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At least 127 records · Page 7Linked to original sources
PubMed2006

Reduction of oxidative stress induced vanadium toxicity by complexing with a flavonoid, quercetin: a pragmatic therapeutic approach for diabetes.

Vanadium compounds are known to lower blood glucose level in diabetes but are associated with toxicity. In vitro cytotoxicity of VOSO(4) and bis(quercetinato) oxovanadium(IV) (BQOV) was examined in CHO cells. Both the agents showed time and dose dependent increase in ROS generation however it was relatively less in BQOV. Moreover, VOSO(4) also caused higher necrosis. Hypoglycemic potential of VOSO(4) and BQOV was tested in streptozotocin-induced diabetic Balb/c mice. A marked difference was observed in the hypoglycemic action of VOSO(4) and BQOV treated mice that lasted only for about 6 h in VOSO(4) as against 24 h in BQOV. Comparison of acute toxicity of the compounds in normal Balb/c mice revealed negligible nephrotoxicity of BQOV. Kidney analyses of VOSO(4) treated animals' revealed high ROS generation and tubular necrosis. Similarly serum levels of urea and creatinine were elevated in these animals indicating kidney dysfunction. No such abnormality was observed in BQOV treated animals. Reduced nephrotoxicity of BQOV could be due to increased catalase activity found in the kidney of BQOV treated animals and BQOV's radical scavenging activity. The data clearly demonstrates immense hypoglycemic activity and reduced toxicity of BQOV thus making the conjugate a suitable candidate for therapeutic utility.

Animals↗
PubMed1996

Genotoxicity of vanadium pentoxide evaluate by the single cell gel electrophoresis assay in human lymphocytes.

Vanadium compounds are extensively used in modern industry and occupational exposure to high doses of Vanadium is quite common. In this study, the genotoxicity of vanadium pentoxide (V2O5) was evaluated directly in whole blood leukocytes and in human lymphocyte cultures using the single-cell gel electrophoresis assay (Comet Assay) to detect DNA damage expressed as DNA strand breaks and alkali labile sites. This chemical produces a clear dose-response in DNA migration in whole blood leukocytes and a significative positive effect only with the highest tested concentration in human lymphocyte cultures. After different recovery times the level of DNA damage returned to the control values. These results indicate that V2O5 is capable to induce DNA single-strand breaks and/or alkali-labile damage.

Adult↗
PubMed2004

Pharmacokinetic study and trial for preparation of enteric-coated capsule containing insulinomimetic vanadyl compounds: implications for clinical use.

To treat patients suffering from diabetes mellitus, we developed several types of orally active vanadyl complexes to replace painful insulin injections, and prepared them in the form of enteric-coated capsules containing vanadium compounds. Pharmacokinetic analysis demonstrated that these capsules enhance the bioavailability of pharmacologically active vanadyl species.

Administration, Oral↗
PubMed2003

Effects of some vanadyl coordination compounds on the in vitro insulin release from rat pancreatic islets.

Many lines of evidence indicate that vanadium inorganic salts possess insulin-mimetic and insulinotropic properties. However, they are poorly absorbed, so high oral doses are required to achieve effective plasma concentrations with possible undesirable toxic side-effects ensuing. Various organically-chelated vanadium compounds have been synthesized that are more potent than inorganic vanadium salts in their insulin-like effects due to their greater bioavailability. Unfortunately, little is known about the possible insulin secretagogue action of organic vanadyl coordination compounds. Hence, we investigated the effect of [VO(metformin)2]H2O, [VO(salicylidene-ethylenedimmine)2] and [VO(pyrrolidine-N-dithiocarbamate)2](VODTC) on insulin release from isolated rat pancreatic islets, and compared it to that of vanadyl sulfate (VOSO4). Of the three coordination compounds, only VODTC was found to exert insulin secretagogue action. VODTC, within concentrations ranging from 0.1 to 1.0 mM, enhanced both basal and glucose (11 mM)-stimulated insulin release. The effect involves calcium channels, since it was not appreciable in Ca2+-free medium. The stimulating action of VODTC required the presence of the whole metal-chelator complex inasmuch as the chelator DTC alone was ineffective. VOSO4 was unable to bring about any significant rise in insulin release from isolated islets. Taken together, our findings indicate that VODTC may be considered a potential elective pharmaceutical tool in the therapy of diabetes, especially of type 2, through its concomitant stimulatory effect on insulin secretion and insulin-mimetic action.

