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 559 records · Page 31Linked to original sources
PubMed1989

Effects of vanadyl sulphate on ornithine decarboxylase and progesterone levels in the ovary of rat.

The effects of vanadyl sulphate in vitro on the levels of ODC activity and progesterone synthesis in ovaries were studied. The levels of ODC in the ovaries were stimulated with high concentration of vanadyl sulphate and at low concentrations there was no change in the levels of ODC activity. On the contrary progesterone levels were stimulated with low concentrations of vanadyl sulphate and were inhibited at higher concentrations. Vanadyl sulphate showed additional stimulation of ODC activity, when it was added with hCG and caused inhibition of hCG induced progesterone biosynthesis. These results show that the effects of vanadyl sulphate on ODC and progesterone are different.

Animals↗
PubMed1995

[Fructose-2,6-bisphosphate system and experimental states].

The molecular mechanisms of the inhibitory action of fructose- 2,6-bisphosphate (F-2,6-P2) on fructose-1,6-biphosphatase (FB-Pase-1), the key enzyme of gluconeogenesis, and the those of the activating action of F-2,6-P2 on phosphofructo-1-kinase (PFK-1), the key enzyme of glycolysis, NMR spectroscopy first provided direct evidence for the fact that F-2,6-P2 was involved in the regulation of the sedoheptulose cycle of a nonoxidative stage of the pentosephosphate pathway. Procedures were developed in measuring the levels of F-2,6-P2 in the cell of experimental animal tissues and human blood lymphocytes. Naturally different emergencies substantially affected the F-2,6-P2 system by triggering these or those mechanisms controlling the activity of enzymes of this system. Vanadium-containing compounds were demonstrated to have a positive action on carbohydrate metabolism in diabetic (streptozotocin-induced) rat hepatocytes.

Animals↗
PubMed1993

Effect of vanadyl sulfate feeding on susceptibility to peroxidative change in diabetic rats.

The effects of vanadyl sulfate treatment on susceptibility to oxidative stress were investigated in streptozotocin-diabetic Wistar rats. A 2 x 2 factorial design was employed, with four groups of animals: 1) untreated, non-diabetic; 2) vanadyl-treated, non-diabetic; 3) untreated, diabetic; and 4) vanadyl-treated, diabetic. Vanadyl sulfate was administered as a 1.00 to 1.25 mg/ml solution in drinking water. Cataract development was entirely suppressed in vanadyl-treated compared to untreated, diabetic rats. STZ-induction of diabetes diminished glutathione (GSH) levels in liver homogenates; whereas vanadyl treatment resulted in restored levels of this nonenzymatic antioxidant. Thiobarbituric acid reactive substances (TBARS), both basal and iron-stimulated, were significantly elevated in all vanadyl-treated animals. Vanadyl treatment lowered liver glutamine synthetase activities in diabetic rats, but not in non-diabetic animals. Thus, vanadyl treatment was antioxidant in terms of cataract formation and reduced glutathione concentration in liver homogenates, pro-oxidant by reason of iron-stimulated TBARS formation and inconclusive with respect to glutamine synthetase activity. These results highlight the importance of using multiple indicators of peroxidative change in evaluating new pro-oxidant/antioxidant treatment regimens.

Administration, Oral↗
PubMed1993

[Study of teratogenicity and sensitive period of vanadium pentoxide in Wistar rats].

