Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Vanadium Compounds”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 361 records · Page 20Linked to original sources
PubMedDate not supplied

Reversal of defective G-proteins and adenylyl cyclase/cAMP signal transduction in diabetic rats by vanadyl sulphate therapy.

Vanadium salts exhibit a wide variety of insulinomimetic effects. In the present studies, we have examined the modulation of G-protein levels and adenylyl cyclase activity in the liver of streptozotocin-induced chronic diabetic rats (STZD) by vanadyl sulfate treatment and compared it with that of insulin. The basal enzyme activity, as well as the stimulatory effects of guanine nucleotides, glucagon, N-Ethylcarboxamideadenosine (NECA), isoproterenol, forskolin and sodium fluoride (NaF) on adenylyl cyclase were significantly increased in STZ-D rat liver as compared to control. In addition, the levels of stimulatory (Gs alpha) as well as inhibitory (Gi alpha-2 and Gi alpha-3) as determined by immunoblotting techniques were also significantly higher in the STZ-D rat liver, however, the inhibitory effects of oxotremorine and low concentrations of GTP gamma S on adenylyl cyclase were not different in the two groups. Vanadyl sulfate and insulin treatments restored the augmented basal enzyme activity, the stimulations exerted by stimulatory inputs on adenylyl cyclase and the G-protein levels to various degrees, however, vanadyl sulfate was more effective than insulin. In addition, unlike vanadyl sulfate, insulin was unable to improve the stimulation exerted by glucagon and isoproterenol on adenylyl cyclase activity in STZD rats. These results suggest that vanadyl sulfate mimics the effects of insulin to restore the defective levels of G-proteins and adenylyl cyclase activity. From these results it may be suggested that one of the mechanisms by which vanadyl sulfate improves the glucose homeostasis in STZ-D rats may be through its ability to modulate the levels of G-proteins and adenylyl cyclase signal transduction system.

Adenylyl Cyclases↗
PubMedDate not supplied

Evidence for selective effects of vanadium on adipose cell metabolism involving actions on cAMP-dependent protein kinase.

The insulin-like effects of vanadium in vivo are likely to be achieved at micromolar concentrations. Demonstrated effects of vanadium on adipose tissue of streptozotocin-diabetic rats include inhibition of basal and stimulated rates of lipolysis and effects on fat cell protein phosphorylation. The studies described below examined the effects of vanadium (to a maximum concentration of 0.5 mM) on adipose cells or tissue in vitro. Vanadium, added as a vanadyl-albumin complex or as sodium orthovanadate, produced a marked (greater than 50%) inhibition of isoproterenol-stimulated lipolysis. Inhibition of lipolysis equivalent to that seen with insulin, was achieved with approximately 100 microM vanadium. In contrast, no insulin-like stimulation of de novo fatty acid biosynthesis was observed with vanadium below 0.5 mM. Surprisingly, the antilipolytic effects of vanadium persisted in the presence of cilostamide, an inhibitor of the insulin-sensitive isoform of cyclic nucleotide phosphodiesterase. Studies with purified preparations of the catalytic subunit of cyclic AMP-dependent protein kinase revealed dose-dependent inhibition with vanadyl-glutathione (to a maximum of approximately 40% inhibition). Equivalent inhibition of cyclic AMP-dependent phosphorylation of Kemptide (approximately 50%) was observed upon incubation of freshly-prepared fat-pad supernatant fractions with vanadyl-glutathione. These results suggest that effects of low concentrations of vanadium may be mediated, at least in part, by actions on the catalytic subunit of cyclic AMP-dependent protein kinase.

Adipocytes↗
PubMedDate not supplied

Long-term correction of STZ-diabetic rats after short-term i.p. VOSO4 treatment: persistence of insulin secreting capacities assessed by isolated pancreas studies.

