Effects Of Sodium Vanadate Research Articles

Effect of sodium vanadate on corrosion of AD31 aluminum alloy in acid media

Scanning electron microscopy, potentiodynamic polarization method, and electrochemical impedance spectroscopy were used to study the corrosion behavior of AD31 (AA6063) aluminum alloy in acid (pH 3) 0.05 M NaCl solutions containing 3 mmol dm–3 of NaVO3 inhibitor. It was found that the corrosion of AD31 alloy in acid sodium chloride solutions predominantly occurs locally at aluminum/intermetallic particle phase boundaries and is limited by the electrochemical stage of charge transfer. It was shown that introduction of sodium vanadate can reduce the rate of selective dissolution of magnesium from the alloy and provides a protective effect on the level of 7–10%.

Effects of Chronic Introduction of Antidepressants on NMDA-Induced Damage to Neurons of the Rat Hippocampus and Cerebral Cortex

In in vitro studies on superfused slices obtained from the rat hippocampus and cortex, we found that 50 μM N-methyl-D-aspartate (NMDA) applied to the slices in the presence of 10 μM glycine for 15 min exerts a significant damaging action to neurons of these structures. One hour after termination of the action of NMDA, this was manifested in more than a twofold decrease in the synaptic reactivity of pyramidal neurons of the hippocampal СА1 area and layers II/III of the cerebral cortex. The excitotoxic effect of NMDA was prevented by application of competitive (D-2-amino-5-phosphonovaleric acid, 50 μM) and noncompetitive (ketamine, 100 μM) blockers of NMDA receptors. A blocker of glycine-binding sites of NMDA receptors (compound ТСВ 24.15, 10 μM) weakened NMDA-induced damage to the neurons. A competitive blocker of glutamate АМРА receptors, 6,7-dinitroquinoxaline-2,3-dione (DNQX, 10 μM), and a local anesthetic, lidocaine hydrochloride (50 μM), did not modify the excitotoxic effect of NMDA. A blocker of voltagedependent L-type calcium channels, verapamil (20 μM), demonstrated some trend to intensification of NMDA excitotoxic action. An inhibitor of tyrosine-protein phosphatases, sodium vanadate, when i.p. injected into rats in a dose of 15 mg/kg 6 h prior to the electrophysiological experiment, decreased the damaging action of NMDA. Two-hour-long treatment of cerebral slices with 1 μM genistein, an inhibitor of tyrosine kinases, weakened the neuroprotective effect of sodium vanadate. Chronic injections (14 days in daily doses of 20 mg/kg) of antidepressants belonging to different functional classes (imipramine, fluoxetine, and pyrazidol) into rats decreased (similarly to blockers of NMDA receptors) the excitotoxic action of NMDA receptors. Neuroprotective effects of antidepressants were weakened upon the action of genistein. We conclude that the neuroprotective activity of antidepressants under conditions of excitotoxic action of NMDA is mainly determined by an increase in the activity of tyrosine kinases in the cytoplasm and/or neuronal nucleus.

Tyrosine Phosphorylation of the Integrin β3 Subunit Regulates β3 Cleavage by Calpain.

Outside-in signaling of β3 integrins induces and requires phosphorylation at tyrosine-747 (Y747) and tyrosine-759 (Y759) of the β3 subunit, but the mechanism for this requirement is unclear. On the other hand, a key consequence of integrin signaling, cell spreading, is inhibited by calpain cleavage of β3 cytoplasmic domain. Here we show that tyrosine phosphorylation in the synthetic β3 cytoplasmic domain peptide inhibits calpain cleavage. In platelets, tyrosine phosphates inhibitor, sodium vanadate, enhances thrombin-induced phosphorylation at Y747 and Y759, which is associated with the reduced integrin cleavage by calpain. The effects of sodium vanadate is unlikely to be caused by its effects on calpain activity but is likely to be caused by the susceptibility of integrin cytoplasmic domain, because sodium vanadate did not affect the calpain cleavage of another substrate, fodrin, in platelets. To further support the protective effect of tyrosine phosphorylation against calpain cleavage, we show that mouse β3 (DiYF) with both Y759 and Y747 mutated to phenylalanine is more susceptible to calpain cleavage than wild type during thrombin-induced platelet aggregation. Furthermore, phosphorylation at Y747 and Y759 of β3 in the focal adhesion sites and the leading edge of spreading platelets was differentially regulated. Selective dephosphorylation of Y759 is associated with calpain cleavage at Y759. Thus, one mechanism by which tyrosine phosphorylation promotes integrin signaling and cell spreading is its inhibition of calpain cleavage of the β3 cytoplasmic domain.

The Grb2/Mek Pathway Represses Nanog in Murine Embryonic Stem Cells

The homeobox gene Nanog is a key intrinsic determinant of self renewal in embryonic stem (ES) cells, and its repression leads ES cells to selectively differentiate into primitive endoderm. Although Nanog repression occurs at the outermost layer of ES cell aggregates independent of the leukemia inhibitory factor (LIF)/STAT3 pathway, it is largely undetermined what external cues and intracellular signals cause the event. Of interest, addition of the tyrosine phosphatase inhibitor, sodium vanadate, selectively repressed Nanog transcription without any detectable changes in upstream transcriptional regulators Oct3/4 and Sox2. Furthermore, sodium vanadate induced primitive endoderm differentiation, even in the inner cells of ES cell aggregates. Expression of Gata6 and Zfp42, two putative downstream Nanog effectors, was also increased and decreased by the addition of sodium vanadate, respectively, but these changes were eliminated by exogenous Nanog expression. The effects of sodium vanadate were abrogated by Grb2 deficiency or by the addition of the Mek inhibitor, PD98059. Indeed, PD98059 prevented Nanog repression induced by ES cell aggregation as well. Furthermore, transfection of a constitutive active Mek mutant into ES cells induced Nanog repression and primitive endoderm differentiation. These data indicate that the Grb2/Mek pathway primarily mediates Nanog gene repression upon ES cell differentiation into primitive endoderm.