Animals↗
PubMedDate not supplied

[Protective effect on nephropathy and on cataract in the streptozotocin-diabetic rat of the vanadium-lazaroid combination].

Experimental work from our laboratory has confirmed the protective power of vanadium compounds on hyperglycemia and glycosuria in streptozotocin (STZ) diabetes. Furthermore, the diabetic cataract too has been partially prevented. The protection slightly increased, when vanadium was administered in combination with vitamin E. This investigation has introduced a combination of Na3VO4 plus the lazaroid U-83836E, a liposoluble antioxidant much more efficacious than tocopherol, in order to improve the insufficient protection when vitamin E was used. Male Wistar rats, rendered diabetic with STZ, were treated for 12 weeks with Na3VO4 in drinking water, U-83836E carried by the food, or both. The most significant metabolic parameters (food and fluid intake, diuresis and excreted feces) were studied monthly by means of metabolic cages. Body weight, glycemia, glycosuria and proteinuria were also recorded. At week 6 and 12 of the treatment, the opaqueness of the eye lenses was controlled. Circulation glycosylated hemoglobin (HbA1c), fructosamine, N-acetyl-beta-D-glucosaminidase (NAG) and fluorescent peroxides were evaluated at the end of the experiment. After the first month of treatment U-83836E improved significantly the protective effect of vanadate alone on polydipsia and polyuria, but more efficiently on hyperglycemia and glycosuria. The further ameliorating effect of the lazaroid was observed also on HbA1c, NAG and, most important, on the cataract. In conclusion, these findings demonstrate that the lazaroid U-83836E succeeds in further protecting the most important symptoms of diabetes treated with vanadate, and that this antioxidant acts effectively even when it is administered per os, in a non invasive manner.

Animals↗
PubMed2003

Vanadium-induced STAT-1 activation in lung myofibroblasts requires H2O2 and P38 MAP kinase.

Vanadium compounds present in air pollution particulate matter activate signal transduction pathways in pulmonary cell types leading to pathological outcomes including aberrant cell proliferation, apoptosis, and cytokine expression. Vanadium has been proposed to activate transcription factors via the generation of hydrogen peroxide (H2O2). We investigated the mechanisms through which vanadium pentoxide (V2O5), the major form of vanadium released from the industrial burning of fuel oil, activated the signal transducer and activator of transcription (STAT)-1. V2O5-induced STAT-1 activation was blocked by catalase and N-acetyl-L-cysteine (NAC), suggesting vanadium-induced generation of H2O2. Surprisingly, however, V2O5 did not increase H2O2 levels released by rat lung myofibroblasts into cell culture supernatants. Instead, these quiescent myofibroblasts spontaneously released micromolar concentrations of H2O2, and the addition of V2O5 reduced H2O2 levels in cell culture supernatants within minutes. V2O5 suppressed H2O2 for as long as 24 h. Differences in the temporal activation of STAT-1 and p38 MAPK were observed following V2O5 or H2O2 treatment, and STAT-1 activation by V2O5 or H2O2 was attenuated by an inhibitor of the EGF receptor tyrosine kinase (AG1478) or p38 MAPK (SB203580). The phosphorylation of p38 MAPK by V2O5 was inhibited by NAC and catalase, yet the EGF receptor inhibitor AG1478 had no effect on V2O5-induced p38 MAPK activation. Collectively, our findings support the novel hypothesis that H2O2 spontaneously generated by myofibroblasts fuels vanadium-induced activation of STAT-1. Moreover, p38 MAPK and EGF receptor activation are required for V2O5-induced STAT-1 activation.

Acetylcysteine↗
PubMed2003

Genotoxic effects of vanadium(IV) in human peripheral blood cells.