We have previously shown that 3 week oral VOSO4 treatment of streptozotocin (STZ, 60 mg/kg)-induced diabetic rats was able to correct diabetes for 13 weeks after treatment withdrawal. In the present study, we investigated whether a short-term (8 days) i.p. VOSO4 treatment was similarly able to reverse the diabetic state. Insulin secretory capacities were assessed at distance of treatment using the isolated pancreas preparation. Seven treatment-groups were performed: high dose VOSO4-treated diabetics (HVD, 1.3 mM/kg/8 days), food-restricted diabetics (FRD, food adjusted to HVD levels), low dose VOSO4-treated diabetes (LVD, 0.06 mM/kg/day), insulin-treated diabetics (ID, dose adjusted to normalize glycaemia) and VOSO4 (0.06 mM/kg/day) + insulin (dose adjusted to normalize glycaemia in the presence of vanadium)-treated diabetics (IVD), in addition to the corresponding untreated non-diabetic controls (C) and diabetics (D). Our results indicate that long-term correction of diabetes (a) can be obtained after an 8 day treatment using i.p. VOSO4 in diabetic animals retaining some degree of pancreatic function, (b) is not obtained with insulin treatment or food restriction although the association of VOSO4 and insulin was found beneficial, (c) can be prolonged in some individuals for at least 4 months, i.e. in conditions such that tissue vanadium concentrations had returned to values close to pre-treatment levels, (d) is associated with improved and in some cases normalized insulin secretion from isolated pancreas. The protective or corrective role of VOSO4 on diabetes-related pancreatic alterations, as well as the potential of the VOSO4-insulin association should be further studied in view of the possible use of vanadium derivatives in the treatment of diabetes.

Animals↗
PubMed2005

Comparative study on the preventing effects of oral vanadyl sulfate and dietary restriction on the age-related glucose intolerance in rats.

BACKGROUND AND AIMS: Aging is associated with a progressive impairment of glucose tolerance. The aim of this study was to explore the protective effects of the chronic oral administration of the insulino-mimetic agent vanadyl sulfate (VOSO4) as compared with those exerted by a long-lasting dietary restriction. METHODS: Male Sprague-Dawley rats, either fed ad libitum (AL) or subjected to 40% dietary restriction (DR), were used. VOSO4 (0.5 mg/mL drinking water) was administered to a subgroup of AL rats for two months, starting at 16 months of age. Rats were subjected to an intravenous glucose tolerance test (IVGTT) at 16 and 18 months of age. Finally, the beta-cell responsiveness to glucose was evaluated in vitro by the isolated perfused pancreas preparation. RESULTS: The IVGTT performed in 16-month-old rats showed that DR prevented the development of the moderate glucose intolerance observed in AL rats. The IVGTT performed at 18 months of age confirmed the beneficial effect of DR and showed that VOSO4 was able to prevent the further age-related progression of glucose intolerance observed in AL rats. Pancreas perfusion studies showed that no increase in insulin secretion occurred in both VOSO4-treated and DR rats with respect to the age-matched AL controls, consistently with the in vivo observation of post-loading insulinaemic changes. CONCLUSIONS: On the basis of these results, we conclude that the beneficial effect of both treatments is mostly related to an improvement of tissue sensitivity to insulin rather than to an insulinotropic effect.

Administration, Oral↗
PubMed2003

Vanadyl sulfate can differentially damage DNA in human lymphocytes and HeLa cells.

Using the comet assay, we showed that vanadyl sulfate induced DNA damage in human normal lymphocytes and in HeLa cells. Vanadyl at 0.5 and 1 mM produced DNA single- and double-strand breaks (SSBs and DSBs) in lymphocytes, whereas in HeLa cells we observed only SSBs. Post-treatment of vanadyl-damaged DNA from lymphocytes with formamidopyrimidine-DNA glycosylase (Fpg), an enzyme recognizing oxidized purines, gave rise to a significant increase in the extent of DNA damage. A similar effect was observed in HeLa cells, but, using endonuclease III, we also detected oxidized pyrimidines in DNA of these cells. There were no differences in the extent of DNA damage in the lymphocytes and HeLa cells in the pH >13 and pH 12.1 conditions of the comet assay, which indicates that strand breaks, and not alkali-labile sites, contributed to the measured DNA damage. Study of DNA repair, determined in the comet assay as an ability of cells to decrease of DNA damage, revealed that HeLa cells retained the ability to repair vanadyl-damaged DNA induced at a ten-fold higher concentration than that in lymphocytes. Incubation of the cells with nitrone spin traps DMPO, POBN and PBN decreased the extent of DNA damage, which might follow from the production of free radicals by vanadyl sulfate. The presence of vitamins A, C or E caused an increase of DNA damage in HeLa cells whereas in lymphocytes such an increase was observed only for vitamin C. Our data indicate that vanadyl sulfate can be genotoxic for normal and cancer cells. It seems to have a higher genotoxic potential for cancer cells than for normal lymphocytes. Vitamins A, C and E can increase this potential.

