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At least 253 records · Page 14Linked to original sources
PubMed1984

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

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

Animals↗
PubMed1991

Evaluation of the efficacy of various chelating agents on urinary excretion and tissue distribution of vanadium in rats.

The effect of repeated intraperitoneal administration of Tiron (4,5-dihydroxy-1,3-benzenedisulfonic acid), ascorbic acid, deferoxamine (DFOA) or 2-mercaptosuccinic acid on urinary excretion and tissue distribution of vanadium was assessed in rats which had previously received 12 intraperitoneal injections of sodium metavanadate (1.84 mg/kg per injection) or vanadyl sulphate trihydrate (6.35 mg/kg per injection) during a 4-week period. Chelating agents were administered daily for 5 days at doses equal to one-eighth of their respective LDSO. Only Tiron significantly decreased the tissue concentration of vanadium, whereas DFOA and Tiron significantly enhanced the urinary excretion of vanadium after repeated parenteral administration of sodium metavanadate. Again, only Tiron significantly increased the urinary elimination of vanadium following vanadyl sulphate administration. The results of this study show that Tiron has potential beneficial effects in the treatment of repeated intraperitoneal vanadium poisoning, while the effectiveness of DFOA is very uncertain. 2-Mercaptosuccinic and ascorbic acids were not effective as antidotes for parenteral vanadium intoxication.

Animals↗
PubMed1993

[A study on developmental toxicity of vanadium pentoxide in Wistar rats].

Timed-pregnant Wistar rats were injected intraperitoneally with V2O5 at 0.33, 1.0 and 3.0 mg/kg/day on days 6-15 of gestation. Maternal toxic symptoms, decreased of weight gain during treatment and placenta weight, increased incidence of embryo-fetus mortality and external or skeletal malformation and fetal growth retardation were observed in the 3.0 mg/kg group. Increased incidence of embryo-fetus mortality and external or skeletal malformation, delayed ossification of bone and decreased placenta weight were observed in the 1.0 mg/kg group. These results indicate that V2O5 is a developmental toxicant with or without obvious maternal toxicity in Wistar rats. Although vanadium can be accumulated in placenta, it could passed through placenta. In this study, vanadium could induce a decrease of placenta weight without obvious maternal toxicity, and an A/D ratio of 3 was noted. These results suggest that vanadium may exert a direct effect on embryo-fetues or a "double effect" on the placenta function and embryo-fetus both. It has been reported that vanadium does not increase mal formation in NIN, Kunming, Swiss, NMRI mice or Syrian golden hamster. The dose for inducing developmental toxicity of vanadium in mice is higher than that in rats. This suggests that rats be more sensitive than mice to the developmental toxicity of vanadium.

Abnormalities, Drug-Induced↗
PubMed1998

[Physical and chemical properties of vanadium and its compounds].

Vanadium is present in the earth crust mainly in the heavy oils, carbons and bituminous materials, where is associated with the heavy fractions. Many live beings have vanadium in their tissues. Their industrial applications are fundamentally based in the physical and chemical properties. From the environmental point of view the vanadium emissions to the atmosphere are produced in areas around siderurgical industries, oil refineries and cities that use fossil fuels for heating. The pollution process in these areas is associated partially with the presence of vanadium compounds, as is the case in the eastern coast of the lake of Maracaibo, Venezuela. Some clinical-epidemiological researches report a high incidence of congenital malformations at the Central Nervous System level, and this has been associated with the intense oil activities of the region. The high incidence of the Central Nervous System congenital malformations could be associated with the vanadium compounds present in the eastern coast of the lake of Maracaibo; here is the interest in the physical and chemical properties knowledge of vanadium and their compounds.

Animals↗
PubMed1981

Effects of vanadium on immunologic functions.