Vanadium has been considered an aneuploidogen; however, there is controversial information about the clastogenic effects of vanadium compounds. In this study, the genotoxicity of vanadium(IV) tetraoxide (V(2)O(4)) was evaluated in human cultured lymphocytes and leukocytes using the mitotic index (MI), the replicative index (RI), chromosome aberrations (CA), sister chromatid exchanges (SCE), satellite associations (SA) and the single cell gel electrophoresis (SCGE) assay. This chemical induced a clear dose-response in MI inhibitions and modifications in the RI. In the CA, including breaks and exchanges and in the SCE, a significant increase appeared in the treated group compared with the controls. The SA test did not reveal an important difference. For the detection of genotoxic properties of vanadium(IV) using the SCGE assay, the 2 h evaluation period was not long enough for the chemical to enter the cell. These results indicate that vanadium(IV) tetraoxide is capable of inducing cytotoxic and cytostatic effects and chromosomal damage.

Adult↗
PubMed1997

Acute and chronic response to vanadium following two methods of streptozotocin-diabetes induction.

Controversial reports on the efficacy and possible toxicity of vanadium obtained from various studies may be attributed to differences in the method of diabetes induction and (or) to differences in animal strains. The objective of this study was to evaluate the contribution of these two factors to the effects of vanadium in the treatment of experimental diabetes. Two methods of streptozotocin induction of diabetes in rats have been used for studying the antidiabetic effects of vanadium. One involves a single intravenous injection of 60 mg/kg streptozotocin, and the other uses two subcutaneous injections of 40 mg/kg streptozotocin, to either Wistar or Sprague-Dawley rats. In a 7-week chronic study, Sprague-Dawley rats appeared to develop a more severe diabetes (indicated by higher plasma cholesterol and higher fasting plasma glucose levels) following the single intravenous injection of streptozotocin than rats made diabetic by two subcutaneous injections of streptozotocin. Irrespective of the method of diabetes induction, the responses of all the diabetic animals to chronic vanadyl sulphate treatment were similar. In an acute study, Wistar diabetic rats were more responsive than Sprague-Dawley diabetic rats to vanadyl sulphate and to lower doses (0.6 and 0.8 mmol/kg) of a new organic vanadium compound, bis(maltolato)oxovanadium(i.v.).

Animals↗
PubMed1998

Reducing agents mitigate protein synthesis inhibition mediated by vanadate and vanadyl compounds in reticulocyte lysates.

Recently, we synthesized and characterized vanadyl saccharides to evaluate the effects of various vanadate and vanadyl complexes, which differ in their oxidation states on various biomacromolecules and cellular activities (1, 2). Here, we report that both vanadate (+V oxidation state) and different vanadyl species (+IV oxidation state) such as vanadyl D-glucose, vanadyl diascorbate, and vanadyl sulfate, impair the formation of polysomes and inhibit the initiation of protein synthesis in hemin-supplemented rabbit reticulocyte lysates. Vanadate inhibits protein synthesis more severely than vanadyl species and is consistent with the idea that vanadate is reduced to vanadyl state intracellularly. The inhibition of protein synthesis caused by low concentrations (10-20 microM) of vanadate and vanadyl species is effectively mitigated by reducing agents such as dithiothreitol, reduced glutathione (GSH), or reduced pyridine dinucleotide. A significant decrease in the protein synthesis inhibition in vanadate-treated lysates by GSH suggests that the mechanism of protein synthesis inhibition by vanadate is different than the action of other oxidants such as heavy metal ions and oxidized glutathione. This suggestion is also consistent with the findings that vanadium compounds do not stimulate phosphorylation of the alpha (alpha) subunit of initiation factor 2 (eIF2) or decrease the guanine nucleotide exchange activity of eIF2B, which is required to exchange GDP for GTP in eIF2.GDP binary complex. The reduction of vanadate to vanadyl state and the subsequent complex formation of vanadyl species with the endogenous reducing compounds or with the -SH groups of certain proteins may be the cause for protein synthesis inhibition in lysates.

