanadium may be considered as a novel anticancer agent.

Animals↗
PubMed1994

Is vanadium of human nutritional importance yet?

The trace element vanadium has been studied by the nutrition community for four decades, yet has not achieved essential status for human beings. It is found in compounds at valences of 2, 3, 4, or 5, with the tetravalent and pentavalent forms being the most common. In human beings, pharmacologic amounts of vanadium (ie, 10 to 100 times normal intake) affect cholesterol and triglyceride metabolism, influence the shape of erythrocytes, and stimulate glucose oxidation and glycogen synthesis in the liver. Vanadium's primary mode of action is as a cofactor that enhances or inhibits enzymes. Recent evidence suggests that vanadium may be essential for higher animals. After their mothers had been fed carefully formulated vanadium-deficient diets, second-generation goat kids suffered skeletal damage and died within 3 days of parturition. Although ubiquitous in air, soil, water, and the food supply, vanadium is generally found in nanogram or microgram quantities, which makes it difficult to measure. Estimates for the American intake of vanadium (based on a food intake of 500 g dry weight) are 10 to 60 micrograms/day. Vanadium levels in diets from five regions of the United States range from 30.9 +/- 1.5 in the Southeast to 50.5 +/- 1.5 micrograms/kg dry weight in the West. Although vanadium is thought to be essential for goats, new data may soon support its essentiality in human beings.

Animals↗
PubMed1983

Minireview: physiological and pharmacological properties of vanadium.

Vanadium is distributed extensively in nature. It is a trace element and is present in almost all living organisms including man. Even though vanadium was originally recognized for its ability to inhibit membrane Na+-K+-ATPase, various laboratory studies now document that this element has the capacity to affect the activity of various intracellular enzyme systems and may modify their physiological functions. Vanadium may be an essential element for normal development and may play an important role in various homeostatic mechanisms, and thus vanadium deficiency may prove to be an important concern. Abnormalities in biological disposition of vanadium may be involved in the pathogenesis of certain neurological disorders or cardiovascular diseases. While the essentiality of this element for living organisms is yet to be established with certainty, vanadium has become an increasingly important element and is used extensively in various heavy industries such as steel, oil, etc.; thus, the incidence of exposure to toxic levels of vanadium to industrial workers has been an increasing concern for toxicologists. To date, little information is available on the physiological or pharmacological actions of vanadium; hence, it is difficult to reach any definitive conclusion concerning its biological significance, essentiality and its role in pathological states. An attempt has been made in this review to broadly document what is known of various biological actions of vanadium.

Animals↗
PubMed1992

Vanadium levels in hair and blood of normal and exposed persons.

Vanadium was determined by both instrumental neutron activation analysis (INAA) and NAA with radiochemical separation (RNAA) in hair of normal children and of children potentially exposed by accidental drinking of vanadium contaminated water (long-term, low-dose exposure). Vanadium hair levels in the two groups did not differ significantly and were in the range 46-313 micrograms/kg (median 98 micrograms/kg) and 24-235 micrograms/kg (median 88 micrograms/kg for the normal and exposed groups, respectively. Using RNAA with proven reliability at the ultratrace level, vanadium was determined in whole blood of the exposed and normal children, normal adults and workers professionally exposed to vanadium in a factory producing vanadium pentoxide. Significantly increased vanadium concentrations were found in blood of exposed children (range 0.018-0.239 micrograms/l, median 0.078 micrograms/l) compared to normal children (range 0.024-0.226 micrograms/l, median 0.042 micrograms/l), while no differences could be detected between blood vanadium levels of normal children and normal adults (range 0.032-0.095 micrograms/l, median 0.056 micrograms/l). Preliminary results for vanadium in blood of occupationally highly exposed persons showed values 2-4 orders of magnitude higher than in normal adults.

Adult↗
PubMed1994

A global biogeochemical budget for vanadium.

Evidence that environmental levels of vanadium are increasing has raised concern over the injection of vanadium into the atmosphere from anthropogenic sources. A simple global mass balance model was developed to demonstrate the influence of anthropogenic vanadium on the global distribution of this trace metal. Vanadium in particulate emissions owing to man's industrial activities were estimated to comprise approximately 53% of total atmosphere vanadium loading and exceeded natural continental or volcanogenic dust by only a narrow margin. Oceanic deposition of vanadium adhering to anthropogenic particles was estimated to comprise approximately 5% of total ocean vanadium loading. There is no suggestion that these inputs of anthropogenic vanadium pose a significant global environmental threat. It is entirely possible, however, that anthropogenic vanadium inputs could pose an environmental hazard given a more restricted area and a specific set of unfavorable circumstances.

Air Pollutants↗
PubMed1992

Haematological effects of vanadium on living organisms.