Ascorbic Acid↗
PubMed2005

Effects of STZ-induced diabetes and its treatment with vanadyl sulphate on cyclosporine A-induced nephrotoxicity in rats.

The aim of this study was to analyze the effect of streptozotocin (STZ)-induced diabetic state and the insulin-like acting, vanadyl sulphate (VS) on cyclosporine A (CyA) related nephrotoxicity in rats. Male Wistar rats were divided into six groups, of 12 animals each: The control, diabetic rats and diabetic rats whose drinking VS in the drinking water in a concentration of 1 mg/ml. Another three similarly treated groups were injected intra-peritoneally (ip) with CyA in a dose of 25 mg/kg/day for ten doses, 10 days after diabetic induction by using a single dose of STZ of 65 mg/kg. Rats were sacrificed 48 h after the last CyA dose and serum as well as kidneys were isolated and analyzed. Treatment with CyA to control normoglycemic rats resulted in significant increases in kidney weight, serum creatinine, urea nitrogen, cholesterol and triglycerides (TG) levels. Also, the kidney tissue of CyA-treated control animals showed significant increases in total nitrate/nitrite (NO(x)) concentration and malondialdehyde (MDA) production level as well as depletion of glutathione (GSH) content and glutathione peroxidase (GSH-P(x)) activity level. Histopathologic evaluation of CyA-treated control rats revealed tubular atrophy, hyaline casts and focal tubular necrosis. However, treatment of diabetic rats with CyA showed significant reduction in serum creatinine and elevation in TG level as well as reductions in the kidney NO(x) concentration and MDA production level and increase in GSH concentration compared to CyA-treated control rats. Moreover, histopathology of the kidney of CyA-treated diabetics showed typical changes of the diabetic controls revealing glomerular hypertrophy and tubular dilation. On the other hand, treatment with CyA to those diabetic animals administered VS in the drinking water resulted in exacerbation of renal dysfunction, manifested by significant increases in serum indices of nephrotoxicity, cholesterol, TG and bilirubin levels. Also, VS administration to CyA-treated diabetics showed significant increase in kidney NO(x) concentration compared to those CyA-treated diabetics drinking plain tap water, and to a level significantly lower than those CyA-treated controls. Histopathologically, kidney of CyA/VS-treated diabetic showed marked CyA related changes. In conclusion, STZ-induced diabetes might provide partial protection against CyA-induced renal dysfunction. Also, treatment of hyperglycemia with VS might exacerbate CyA related nephrotoxicity.

Animals↗
PubMed2003

Antitumoral properties of two new vanadyl(IV) complexes in osteoblasts in culture: role of apoptosis and oxidative stress.

BACKGROUND: Vanadium derivatives have been reported to display different biological effects, and in particular antineoplastic activity has been demonstrated in both in vivo and in vitro studies. PURPOSE. To study the effect of two new organic vanadyl(IV) complexes (one with glucose, GluVO, and the other with naproxen, NapVO) in osteosarcoma cells. METHODS: UMR106 osteosarcoma cells and, for comparison, nontransformed MC3T3E1 osteoblasts were used. Proliferation and differentiation were assessed using the crystal violet assay and ALP specific activity, respectively. Morphological alterations were assessed by light microscopy. Lipid peroxidation was evaluated in terms of production of thiobarbituric acid-reactive substances (TBARS) and apoptosis was measured using annexin V. Extracellular regulated kinase (Erk) activation was investigated by Western blotting. RESULTS: Vanadium complexes caused morphological alterations and they strongly inhibited UMR106 cell proliferation and differentiation. In contrast, in MC3T3E1 cells, these vanadium derivatives had a relatively weak action. In UMR106 tumoral cells there was a significant increase in TBARS production. Both vanadium complexes induced apoptosis and activation of Erk. PD98059, an inhibitor of Erk phosphorylation, did not block the vanadium-induced antitumoral action. However, the antioxidants vitamins C and E abrogated the apoptosis and TBARS production induced by the vanadium complexes. CONCLUSIONS: GluVO and NapVO exerted an antitumoral effect in UM106 osteosarcoma cells. They inhibited cell proliferation and differentiation. While the Erk cascade seems not to be directly related to the bioactivity of these vanadium derivatives, the action of both vanadium complexes with organic ligands may be mediated by apoptosis and oxidative stress.