Exposure of mice to vanadium caused a dose-related but nonsignificant decrease in the antibody-forming cells in the spleen of animals challenged with sheep erythrocytes. Delayed hypersensitivity reaction was not affected in similarly sensitized animals. Serum immunoglobulins were also not altered by the vanadium treatment. Splenic lymphocytes obtained at 1, 4, 8 and 13 wk of exposure to 0, 1, 10, and 50 mg of vanadium per liter of drinking water showed an increased DNA synthesis related to vanadium treatment when cultured in the presence of phytohemagglutinin and pokeweed mitogen but not with bacterial lipopolysaccharide. Addition of vanadium to splenic cultures in vitro caused a marked enhancement of lymphocyte transformation at low concentrations, whereas a decreased cellular proliferation was observed at high concentrations of vanadium.

Animals↗
PubMed1999

Vanadium and diabetes.

Vanadium is an ultratrace element, widely distributed in nature, yet with no presently known specific physiological function in mammals. The apparent role of vanadium in regulation of intracellular signaling, as a cofactor of enzymes essential in energy metabolism, and as a possible therapeutic agent in diabetes is of increasing interest as more and more research reports present evidence of vanadium's potentially unique biological function. In this mini-review, the author summarizes current knowledge of the bioinorganic chemistry of vanadium, the basic features of diabetes mellitus and its metabolic sequelae, and the in vitro and in vivo effects of both inorganic and organically-chelated vanadium compounds. Results of clinical trials to date, as well as kinetic studies of tissue uptake are covered. Examples of ways to enhance the positive effects of vanadium as an oral therapeutic adjunct in diabetic control, while minimizing potential toxicity, are compared with regard to desirable features and possible drawbacks.

Animals↗
PubMed2006

Vanadium limits the expression of proliferating cell nuclear antigen and inhibits early DNA damage during diethylnitrosamine-induced hepatocellular preneoplasia in rats.

Previous studies from our laboratory have shown that vanadium stabilizes xenobiotic metabolizing enzymes and antioxidant status and suppresses DNA-protein crosslinks during chemically-induced hepatocarcinogenesis in rats. In the present study, we have further investigated the in vivo antitumor potential of this micronutrient by determining the effect of 0.5 ppm vanadium in drinking water on biomarkers for the early stages of hepatocarcinogenesis; the biomarkers included gamma-glutamyl transpeptidase (GGT)-positive foci and glycogen-storage foci, in situ expression of proliferating cell nuclear antigen (PCNA), and genotoxic DNA damage assessed by the alkaline Comet assay. Histomorphometry also was assessed during the study. Hepatocarcinogenesis was induced by treating 4-week-old male Sprague-Dawley rats with a single, necrogenic, intraperitoneal (i.p.) injection of 200 mg/kg body weight diethylnitrosamine (DEN). Compared to the carcinogen control, vanadium administration over the 32 weeks of the experiment reduced the relative liver weight by 30%, the incidence of nodules by 69.34%, the total number and multiplicity of nodules by 80.77%, and remodeled the hepatocellular premalignant architecture towards a normal phenotype. Moreover, long-term vanadium treatment reduced the development of GGT foci by 76.2% (P < 0.001), decreased periodic acid-Schiff's reactivity by 59.49% (P < 0.01), and decreased PCNA expression, with the concomitant reduction in PCNA immunolabeling index by 93.36% (P < 0.001). Finally, vanadium inhibited early DNA damage (DNA strand-breaks) in DEN-treated rat hepatocytes as expressed in the Comet assay by a 60.04% reduction in the length:width value of DNA mass (P < 0.01) and a 51.54% reduction in the tail length of the DNA comets (P < 0.001). Our results indicate that continuous supplementation with 0.5 ppm vanadium suppresses hepatocellular neoplastic transformation in rats.

Animals↗
PubMed1994

Cellular uptake of titanium and vanadium from addition of salts or fretting corrosion in vitro.

The use of titanium and titanium-6% aluminum-4% vanadium alloy for dental and orthopedic implants has increased in the last decade. The implants are presumed to be compatible because osseointegration, bony apposition, and cell attachment are known. However, the cellular association of titanium and vanadium have remained unknown. This study examined the uptake of salts or fretting corrosion products. Titanium was not observed to be toxic to the cells. Vanadium was toxic at levels greater than 10 micrograms/mL. The percentage of cellular association of titanium was shown to be about 10 times that of vanadium. The percentage of cellular association of either element was greater from fretting corrosion than from the addition of salts. The presence of vanadium did not affect the cellular uptake of titanium. The presence of titanium decreased the cell association of vanadium.