Although vanadium has been of great interest for many researchers over a number of years, its biochemical and physiological role is not yet fully clear. There are many papers describing the haematological consequences of its excess in living organisms and most of their data are quoted in this mini-review. The authors of these papers used various laboratory animals, different vanadium compounds, frequently different routes of administration and duration of intoxication. Hence a checklist and comparison of the results are rather difficult. Vanadium reduces the deformability of erythrocytes, and such cells are rather frequently retained in the reticuloendothelial system of the spleen and eliminated faster from the blood stream (Kogawa et al., 1976). Vanadium produces peroxidative changes in the erythrocyte membrane, this leading to haemolysis. Therefore, the depressed erythrocyte count in animals intoxicated with vanadium may be the consequence of both the haemolytic action of vanadium and the shortened time of survival of erythrocytes. Changes of the haem precursor level in blood serum and urine observed in humans exposed occupationally to vanadium suggest an influence of this element on haem synthesis. This problem requires, however, further studies and observations. Changes occurring under the influence of vanadium on the leukocyte system of animals suggest the influence of this element on the resistance of the organism, but the mechanism of the action of vanadium still requires elucidation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2005

Differences in plasma homocysteine levels between Zucker fatty and Zucker diabetic fatty rats following 3 weeks oral administration of organic vanadium compounds.

PURPOSE: Recently, our laboratory group has reported that rats with Type 1 diabetes have decreased plasma homocysteine and cysteine levels compared to non-diabetic controls and that organic vanadium treatment increased plasma homocysteine concentrations to non-diabetic concentrations. However, to date, no studies have been done investigating the effects of organic vanadium compounds on plasma homocysteine and its metabolites in Type 2 diabetic animal model. These studies examined the effect of organic vanadium compounds [bis(maltolato)oxovanadium(IV) and bis(ethylmaltolato)oxovanadium(IV); BMOV and BEOV] administered orally on plasma concentrations of homocysteine and its metabolites (cysteine and cysteinylglycine) in lean, Zucker fatty (ZF) and Zucker diabetic fatty (ZDF) rats. ZF rats are a model of pre-diabetic Type 2 diabetes characterized by hyperinsulinemia and normoglycemia. The ZDF rat is a model of Type 2 diabetes characterized by relative hypoinsulinemia and hyperglycemia. METHODS: Zucker lean and ZF rats received BMOV in the drinking water at a dose of 0.19 +/- 0.02 mmol/kg/day. Lean and ZDF rats received BEOV by oral gavage daily at dose of 0.1 mmol/kg. The treatment period for both studies was 21 days. At termination, animals were fasted overnight (approximately 16 h) and blood samples were collected by cardiac puncture for determination of plasma glucose, insulin and homocysteine levels. Plasma homocysteine and its metabolites levels were determined using high-pressure liquid chromatography. Plasma glucose was determined using a Glucose Analyzer 2. Plasma insulin levels were determined by radioimmunoassay. Plasma triglycerides were determined by an enzymatic assay methodology. RESULTS: ZF (n = 4) and ZDF (n = 10) rats had significantly lower plasma homocysteine as compared to their respective lean groups (ZF 0.78 +/- 0.1 micromol/L vs. Zucker lean 2.19 +/- 0.7 micromol/L; ZDF 1.71 +/- 0.2 micromol/L vs. Zucker lean 3.02 +/- 0.3 micromol/L; p < 0.05). BMOV treatment in ZF rats restored plasma homocysteine levels to those observed in lean untreated rats (ZF treated: 2.04 +/- 0.2 micromol/L; lean 2.19 +/- 0.7 micromol/L). There was a modest effect of BMOV treatment on plasma glucose levels in ZF rats. BEOV treatment significantly decreased the elevated plasma glucose levels in the ZDF rats (lean 7.9 +/- 0.1 mmol/L; lean + vanadium 7.7 +/- 0.2 mmol/L; ZDF 29.9 +/- 0.4 mmol/L; ZDF + vanadium 17.4 +/- 0.3 mmol/L, p < 0.05). Organic vanadium treatment reduced cysteine levels in both ZF and ZDF rats. No differences in total plasma cysteinylglycine concentrations were observed. CONCLUSION: Plasma homocysteine levels are significantly reduced in a pre-diabetic model of Type 2 diabetes, which was restored to lean levels upon vanadium treatment; however, this restoration of plasma homocysteine levels was not seen in ZDF Type 2 diabetic rats following vanadium treatment. In the latter case vanadium treatment may not have totally overcome the insulin resistance seen in these animals.

Administration, Oral↗
PubMed2003

Vanadium(IV/V) speciation of pyridine-2,6-dicarboxylic acid and 4-hydroxy-pyridine-2,6-dicarboxylic acid complexes: potentiometry, EPR spectroscopy and comparison across oxidation states.