Animals↗
PubMed2005

Macrophage activation by a vanadyl-aspirin complex is dependent on L-type calcium channel and the generation of nitric oxide.

Bone homeostasis is the result of a tight balance between bone resorption and bone formation where macrophage activation is believed to contribute to bone resorption. We have previously shown that a vanadyl(IV)-aspirin complex (VOAspi) regulates cell proliferation and differentiation of osteoblasts in culture. In this study, we assessed VOAspi and VO effects and their possible mechanism of action on a mouse macrophage cell line RAW 264.7. Both vanadium compounds inhibited cell proliferation in a dose-dependent manner. Nifedipine completely reversed the VOAspi-induced macrophage cytotoxicity, while it could not block the effect of VO. VOAspi also stimulated nitric oxide (NO) production, the oxidation of dihydrorhodamine 123 (DHR-123) and enhanced the expression of both constitutive and inducible isoforms of nitric oxide syntases (NOS). All these effects were abolished by nifedipine. Altogether our finding give evidence that VOAspi-induced macrophage cytotoxicity is dependent on L-type calcium channel and the generation of NO though the induction of eNOS and iNOS. Contrary, the parent compound VO exerted a cytotoxic effect by mechanisms independent of a calcium entry and the NO/NOS activation.

Animals↗
PubMed2006

Inhibition of cyclic AMP dependent protein kinase by vanadyl sulfate.

Vanadium salts influence the activities of a number of mammalian enzymes in vitro but the mechanisms by which low concentrations of vanadium ameliorate the effects of diabetes in vivo remain poorly understood. The hypothesis that vanadium compounds act by inhibiting protein tyrosine phosphatases has attracted most support. The studies described here further evaluate the possibility that vanadyl sulfate trihydrate (VS) can also inhibit 3',5'-cyclic adenosine monophosphate (cAMP) dependent protein kinase (PKA). Using conventional assay conditions, VS inhibited PKA only at high concentrations (IC50>400 microM); however, PKA inhibition was seen at dramatically lower concentrations of VS (IC50<10 microM) when sequestration of vanadyl ions was minimized. Vanadyl appears to be the effective PKA inhibitor because sodium orthovanadate did not inhibit PKA and inhibition by vanadyl was abolished by potential chelators such as ethylenediaminetetraacetic acid or glycyl peptides. PKA inhibition by vanadyl appears to be mixed rather than strictly competitive or uncompetitive and may replicate the inhibitory effects of high concentrations of Mg2+. The effect of vanadyl on PKA provides a possible explanation for the effects of vanadium salts on fat tissue lipolysis and perhaps on other aspects of energy metabolism that are controlled by cAMP-dependent mechanisms. Considering the high degree of conservation of the active sites of protein kinases, vanadyl may also influence other members of this large protein family.

Animals↗
PubMed2003

Vanadium-induced HB-EGF expression in human lung fibroblasts is oxidant dependent and requires MAP kinases.

Vanadium pentoxide (V(2)O(5)) is a transition metal derived from the burning of petrochemicals that causes airway fibrosis and remodeling. Vanadium compounds activate many intracellular signaling pathways via the generation of hydrogen peroxide (H(2)O(2)) or other reactive oxygen species. In this study, we investigated the regulation of heparin-binding epidermal growth factor-like growth factor (HB-EGF) in human lung fibroblasts after V(2)O(5) treatment. V(2)O(5)-induced HB-EGF mRNA expression was abolished by N-acetyl-l-cysteine, suggesting an oxidant-mediated effect. Exogenous H(2)O(2) (>10 microM) mimicked the effect of V(2)O(5) in upregulating HB-EGF expression. Fibroblasts spontaneously released low levels of H(2)O(2) (1-2 microM), and the addition of V(2)O(5) depleted the endogenous H(2)O(2) pool within minutes. V(2)O(5) caused a subsequent increase of H(2)O(2) into the culture medium at 12 h. However, the burst of V(2)O(5)-induced H(2)O(2) occurred after V(2)O(5)-induced HB-EGF mRNA expression at 3 h, indicating that the V(2)O(5)-stimulated H(2)O(2) burst did not mediate HB-EGF expression. Either V(2)O(5) or H(2)O(2) activated ERK-1/2 and p38 MAP kinase. Inhibitors of the ERK-1/2 pathway (PD-98059) or p38 MAP kinase (SB-203580) significantly reduced either V(2)O(5)- or H(2)O(2)-induced HB-EGF expression. These data indicate that vanadium upregulates HB-EGF via ERK and p38 MAP kinases. The induction of HB-EGF is not related to a burst of H(2)O(2) in V(2)O(5) treated cells, yet the action of V(2)O(5) in upregulating HB-EGF is oxidant dependent and could be due to the reaction of V(2)O(5) with endogenous H(2)O(2).