Alloys↗
PubMed1992

Structure and function of vanadium compounds in living organisms.

Vanadium has been recognized as a metal of biological importance only recently. In this mini-review, its main functions uncovered during the past few years are addressed. These encompass (i) the regulation of phosphate metabolizing enzymes (which is exemplified for the inhibition of ribonucleases by vanadate), (ii) the halogenation of organic compounds by vanadate-dependent non-heme peroxidases from seaweeds, (iii) the reductive protonation of nitrogen (nitrogen fixation) by alternative, i.e. vanadium-containing, nitrogenases from N2-fixing bacteria, (iv) vanadium sequestering by sea squirts (ascidians), and (v) amavadine, a low molecular weight complex of V(IV) accumulated in the fly agaric and related toadstools. The function of vanadium, while still illusive in ascidians and toadstools, begins to be understood in vanadium-enzyme interaction. Investigations into the structure and function of model compounds play an increasingly important role in elucidating the biological significance of vanadium.

Animals↗
PubMed1996

Induction of vanadium accumulation and nuclear sequestration causing cell suicide in human Chang liver cells.

Very little is known about the modulation of vanadium accumulation in cells, although this ultratrace element has long been seen as an essential nutrient in lower life forms, but not necessarily in humans where factors modulating cellular uptake of vanadium seem unclear. Using nuclear microscopy, which is capable of the direct evaluation of free and bound (total) elemental concentrations of single cells we show here that an NH4Cl acidification prepulse causes distinctive accumulation of vanadium (free and bound) in human Chang liver cells, concentrating particularly in the nucleus. Vanadium loaded with acidification but leaked away with realkalinization, suggests proton-dependent loading. Vanadyl(4), the oxidative state of intracellular vanadium ions, is known to be a potent source of hydroxyl free radicals (OH). The high oxidative state of nuclei after induction of vanadyl(4) loading was shown by the redox indicator methylene blue, suggesting direct oxidative damage to nuclear DNA. Flow cytometric evaluation of cell cycle phase-specific DNA composition showed degradation of both 2N and 4N DNA phases in G1, S and G2/M cell cycle profiles to a solitary IN DNA peak, in a dose-dependent manner, effective from micromolar vanadyl(4) levels. This trend was reproduced with microccocal nuclease digestion in a time response, supporting the notion of DNA fragmentation effects. Several other approaches confirmed fragmentation occurring in virtually all cells after 4mM V(4) loading. Ultrastructural profiles showed various stages of autophagic autodigestion and well defined plasma membrane outlines, consistent with programmed cell death but not with necrotic cell death. Direct intranuclear oxidative damage seemed associated with the induction of mass suicide in these human Chang liver cells following vanadium loading and nuclear sequestration.

Ammonium Chloride↗
PubMed1999

Vanadium accumulation in pinnipeds.

Vanadium in four species of pinnipeds (northern fur seals [Callorhinus ursinus], Steller sea lions [Eumetopias jubatus], harbor seals [Phoca vitulina], and ribbon seals [Phoca fasciata]) caught in the Northern Pacific was analyzed using ICP-MS to understand its accumulation and distribution. In northern fur seals, relatively high concentrations of vanadium were observed in the liver, hair, and bone. Ninety percent of the vanadium burden in the body was concentrated in these three tissues, which comprise <20% of total body weight. Hepatic vanadium concentrations in the four pinniped species were significantly correlated to age, although the levels varied with species. An increase in vanadium accumulation in the liver of northern fur seals was caused by an increase of retention in nuclei and mitochondria fraction in the cells. Vanadium concentrations in liver were significantly correlated with mercury, silver, and selenium concentrations in northern fur seals, Steller sea lions, and harbor seals.

Alaska↗
PubMed2003

Expressed sequence tag analysis of vanadocytes in a vanadium-rich ascidian, Ascidia sydneiensis samea.