Pregnant Wistar rats were administered with vanadium pentoxide (V2O5) in three different ways single intraperitoneal injection (ip) of V2O5 5mg/kg on days 9, 10, and 11 of gestation; ip 5mg/kg/day on days 9-12 of gestation; and ip 3mg/kg/day on days 6-15 of gestation. The results showed that the female rats had such toxic symptoms as decreased weight gain, increase fetal mortality, decreased fetal weight and crown-rump, retarded ossification of the bone, increased incidence of subcutaneous hemorrhage, rib wavy, dilation of lateral ventricles and renal pelvis in the two groups, i.e., on days 6-15, and 9-12 of gestation, Decreased weight gain, increased incidence of subcutaneous hemorrhage and visceral anomalies were found on day 11 of gestation group. Increased incidence of fetal death, retarded ossification of the bone on day 10 of gestation group; and increased incidence of subcutaneous hemorrhage and visceral anomalies on days 9, and 10 of gestation were observed. These data suggest that V2O5 can induce teratogenicity in Wistar rat with or without obvious maternal toxicity. There was no obvious teratogenic sensitive period of V2O5 on embryo, but as for single treatment, it was more sensitive on gestation day 10 than on gestational day 11 or 9; as for multi-treatment, it was more sensitive on days 9-12 than on days 6-15 of gestation for teratogenicity and fetal death. It is suggested that V2O5 may act mainly on the middle or late stage of organogenetic period.

Abnormalities, Drug-Induced↗
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↗
PubMed1995

[Toxicity of vanadium to Leydig cells in vitro].

The levels of testosterone secreted by rat's Leydig cells in varied concentrations of V2O5 (0.125, 0.,25, 0.5, 2 and 3 mmol/L) were assayed. The result showed there was no obvious relation between the level of testosterone and the concentration of V2O5. This in vitro study in accord with the result of whole animal research indicates that Leydig cell is not the target of V2O5.

Animals↗
PubMed1997

Characterization of vanadyl sulfate effect on vascular contraction: roles of calcium and tyrosine phosphorylation.

In order to explore the mechanism of action of vanadyl sulfate (VOSO4), previously described as an antidiabetic and antihypertensive agent, we have investigated the role of calcium and tyrosine phosphorylation in the contractile responses of rat aorta or skinned rabbit mesenteric artery rings. VOSO4 induced a concentration-dependent contraction of aorta (pD2 = 3.2), which was potentiated by endothelium removal (pD2 = 4.2). After a first exposure to VOSO4, no change in responsiveness was observed even though high vanadium concentrations had accumulated in the aortic tissue (approximately 4 x 10(-3) M). VOSO4 induced, in calcium-free medium, a significant response that, relative to contractions measured in Krebs-Henseleit buffer, was higher (36%) than norepinephrine (16%)-, arginine-vasopressin (8%)- or KCI (5%)-induced responses. 8-(N,N-diethylamino)octyl 3,4,5-trimethoxybenzoate hydrochloride (TMB-8), an intracellular calcium release inhibitor, did not modify VOSO4-induced response either in the presence or in the absence of ambient calcium. On skinned preparations, VOSO4 antagonized Ca++-induced contraction. The tyrosine kinase inhibitors tyrphostin 23 (T23) and tyrphostin 47 (T47) potentiated by 4- and 14-fold, respectively, the activity of VOSO4, in contrast to the lack of effect of T47 on pervanadate-induced contraction. When phosphotyrosine content was revealed by Western blotting, VOSO4 had no effect alone, but in the presence of T47, it dramatically increased the phosphotyrosine content. This result contrasts again with PV-induced tyrosine phosphorylation, which was blocked by T47. These data suggest that the signaling events involved in vascular effects of VOSO4, although they depend little on calcium mobilization, are related to tyrosine phosphorylation, likewise through a pathway different from that of pervanadate.

Animals↗
PubMed1997

Islet amyloid polypeptide in Psammomys obesus (sand rat): effects of nutritionally induced diabetes and recovery on low-energy diet or vanadyl sulfate treatment.