Cell Line↗
PubMed2001

Decrease of hypothalamic neuropeptide Y gene expression by vanadyl sulfate in streptozotocin-induced diabetic rats.

In an attempt to elucidate the effect of vanadium compounds on the gene expression of neuropeptide Y (NPY), vanadyl sulfate (VOSO4) was orally administrated at the dose of 1 mg/kg body weight into streptozotocin-induced diabetic rats (STZ-diabetic rats) three times daily for 1 week. We found a marked lowering of plasma glucose with a significant decrease of food and water intake in these STZ-diabetic rats treated with VOSO4, although the weight gain was unaffected. The increase of hypothalamic NPY, both the mRNA level and peptide concentration, in STZ-diabetic rats was also reduced by this oral treatment of VOSO4. However, similar treatment of VOSO4 in normal rats failed to modify the feeding behavior and hypothalamic NPY gene expression. These data suggest that decrease of hypothalamic NPY gene expression by VOSO4 is related to the recovery of hyperphagia in diabetic rats lacking insulin.

Animals↗
PubMed1997

Oral vanadyl sulphate does not affect blood cells, viscosity or biochemistry in humans.

Vanadyl sulphate (VOSO4) is used to improve performance in weight training athletes. Concerns about its safety have arisen because vanadium compounds may cause anaemia and changes in the leukocyte system. In this study, the effects of oral VOSO4 (0.5 mg/kg/day) on haematological indices (red and white cell and platelet counts, red cell mean cell volume and haemoglobin level), blood viscosity (haematocrit, plasma viscosity and blood viscosity at 10s-1 and 100s-1 shear rates) and biochemistry (lipids and indices of liver and kidney function) were investigated in a twelve week, double blind, placebo controlled trial in 31 weight training athletes. Blood viscosity was evaluated at 0, 2, 4, 8 and 12 weeks and haematological indices and biochemistry were measured before and at the end of treatment. Both the treatment group and placebo group showed increases in haematocrit (3.3-3.6%) and blood viscosity (9-11% at 100s-1 shear; 35-38% at 10s-1 shear) but there were no significant effects of treatment. Similarly there were no treatment effects on haematological indices and biochemistry. Concerns about the adverse effects of oral vanadyl sulphate on blood are not supported by the results of this trial.

Adult↗
PubMed2002

Effect of acute and short-term administration of vanadyl sulphate on insulin sensitivity in healthy active humans.

Vanadium compounds have been shown to have insulin-like properties in rats and non-insulin-dependent diabetic humans. The purpose of the present study was to examine whether the effects of acute and short-term administration of vanadyl sulfate (VA) on insulin sensitivity also exist in healthy active individuals. Five male and two female participants (age: 24.9 +/- 1.5 years; height: 176.1 +/- 2.9 cm; body mass: 70.1 +/- 2.9 kg) underwent 3 oral glucose tolerance tests (OGTT). The first OGTT was performed to obtain a baseline index of insulin sensitivity (ISI). On the night preceding the second OGTT, participants ingested 100 mg of VS, and the acute effects of VS on ISI were examined. For the next 6 days, participants were instructed to ingest 50 mg of VS twice daily, and a final OGTT was performed on day 7 to determine the short-term effects of VS on ISI. No differences were found in fasting plasma glucose and insulin concentrations after VS administration. Furthermore, ISI after 1 day and 7 days of VS administration was not different compared with baseline ISI (4.8 +/- 0.1 vs. 4.7 +/- 0.1 vs. 4.7 +/- 0.1, respectively). These results demonstrate that there are no acute and short-term effects of VS administration on insulin sensitivity in healthy humans.