Some species in the family Ascidiidae accumulate vanadium at concentrations in excess of 350 mM, which corresponds to about 10(7) times higher than that in seawater. In these species signet ring cells, with a single huge vacuole in which vanadium ion is contained, function as vanadium-accumulating cells, vanadocytes. To investigate the mechanism underlying this phenomenon, we performed an expressed sequence tag (EST) analysis of a complementary DNA library from vanadocytes of a vanadium-rich ascidian, Ascidia sydneiensis samea. We determined the nucleotide sequences of 1000 ESTs and performed a BLAST analysis against the SwissProt database. We found 93 clones of metal-related gene homologues, including the ferritin heavy subunit, hemocyanin, and metallothionein. Two ESTs, in particular, exhibited significant similarity to vanabins that have been extracted from A. sydneiensis samea blood cells as low molecular weight vanadium-binding proteins. We have named the genes encoding these ESTs vanabin3 and vanabin4. Immobilized metal ion affinity chromatography revealed that these novel vanabin homologues bind vanadium(IV) ions.

Amino Acid Sequence↗
PubMed1990

A kinetic method for determination of free vanadium(IV) and (V) at trace level concentrations.

A kinetic method based on alkaline phosphatase has been developed to measure free trace levels of vanadium(IV) and (V). The method involves measuring the rate of the alkaline phosphatase-catalyzed hydrolysis of p-nitrophenyl phosphate with (Vi) and without (Vo) a competitive inhibitor in the assay. Michaelis-Menten kinetics for a competitive inhibitor was used to express the relationship between Vo/Vi and the inhibitor concentration. Measuring both Vo and Vi thus yields a Vo/Vi ratio that allows calculation of the competitive inhibitor concentration. Determination of free vanadium in complex fluids can be accomplished by comparing the ratio of rates of p-nitrophenyl phosphate hydrolysis with and without a sequestering agent to the ratios of rates measured on addition of a known vanadium concentration. Free vanadium(V) can conveniently be measured from 10(-7) to 10(-5) M and free vanadium(IV) can be measured at 10(-8) M and above. The error limits on the vanadium determinations range from +/- 3 to +/- 12% of the concentration under investigation depending on the conditions under which the assay was conducted.

Alkaline Phosphatase↗
PubMed1993

Role of vanadium in nutrition: metabolism, essentiality and dietary considerations.

Vanadium is a pervasive element of biological systems, being widely distributed across the food supply. Food refining and processing appear to increase vanadium content. At higher intakes, it accumulates in body tissues such as liver, kidney and bone. Essentiality of the nutrient has been established in lower life forms but the significance and extent of vanadium's role in humans has been overshadowed by the absence of deficiency symptoms in man. While the pharmacological properties of vanadium have stimulated much interest, knowledge of basic metabolic processes regulating vanadium remains incomplete. Ultimate determination of essentiality for humans will depend on greater understanding of the fundamental biochemical roles of vanadium.

Animal Nutritional Physiological Phenomena↗
PubMed1978

Vanadium in foods and in human body fluids and tissues.

Using neutron activation analysis, vanadium was analysed in a range of foods, human body fluids and tissues. On the basis of these results and those of other workers, it was concluded that daily dietary intake amounts to some tens of micrograms. Analysis of body fluids (including milk, blood and excreta) and organs and tissues provided an estimate for the total body pool of vanadium in man of about 100 microgram. Vanadium was not detectable in blood and urine at the level of 0.3 ng/g, while low levels were found in muscle, fat, bone, teeth and other tissues. The relationship between dietary intake to pulmonary absorption is discussed in relation to the occurrence of vanadium in man-made air particulates. The very low levels found in milks and eggs suggest minimal vanadium requirements in growth. The findings are discussed in the light of previous results and also in relation to the possible essentiality of vanadium.

Air↗
PubMed1989

Vanadium in particles and sediments of the northern Saronikos Gulf, Greece.