Animals↗
PubMed1998

Vanadyl ions stimulate K+ uptake into isolated perfused rat liver via the Na+/K+-pump by a tyrosine kinase-dependent mechanism.

Vanadium salts mimic most metabolic effects of insulin in vitro. We report here that vanadyl sulfate (VOSO4) and sodium vanadate (NaVO3) stimulate net K+ uptake in isolated perfused rat liver. Stimulation was evident at low concentrations of vanadyl ions (range 1-20 microM) and occurred within minutes following the addition of VOSO4. By comparison with VOSO4, insulin had less of a stimulatory effect on K+ uptake. Ouabain prevented the activating effect of VOSO4 on K+ uptake. Following a VOSO4 challenge, measured intracellular Na+ concentration ([Na+]i) fell (control, 17.1 +/- 1.2; VOSO4-treated, 13.0 +/- 1.1 mmol.g-1 wet weight, P = 0.027). The results indicate that active K+ uptake via the Na+/K+-ATPase was stimulated by vanadyl ions. An indirect mechanism due to changes in [Na+]i can be excluded. The tyrosine kinase inhibitor genistein was found to inhibit stimulation of K+ by vanadyl and vanadate ions which are known inhibitors of phosphotyrosine phosphatases. We conclude that stimulation of active K+ influx involves a tyrosine kinase. Possible mechanisms include phosphorylation at tyrosine residues and direct activation of the Na+/K+-ATPase, or phosphorylation of other proteins that regulate the activity or number of pumps in the cells.

Animals↗
PubMed2006

Pentavalent vanadium at concentration of the underground water level enhances the sweet taste sense to glucose in college students.

Underground water in volcanic areas contains vanadium when the basalt layer exists among igneous rocks. The concentration of vanadium in drinking water sometimes exceeds 0.8 microM in these areas, however, the physiological effects of vanadium, especially non-toxic effects, at concentrations lower than 1 microM are unknown. In the present experiments, we examined the effect of pentavalent vanadium and tetravalent vanadium at 0.8 and 8.0 microM concentrations on the recognition threshold to taste substances in healthy college students. Pentavalent vanadium, ammonium vanadate, lowered the sweet taste threshold to glucose at 0.8 and 8.0 microM as well. Tetravalent vanadium, vanadium sulfate, did not alter the threshold to glucose either at 8.0 microM or at 0.8 microM. Ammonium vanadate also decreased the sweet taste threshold to L-proline at 8.0 microM. Ammonium vanadate did not influence the sour taste threshold to hydrogen chloride. Neither ammonium sulfate nor ammonium bicarbonate altered the sweet taste threshold to glucose. Therefore, the effect of ammonium vanadate on the sweet taste threshold is attained by vanadium but not by ammonium. It was concluded that pentavalent vanadium at 0.8 microM intensifies the sweet taste sense to glucose rather specifically. We have first shown the physiological effect of vanadium at the concentration of the underground water level.

Adolescent↗
PubMed2005

The effects of peroxovanadate and peroxovanadyl on glucose metabolism in vivo and identification of signal transduction proteins involved in the mechanism of action in isolated soleus muscle.

The insulin-like effects of peroxovanate (POV) and peroxovanadyl (PSV) on rates of lactate formation and glycogen synthesis were measured in isolated incubated soleus muscle preparations. In another experiment rats were made insulin deficient by streptozotocin injection and treated with POV and PSV (0.25 mM) administered in the drinking water and in the course of 7 days glycemia were determined. Also, signal transduction proteins ERK 1 and ERK 2 involved in the insulin signaling were measured in soleus muscle of diabetic rats treated with POV and PSV. Peroxides of vanadate and vanadyl significantly stimulated glucose utilization in soleus muscle preparations in vitro. The stimulation of glycogen synthesis and lactate formation by POV and PSV was similar to insulin stimuli. Rats treated with POV or PSV presented reduction of glycemia, food and fluid intake with amelioration of the diabetic state during the short period of treatment (7 days). POV and PSV modulated ERK1/2 phosphorilation and the insulin administration in these rats caused an addictive effect on phosphorilation state of these proteins.

Animals↗
PubMed2006

Vanadyl sulfate administration protects the streptozotocin-induced oxidative damage to brain tissue in rats.