Administration, Oral↗
PubMed1995

Skeletal muscle mitogen-activated protein kinases and ribosomal S6 kinases. Suppression in chronic diabetic rats and reversal by vanadium.

The mitogen-activated protein (MAP) kinases and ribosomal S6 protein kinases in the skeletal muscle of insulin-resistant long-term (2 and 6 months' duration) diabetic rats were investigated to understand further the changes in insulin intracellular signaling pathways that accompany diabetes. The effects of insulin-mimetic vanadium compounds on the activity of these kinases were also examined. In the insulin-resistant 2-month diabetic rats, the basal activities of MAP kinases were relatively unchanged, while the basal activities of S6 kinases were significantly increased. Intravenous injection of insulin moderately activated both the 42-kDa MAP kinase (p42mapk) and a 44-kDa MAP kinase (p44erk1) in the 2-month control rats but not in the 2-month diabetic rats. Insulin treatment markedly stimulated the activity of a novel 31-kDa S6 kinase and the previously described 90-kDa ribosomal S6 kinase encoded by one of the rsk genes (p90rsk) in the 2-month control rats, while the effect was substantially reduced in the diabetic rats. In the 6-month diabetic rats, the basal phosphotransferase activities of both MAP kinases were depressed threefold or greater. This correlated with reductions in the amount of immunoreactive p42mapk and p44erk1 proteins in extracts from the diabetic rats. The basal activity of the 31-kDa S6 kinase activity was also reduced fourfold in the 6-month diabetic rats. Treatment of the 2-month diabetic rats with vanadyl sulfate resulted in euglycemia, prevented the increase in the basal activity of S6 kinase, and improved the activation of S6 kinase by insulin.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

Influence of chelation and oxidation state on vanadium bioavailability, and their effects on tissue concentrations of zinc, copper, and iron.

Today, vanadium compounds are frequently included in nutritional supplements and are also being developed for therapeutic use in diabetes mellitus. Previously, tissue uptake of vanadium from bis(maltolato)oxovanadium(IV) (BMOV) was shown to be increased compared to its uptake from vanadyl sulfate (VS). Our primary objective was to test the hypothesis that complexation increases vanadium uptake and that this effect is independent of oxidation state. A secondary objective was to compare the effects of vanadium complexation and oxidation state on tissue iron, copper, and zinc. Wistar rats were fed either ammonium metavanadate (AMV), VS, or BMOV (1.2 mM each in the drinking water). Tissue uptake of V following 12 wk of BMOV or AMV was higher than that from VS (p < 0.05). BMOV led to decreased tissue Zn and increased bone Fe content. The same three compounds were compared in a cellular model of absorption (Caco-2 cells). Vanadium uptake from VS was higher than that from BMOV or AMV at 10 min, but from BMOV (250 microM only, 60 min), uptake was far greater than from AMV or VS. These results show that neither complexation nor oxidation state alone are adequate predictors of relative absorption, tissue accumulation, or trace element interactions.

Animals↗
PubMed1990

Bioaccumulation of nickel and vanadium in tissues of the catfish Clarias batrachus.

Bioaccumulation of nickel and vanadium in the tissues of the liver, kidney, gill, and intestine has been studied following 4 days and 30 days of exposure at sublethal concentrations of nickel and vanadium compounds in the catfish Clarias batrachus. Nickel and vanadium have been found to accumulate in all four tissues observed. High concentrations of nickel and vanadium have been found in the order kidney greater than gill greater than liver greater than intestine during the 4 days and 30 days treatment. A dose-response effect was seen, as the concentration of metals in the tissues increased with concentration and exposure time. The effect on bioaccumulation in the specific tissue provides a better basis for monitoring exposures than whole-body analysis.

Animals↗