Evaluation of stability of vanadium(IV) and (V) complexes under similar conditions is critical for the interpretation and assessment of bioactivity of various vanadium species. Detailed understanding of the chemical properties of these complexes is necessary to explain differences observed their activity in biological systems. These studies are carried out to link the chemistry of both vanadium(IV) and (V) complexes of two ligands, 2,6-pyridinedicarboxylic acid (dipicolinic acid, H(2)dipic) and 4-hydroxy-2,6-pyridinedicarboxylic acid (H(2)dipic-OH). Solution speciation of the two 2,6-pyridinedicarboxylic acids with vanadium(IV) and vanadium(V) ions was determined by pH-potentiometry at I=0.2 M (KCl) ionic strength and at T=298 K. The stability and the metal affinities of the ligands were compared. Vanadium(V) complexes were found to form only tridentate coordinated 1:1 complexes, while vanadium(IV) formed complexes with both 1:1 and 1:2 stoichiometries. The formation constant reflects hindered coordination of a second ligand molecule, presumably because of the relatively small size of the metal ion. The most probable binding mode of the complexes was further explored using ambient and low temperature EPR spectroscopy for vanadium(IV) and 51V NMR spectroscopy for vanadium(V) systems. Upon complex formation the pyridinol-OH in position 4 deprotonates with pK approximately 3.7-4.1, which is approximately 6 orders of magnitude lower than that of the free ligand. The deprotonation enhances the ligand metal ion affinity compared to the parent ligand dipicolinic acid. In the light of the speciation and stability data of the metal complexes, the efficiency of the two ligands in transporting the metal ion in the two different oxidation states are assessed and discussed.

Electron Spin Resonance Spectroscopy↗
PubMed1995

Inhibitory effect of vanadium on rat liver carcinogenesis initiated with diethylnitrosamine and promoted by phenobarbital.

The chemoprotective effect of vanadium, a dietary micronutrient, against chemically induced hepatocarcinogenesis in rats was investigated. Initiation was performed by a single intraperitoneal injection of diethylnitrosamine (DENA; 200 mg kg-1) followed by promotion with phenobarbital (0.05%) in the diet. Supplementary vanadium (0.5 p.p.m.) in the drinking water was provided ad libitum throughout the experiment, before the initiation or during the promotion period. At the end of the study (20 weeks), vanadium supplementation throughout the experiment reduced the incidence (P < 0.01), total number and multiplicity (P < 0.001) and altered the size distribution of visible persistent nodules (PNs) as compared with DENA control animals. Mean nodular volume (P < 0.05) and nodular volume as a percentage of liver volume (P < 0.01) were also attenuated following long-term vanadium treatment. It also caused a large decrease in the number (P < 0.001) and surface area (P < 0.01) of gamma-glutamyltranspeptidase (GGT)-positive hepatocyte foci and in the labelling index (P < 0.001) of focal cells, coupled with increased (P < 0.01) remodelling. The activity of GGT, measured quantitatively, was found to be significantly less in the PNs (P < 0.001) and non-nodular surrounding parenchyma (P < 0.01) of vanadium-supplemented rats. The anticarcinogenic effect of vanadium was also reflected in the histopathological analysis of liver sections that showed a well-maintained hepatocellular architecture as compared with DENA control. Similar results were observed when vanadium was given only before the initiation. However, supplementation of vanadium during the promotion period did not result in significant alterations of these parameters. Our results, thus, strongly suggest that vanadium may have a unique anti-tumour potential which is primarily exerted on the initiation phase and only secondarily on the promotion stage.

Animals↗
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↗
PubMed2003

Lung deposition and clearance of inhaled vanadium pentoxide in chronically exposed F344 rats and B6C3F1 mice.

Female F344 rats and B6C3F1 mice were exposed to vanadium pentoxide (V2O5) at concentrations of 0, 0.5, 1, or 2 mg/m3 (rats) and 0, 1, 2, or 4 mg/m3 (mice) for 6 h/day, 5 days/week (for up to 18 months), by whole-body inhalation. Lung weights and lung burdens of vanadium were determined for exposed animals after 1, 5, and 12 days and after 1, 2, 6, 12, and 18 months of V2O5 exposure. Blood vanadium concentrations were determined at 1, 2, 6, 12, and 18 months for all animals including controls. A model that assumed a first-order deposition rate and a first-order elimination rate for vanadium was employed to fit the lung burden data. Comparisons between exposed groups indicated a progressive increase in lung weight with exposure concentration and time on exposure for both species. The vanadium lung burdens appeared to reach steady state in the lowest exposure groups (0.5 and 1 mg/m3 for rats and mice, respectively) but showed a decline in the higher exposure groups. This deposition pattern was similar between rats and mice but the maximum lung burdens were observed at different times (1 or 2 months in mice vs. 6 months in rats). The vanadium deposition rate decreased faster in mice, while the elimination half-lives of vanadium lung burdens were about six- to nine-fold shorter in mice than in rats at 1 and 2 mg/m3. Thus, the retention of vanadium in the lungs at 18 months was lower in mice (approximately 2% retained) compared with rats (13-15% retained) at the common exposure concentrations of 1 and 2 mg/m3. The lung burden data were approximately proportional to the exposure concentration in both species, likely due to concomitant decreases in deposition and elimination to a similar extent with increasing exposure. The area under the lung burden versus time curves and the area under the blood concentration (control-normalized) versus time curves were also proportional to exposure concentration. The progression of pathological changes in the lung with exposure and time is thought to affect the pattern and/or extent of vanadium deposition in the lungs following repeated exposures to V2O5.

Administration, Inhalation↗