Diabetes mellitus manifests itself in a wide variety of complications and the symptoms of the disease are multifactorial. The present study was carried out to investigate the effects of vanadyl sulfate on biochemical parameters, enzyme activities and brain lipid peroxidation, glutathione and nonenzymatic glycosylation of normal- and streptozotocin-diabetic rats. Streptozotocin (STZ) was administered as a single dose (65 mg/kg) to induce diabetes. A dose of 100 mg/kg vanadyl sulfate was orally administered daily to STZ-diabetic and normal rats, separately until the end of the experiment, at day 60. In STZ-diabetic group, blood glucose, serum sialic and uric acid levels, serum catalase (CAT) and lactate dehydrogenase (LDH) activities, brain lipid peroxidation (LPO) and nonenzymatic glycosylation (NEG) increased, while brain glutathione (GSH) level and body weight decreased. In the diabetic group given vanadyl sulfate, blood glucose, serum sialic and uric acid levels, serum CAT and LDH activities and brain LPO and NEG levels decreased, but brain GSH and body weight increased. The present study showed that vanadyl sulfate exerted antioxidant effects and consequently may prevent brain damage caused by streptozotocin-induced diabetes.

Administration, Oral↗
PubMed1990

Vanadium uptake by yeast cells.

During incubation with vanadyl, Saccharomyces cerevisiae yeast cells were able to accumulate millimolar concentrations of this divalent cation within an intracellular compartment. The intracellular vanadyl ions were bound to low molecular weight substances. This was indicated by the isotropic nature of the electron paramagnetic resonance (EPR) spectra of the respective samples. Accumulation of intracellular vanadyl was dependent on presence of glucose during incubation. It could be inhibited by various di- and trivalent metal cations. Of these cations lanthanum displayed the strongest inhibitory action. If yeast cells were exposed to more than 50 microM vanadyl sulfate at a pH higher than 4.0, a potassium loss into the medium was detected. The magnitude of this potassium loss suggests a damage of the plasma membrane caused by vanadyl. Upon addition of vanadate to yeast cells surface-bound vanadyl was detectable after several minutes by EPR. This could be the consequence of extracellular reduction of vanadate to vanadyl. The reduction was followed by a slow accumulation of intracellular vanadium, which could be inhibited by lanthanum or phosphate. Therefore, permeation of vanadyl into the cells can be assumed as one mechanism of vanadium accumulation by yeast during incubation with vanadate.

Cations, Divalent↗
PubMed1992

DNA cleavage by hydroxyl radicals generated in a vanadyl ion-hydrogen peroxide system.

Vanadyl ion (+4 oxidation state) has been shown to be an effective agent for chemoprotection of cancers in animals. For understanding the mechanism, distribution of vanadium was studied. More vanadium was found to accumulate in the nuclei of the liver of rats when it was given as vanadyl sulfate than when it was given as sodium vanadate (+5 oxidation state). The reactivity of vanadyl ion with DNA was investigated by the DNA cleavage technique and the reaction mechanism by ESR spectroscopy. Incubation of double-strand DNA with vanadyl ion and hydrogen peroxide resulted in marked concentration- and pH-dependent DNA cleavage. Studies by the ESR spin-trap method demonstrated that hydroxyl radicals are generated during the reactions of vanadyl ion with hydrogen peroxide. Thus the antineoplastic action of vanadyl ion is proposed to be due to DNA cleavage by hydroxyl radicals generated in the cells.

Animals↗
PubMed1996

Measurement of phospholipase A2 and 1-alkylglycerophosphocholine acetyltransferase activities in stimulated alveolar macrophages by HPLC analysis of NBD-labeled ether lipids.

The importance of phospholipases in cellular signaling and 1-alkylglycerophosphocholine acetyltransferase in the formation of platelet-activating factor (PAF) has stimulated demand for methods to measure these enzyme activities in inflammatory cells. Most of the assays currently used rely on radiolabeled substrates. We have synthesized NBD-labeled ether lipids as substrates for measuring enzyme activities of the PAF cycle and of lysosomal phospholipase A2 (PLA2). The fluorescent lipids were incubated with homogenates of stimulated bovine alveolar macrophages. The generated products were separated from the substrates by HPLC on a normal phase and monitored with a fluorescence detector. NBD-lyso-PAF was well accepted by acetyl- and acyltransferases of the cell-free preparations, which metabolized the substrate into NBD-PAF and NBD-alkyl-acylglycerophosphocholines. Homogenates of stimulated cells showed an enhanced production of NBD-PAF. The increased formation of the biological mediator was dependent on the nature of the stimuli and the time of stimulation. Lysosomal PLA2 was measured with 1-O-(12-NBD-aminododecyl)-2-acyl-sn-glycero-3-phosphocholine as substrate. By varying the pH and the calcium concentration, it was possible to distinguish between the cytosolic PLA2 and the lysosomal PLA2 activity. Optimal conditions for the determination of the lysosomal PLA2 were obtained at pH 4.5 and in the presence of EDTA. Stimulation with particulate agonists induced an enhancement of the lysosomal PLA2 activity in macrophages.