We investigated the possible relationship between islet amyloid polypeptide (IAPP) and the hyperinsulinemia and/or hyperglycemia that is seen in the desert-adapted gerbil Psammomys obesus, when the animal is transferred from a low-energy (LE) diet to a high-energy (HE) diet. The effects of vanadyl sulfate and transition from a HE to a LE diet on the diabetic state of the Psammomys were also studied. Psammomys maintained on a LE diet, showing normoinsulinemia and normoglycemia (group A), were used as controls. IAPP and insulin immunoreactivity in the islets of Langerhans was studied using the peroxidase-antiperoxidase technique and plasma levels of the two hormones were determined by radioimmunoassays. The islet immunoreactivity of both IAPP and insulin was significantly weaker in the hyperinsulinemic and hyperglycemic Psammomys (group C) compared to group A. Transfer to a LE diet resulted in complete recovery of the IAPP- and insulin-staining pattern to that seen in group A [group A--Rec (nutrition)]. The plasma IAPP levels of the group C animals were not significantly higher than in group A, while after vanadyl sulfate treatment the IAPP levels and IAPP/insulin ratios remained significantly higher [group A--Rec (vanadyl)]. At the same time the circulating levels of glucose and insulin were restored to normal. Conclusively, islet IAPP and insulin immunoreactivity disappeared and reappeared in parallel in Psammomys transferred to a HE diet and back to a LE diet. Furthermore, vanadyl sulfate treatment of the hyperinsulinemic and hyperglycemic animals normalized circulating glucose and insulin levels, but not IAPP levels, possibly due to a negative feedback effect of IAPP on insulin release.

Amyloid↗
PubMed1997

Effects of vanadyl sulphate on glucose homeostasis in severe diabetes induced by streptozotocin in rats.

Rats made severely diabetic by an i.v. injection of 50-55 mg/kg streptozotocin (STZ), 15 days later showed blood glucose > 500 mg/dl, quadrupled daily water intake and plasma insulin of 14 +/- 3 microU/ml, about 25 per cent that of normal rats. Subsequently, these rats in two groups, received 0.5-1 mg/ml vanadyl sulphate in base solution (vanadyl) orally (Group I) and base solution containing 50 mEq/1 NaCl (Group II). Since 90 days of vanadyl therapy could not decrease blood glucose of group I (420 +/- 10 mg/dl) to normal levels, euglycaemia was achieved for a period of two months by intraperitoneal (i.p.) injection of NPH insulin. The required daily doses of insulin in vanadyl-treated rats of group I (8 +/- 1 U/kg/day) were only 8 per cent of those in group II animals (103 +/- 7 U/kg/day). In conclusion, it seems that vanadyl per se cannot induce normoglycaemia in diabetic rats with very low plasma insulin levels, but can augment the sensitivity of peripheral tissues to insulin.

Animals↗
PubMed1997

Improvement of impaired glucose tolerance by oral administration of vanadyl sulfate by gavage in streptozotocin-induced diabetic rats.

We examined the effect of oral administration of vanadyl sulfate by gavage on the levels of blood glucose and plasma insulin during oral glucose tolerance test (OGTT) in diabetic rats. Diabetes was induced by intravenous injection of streptozotocin at the dose of 32 mg/kg. Nondiabetic control animals were injected with an equal volume of saline. Vanadyl sulfate at a dose of 25, 50, or 75 mg/kg was given orally by gavage for 2 weeks, starting 12 hours after streptozotocin injection. When vanadyl sulfate was given twice a day, half of the one-day-dosage was given in the morning and the remaining half in the evening. Glucose tolerance test with 5 g/kg of glucose was carried out 2 weeks after administration of vanadyl sulfate. The fasting the blood glucose level in the diabetic rats was higher than that in the non-diabetic rats, whereas the plasma insulin level in the diabetic rats was lower. An increase in blood glucose seen in the glucose tolerance test was significantly greater in the diabetic rats than in the non-diabetic rats. The level of plasma insulin was increased by glucose tolerance test in the non-diabetic rats, while it was not changed in diabetic rats. Oral administration of vanadyl sulfate by gavage significantly improved the impaired glucose tolerance in the the diabetic rats in a dose-dependent manner without any change in plasma insulin level. In conclusion, oral administration of vanadyl sulfate by gavage is effective on impaired glucose tolerance in streptozotocin-induced diabetic rats.

Animals↗
PubMedDate not supplied

Beneficial effects of a vanadium complex with cysteine, administered at low doses on benzo(alpha)pyrene-induced leiomyosarcomas in Wistar rats.