This study provides data for total and non-residual vanadium distributions in the northern Saronikos Gulf and shows that close to the Athens sewage outfall (ASO), the combined domestic and industrial wastes have resulted in a considerable increase in concentrations of vanadium in sediments and suspended solids. This appears to be the main vanadium source in the area; a second major source is a fertilizer plant (FP) near the entrance of Piraeus Harbour (PH), the impact of which is also important. Atmospheric inputs from the Piraeus industrial site and frequent crude oil spillages from ships and land-based sources seem to contribute significantly to the observed vanadium distribution, which is clearly affected by the prevailing circulation of surface waters and winds. The high percentage of the 0.5 NHCl-leachable vanadium fraction in the most polluted sediments, together with positive correlation with organic carbon and certain other trace metals (i.e. Ag, Co, Cr, Fe, Zn) and negative correlation coefficients with Al and Sc, indicate that a considerable portion of the vanadium is of "anthropogenic" origin not related to lithogenous particles. It enters the system in association with relatively large organic aggregates, either authigenic or derived from sewage.

Greece↗
PubMed1993

The chloroperoxidase from the fungus Curvularia inaequalis; a novel vanadium enzyme.

The presence of vanadium-containing bromoperoxidases in various types of seaweed is well-documented. We now report that the terrestrial fungus Curvularia inaequalis excretes a novel chloroperoxidase which also contains vanadium as a prosthetic group. The chloroperoxidase is excreted in the medium as the only protein and is, therefore, almost purely obtained. Atomic absorption spectroscopy measurements showed that the chloroperoxidase contained vanadium, which was essential for enzymatic activity, in a stoichiometry of 1 mol vanadium per mol of enzyme. When the fungus was grown in media containing low concentrations of vanadate (VO4(3-)) or when vanadate was absent, the enzyme was excreted in an apoform. Addition of vanadate to the apoenzyme purified from the medium, dialyzed holo-enzyme or growth medium led to incorporation of the metal and to a subsequent increase in specific activity from 0.7 to about 7.5 units/mg. The reduced enzyme showed an axially symmetric EPR spectrum (g(o) = 1.971, Ao = 91.7 x 10(-4) cm-1) with 16 hyperfine lines that is essentially the same as the EPR spectrum of the vanadium-containing bromoperoxidase of the seaweed Ascophyllum nodosum. This demonstrates that the active sites in the two enzymes are very similar. The chlorinating and brominating activities of the chloroperoxidase from C. inaequalis were also studied and compared to those of the vanadium bromoperoxidase from A. nodosum. The chlorinating reaction catalyzed by the chloroperoxidase had a pH optimum around 5.5 and the Km for Cl- was small (0.25 mM at pH 4.5), but the logarithm of its value increased linearly with increasing pH. At high bromide concentrations, the pH optima of chloroperoxidase and bromoperoxidase in the brominating reaction were about the same (5.5). However, at low bromide concentrations the pH optimum of the chloroperoxidase was at higher pH values than that of the bromoperoxidase.

Chloride Peroxidase↗
PubMed1989

Contractile responses of the guinea-pig vas deferens to the combination of vanadium ions with ouabain.

1. Vanadate and vanadyl ions (10(-5)-10(-2) M) induced dose-dependent rhythmic contractions of the vas deferens of reserpine-treated guinea-pigs. The Na, K-ATPase blocker ouabain (10(-5)-10(-3) M) induced similar, though smaller, effects. Experiments were performed to verify if these effects are due to an interaction with the same receptor population. 2. Ouabain caused a striking potentiation of vanadium effects, which was also observed in denervated organs, indicating that a release of neuronal substances is not involved in potentiation. Similar potentiations were observed by combining vanadium with K-free solutions instead of ouabain, corroborating the involvement of the latter drug with Na, K, ATPase. 3. From the analysis of time-response and concentration-response curves, there are at least three indications that vanadium and ouabain interact with different sites: (a) the combined effect of both agonists was several times higher than the corresponding isolated effects; (b) the combined effect, expected to be independent of the order of addition of the agonist, was higher if vanadium was added before, than after ouabain; (c) the combined effect on the time elapsed between the addition of the two agonists, being higher if an interval of at least 10 min was allowed between vanadium and ouabain additions. 4. In conclusion, our results do not support the hypothesis that vanadium compounds and ouabain have a similar mechanism of action for the contraction induced in guinea-pig vas deferens.

Animals↗