4-Chloro-7-nitrobenzofurazan↗
PubMed1994

Comparison of the effects of various vanadium salts on glucose homeostasis in streptozotocin-diabetic rats.

Oral administration of vanadium salts to severely diabetic rats lead to a spectacular decrease of plasma glucose levels in spite of the insulin deficiency of the animals. The insulin-like properties of vanadium have been attributed to the cationic form, vanadyl, into which the anionic form, vanadate, is reduced within cells. This has led to the suggestion that vanadyl is the form of choice for the treatment. In this study, rats made insulin-deficient and diabetic with streptozotocin were treated with three salts of vanadium: sodium orthovanadate, sodium metavanadate and vanadylsulfate. The salts were added to the drinking water, in concentrations that led to ingestion of the same amount of vanadium element by the three groups of rats (approximately 8 mg/kg per day). The initial, transient, loss of weight that affected the treated rats was slightly smaller in the vanadyl-treated group than in the vanadate-treated groups. However, during steady-state treatment, the three groups exhibited a similar food intake (lower than in controls) and growth rate (higher than in controls). The decreases in plasma glucose levels, in urinary volume and in glucosuria, and the improvement of the tolerance to an oral glucose load were similar regardless of the type of vanadium salt. Withdrawal of the treatment after 14 weeks was followed by a rapid increase in plasma glucose levels which, however, remained clearly lower than in controls for at least 4 weeks, whereas plasma insulin levels increased only transiently. A smaller glucosuria and a slightly better tolerance to oral glucose than in controls were still observed in the previously treated rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1996

UV-B- and oxidative stress-induced increase in nicotinamide and trigonelline and inhibition of defensive metabolism induction by poly(ADP-ribose)polymerase inhibitor in plant tissue.

Nicotinamide and trigonelline contents increased in Catharanthus roseus tissue culture after exposure to 2,2'-azobis(2-amidinopropane)dihydrochloride (AAPH) or vanadylsulfate and in Pisum sativum leaves after exposure to UV-B radiation. Vanadylsulfate increased phenylalanine ammonia-lyase (PAL) activity and the content of reduced and oxidized gluthathione in C. roseus tissue culture. The increases in PAL activity caused by 2 mM AAPH or 0.2mM vanadylsulfate were prevented by 0.1 mM 3-aminobenzamide (3-AB), an inhibitor of poly(ADP-ribose)polymerase. Present results support the hypothesis [Berglund, T., FEBS Lett. (1994) 351, 145-149] that nicotinamide and/or its metabolites may function as signal transmittors in the response to oxidative stress in plants and that poly(ADP-ribose)polymerase has a function in the induction of defensive metabolism.

Alkaloids↗
PubMed1985

Effect of vanadate and pyridoxal phosphate on S-adenosylmethionine.

Vanadate in the presence of pyridoxal phosphate promotes the decarboxylation of S-adenosylmethionine. Pyridoxal has a lower effect; pyridoxine none. The rate of decarboxylation depends on pyridoxal phosphate and vanadate concentration. Vanadate as low as 10(-7) M gives significant decarboxylation. The reaction seems to occur through the formation of a Schiff base. The spectral shift elicited by S-adenosylmethionine on pyridoxal phosphate due to the presence of the sulfonium function is influenced by vanadate. Orthovanadate is a little less effective then metavanadate; vanadyl sulfate is even less efficient, and the effect of Cu2+ at the same concentration is still lower. Bleomycin partially prevents the vanadium effect. In vivo, vanadate promotes a marked increase in chicken liver S-adenosylmethionine and S-adenosylhomocysteine concentration, whereas the polyamine concentration is unaffected.

Animals↗