BACKGROUND: Vanadium is a potent environmental and body metal, possessing remarkable antitumor and antidiabetic properties. Vanadium salts and complexes have been widely investigated for their anticarcinogenic properties in experimental carcinogenesis. In the present study the antitumor effects of a new vanadium complex with cysteine in relation to identical doses of vanadyl sulfate and cysteine, in tumor bearing rats are investigated. MATERIALS AND METHODS: Male wistar rats were injected with benzo(alpha)pyrene and divided into four groups of 21 rats each. Control group was treated only with BaP. The first group(TR-1) was treated by vanadyl sulfate per os at daily doses of 0.5 mg of V/kg b.w per day. The second (TR-2) by cysteine at doses of 4.5 mg/kg b.w per day and the third group (TR-3), by the complex V(III)-cysteine at daily doses of V 0.5 mg/kg b.w (containing cysteine at concentrations of 4.5 mg/b.w). Treatment was started when tumors were developed (evidenced from a palbable mass at the site of Bap injection) and went on till death. Toxicological tests were performed in 27 rats divided into a control group and two test groups; T-1 administered with vanadyl sulfate at daily doses of 18.5 mg V/kg b.w and T-2 group with V(III)-cysteine complex at daily doses of 18.5 V/kg b.w, for 9 weeks. Mean survival time, death rate, tumor growth rate, the carcinogenic potency of BaP, and the anticarcinogenic potency in relation to histological findings in each treatment group were calculated in each group in order to evaluate the antitumor effects of the substances used. RESULTS: Vanadyl sulfate, cysteine and V(III)-cysteine exerted antitumor effects on leiomyosarcoma bearing Wistar rats. However, V(III)-complex exerted much more potent effects than the other treatments, significantly prolonging mean survival time, retarding tumor growth rate and decreasing the carcinogenic potency of BaP in the TR-3 group, in comparison to the control and the TR-1 and TR-2 groups. Moreover V(III)-cysteine complex resulted in complete remission of 4 (19.7%) of the tumor bearing rats. Blood, urine, biochemical routine tests as well as autopsy did not reveal any toxic effects either of vanadyl sulafate or V(III)-cysteine complex. CONCLUSIONS: Vanadyl sulfate, cysteine and V(III)-cysteine complex exerted antitumor effects in tumor bearing rats. The V(III)-cysteine complex, however, exerts much more potent effects, as evident from the results of the present study. These beneficial effects of the above complex, in combination with its low toxicity provide evidence suggest its possible application in the treatment of human malignant diseases.

Animals↗
PubMed1996

Vanadium salts as insulin substitutes: mechanisms of action, a scientific and therapeutic tool in diabetes mellitus research.

Vanadium and its compounds exhibit a wide variety of insulin-like effects. In this review, these effects are discussed with respect to the treatment of type I and type II diabetes in animal models, in vitro actions, antineoplastic role, treatment of IDDM and NIDDM patients, toxicity, and the possible mechanism(s) involved. Newly established CytPTK plays a major role in the bioresponses of vanadium. It has a molecular weight of approximately 53 kDa and is active in the presence of Co2+ rather than Mn2+. Among the protein-tyrosine kinase blockers, staurosporine is found to be a potent inhibitor of CytPTK but a poor inhibitor of InsRTK. Vanadium inhibits PTPase activity, and this in turn enhances the activity of protein tyrosine kinases. Our data show that inhibition of PTPase and protein tyrosine kinase activation has a major role in the therapeutic efficacy of vanadium in treating diabetes mellitus.

Animals↗
PubMed2002

Behaviour of vanadate and vanadium-transferrin complex on different anion-exchange columns. Application to in vivo 48V-labelled rat serum.

The behaviour of free [48V]vanadate and [48V]vanadium-transferrin complex was investigated on five different anion-exchange columns (Mono Q 5/5 HR, Hitrap Q HP, Sepharose Q FF, Sepharose DEAE FF and Hitrap Q XL). The recovery of both V-compounds was quantitative. The peak shape and retention time of vanadate varied according to the type of column. The vanadium-transferrin complex also showed different elution patterns depending on the type of column. Especially in case of the Sepharose Q FF, Mono Q 5/5 HR and Hitrap Q XL columns the vanadium-transferrin binding was degraded during elution on the column. The results clearly prove that care should be taken as to the choice of column for speciation purposes of vanadium compounds in order to prevent various artefacts showing up in the chromatograms. A Hitrap Q HP column was used to fractionate different vanadium compounds in rat serum.

Animals↗
PubMed2003

Short-term inhalation of particulate transition metals has little effect on the electrocardiograms of dogs having preexisting cardiac abnormalities.

There is growing epidemiological evidence for statistical associations between increases in air pollution, especially particulate matter, and increases in cardiovascular morbidity and mortality. Laboratory studies have shown that transition metals contribute strongly to the effects of high lung doses of model particles on changes in the electrocardiograms of animals. The present study evaluated the effects of short-term inhalation exposure to respirable particles of specific oxide and sulfate forms of transition metals on heart rate and the electrocardiogram of old dogs having preexisting cardiac abnormalities. Conscious beagle dogs were exposed by oral inhalation for 3 h on each of 3 successive days to aerosols of manganese, nickel, vanadium, iron, and copper oxides, and nickel and vanadium sulfates as single compounds at concentrations of 0.05 mg/m(3). Electrocardiograms were recorded and evaluated for exposure-related changes in heart rate, heart rate variability, and abnormalities of waveforms. Although the electrocardiograms of this population of dogs having potential age and cardiovascular susceptibility factors reflected their underlying clinical abnormalities, no significant effect of exposure to the transition metal aerosols was observed.

Administration, Inhalation↗
PubMed1998

Ferro- and Antiferromagnetic Exchange in Decamethylbimetallocenes.

With the aim of studying next-neighbor magnetic interactions in polymeric metallocenes the paramagnetic decamethylbimetallocenes (M'M') have been chosen as most simple model compounds. They have been synthesized for vanadium, cobalt, and nickel (to yield V'V', Co'Co', and Ni'Ni', respectively) by starting from dilithium and dithallium salts of the fulvalene dianion. The latter have been characterized by (13)C NMR spectroscopy. Decamethylbiferrocene has been synthesized as a diamagnetic standard compound, and decamethylbicobaltocenium hexafluorophosphate, as a precursor to Co'Co'. While the methylated M'M' species were stable when protected from air, the synthesis of the parent binickelocene (Ni'Ni') was accompanied by the formation of the ternickelocene NiNiNi. According to (1)H NMR spectroscopy NiNi and NiNiNi were antiferromagnetic and underwent ligand exchange to nickelocene and bisfulvalenedinickel. Unlike the usually green nickelocenes Ni'Ni' was deep red-violet owing to a new band at 528 nm. Measurements of the magnetic susceptibility (chi(m)) and the magnetization established a rare example of ferromagnetic interaction within a purely organometallic compound for Co'Co'. By contrast, V'V' and Ni'Ni' were antiferromagnetic (J = -1.6 and -180 cm(-)(1), respectively, with H = -JS(A).S(B)). The (1)H and (13)C NMR spectra confirmed the expected structures of Co'Co' and Ni'Ni', while the synthesis of V'V'-d(8) and (2)H NMR spectroscopy were necessary to fully establish the vanadium compound. Temperature-dependent measurements of the (1)H NMR signal shifts and of chi(m) yielded similar J values for Ni'Ni'. MO calculations were carried out for M'M', and the results were converted into theoretical NMR spectra of the bridging fulvalene ligand depending on the spin-carrying MO. This allowed the full assignment of the NMR signals and showed that the spin is delocalized to more than one MO. The MOs were shown to have different magnetic coupling capabilities, and the different magnetic behavior of M'M' was attributed to the near-degeneracy of the magnetic orbitals.

Journal Article↗