Effects of sodium vanadate on contractility of vascular smooth muscle

Effects of sodium vanadate on contractility of vascular smooth muscle

Protein tyrosine phosphorylation and regulation of the receptor for platelet-activating factor in rat Kupffer cells. Effect of sodium vanadate.

Platelet-activating factor (1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine, AGEPC) and sodium vanadate (a phosphotyrosine phosphatase inhibitor) induced a time- and concentration-dependent increase in phosphotyrosine in several proteins and stimulated prostaglandin (PG) E2 production in cultured rat Kupffer cells. In addition, vanadate induced a decrease in the surface expression of AGEPC receptors and, as a consequence, inhibited AGEPC-stimulated PGE2 production. The vanadate-induced decrease in the surface expression of AGEPC receptors was time- and concentration-dependent and was partially prevented by genistein, a putative tyrosine kinase inhibitor. Upon removal of vanadate from the culture medium and re-incubation of cells in vanadate-free medium, the surface AGEPC receptors were restored within 7 h after the removal of vanadate. Both AGEPC- and vanadate-stimulated PGE2 formation was attenuated by genistein. Thus the present investigation demonstrates that both AGEPC and sodium vanadate stimulate tyrosine phosphorylation of cellular proteins, and vanadate induces a decrease in the number of the surface AGEPC receptors. These results suggest that protein tyrosine phosphorylation may play a role, directly or indirectly, in the regulation of surface expression of AGEPC receptors as well as in PGE2 production in response to vanadate and AGEPC.

Potentiation of twitch contraction in guinea pig ureter by sodium vanadate

The effect of sodium vanadate on action potential and twitch contraction of guinea pig ureter was studied and compared with that of ouabain, elevated K+, low temperature, and a Ca agonist (BAY K 8644), which can be expected to exert certain comparative effects. Sodium vanadate markedly potentiated twitch contraction. Potentiation by vanadate was associated with marked prolongation of relaxation time. Sodium vanadate caused only slight depolarization of the membrane but marked changes in action potential. The duration of action potential was prolonged and the number of oscillatory spike potentials increased. These effects were different from those of other treatments. It is concluded that prolongation of action potential and the increase in the number of spikes are the main cause of potentiation of twitch contraction by sodium vanadate. In addition, inhibition of Ca pump activity of the smooth muscle membrane system by vanadate might also be involved in potentiation of twitch contraction.

The relaxation and Ca-pump inhibition in mesenteric artery of normotensive and stroke-prone spontaneously hypertensive rats

The influences of low temperature and vanadate, both of which have been known to inhibit the Ca-pump activity of membranous systems of smooth muscle cells, on the relaxation of mesenteric artery of stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar-Kyoto rats (WKY) were studied. Relaxation was induced by the removal of extracellular Ca in high-K-depolarized preparations, so that the involvement of receptor kinetics and changes in membrane potential could be excluded. Relaxation was significantly slower in the preparation from SHRSP than in that from SHRSP. Low temperature prolonged relaxation in preparations from both SHRSP and WKY. No difference in the effect of low temperature was observed between the preparations, which showed Q 10 values between 2.8 and 3.5 for 50 and 80% relaxation time. Sodium vanadate also prolonged the time course of relaxation in both preparations. No difference in the effect of sodium vanadate was observed between the preparations from WKY and SHRSP. These results suggest that Ca-pump activity is involved in the relaxation of K-depolarized smooth muscle of mesenteric arteries from both WKY and SHRSP. However, the difference in the pump activity may not contribute greatly to the difference in the relaxation of K-depolarized preparations by the removal of extracellular Ca.

Effects of sodium vanadate on the smooth muscle of the rat portal vein.

The effects of vanadate on the mechanical and electrical activity of the rat portal vein were examined. Vanadate increased the height of the spontaneous contractions of the portal vein without affecting basal tension. This effect was not blocked by alpha-blockers or atropine. Vanadate did not exert any effect when the spontaneous contractions were abolished by high concentrations of verapamil or in the absence of Ca. Vanadate did not change the resting membrane potential of the smooth muscle cells of the vein, but it increased the rate of rise and the amplitude of the action potentials and the number of action potentials per burst. The intracellular Na content was increased slightly by vanadate. However, the effects of Na,K-pump inhibition by ouabain or K-removal were quite different from those of vanadate, and these procedures did not block the effect of vanadate, although they attenuated it. Vanadate also potentiated the K-contracture of the portal vein. These results indicate that vanadate increases the amplitude of the spontaneous contractions through an increase in the number of action potentials per burst which underly the contraction. These effects are not mediated by intrinsic nerve excitation or inhibition of Na,K pump activity. The facilitation of Ca entry through the voltage dependent Ca channel may be the main cause of the effect of vanadate on mechanical activity.

Effects of sodium vanadate on smooth muscles of guinea-pig ureter and their relation to extracellular Ca.

The effects of sodium vanadate on electrical and mechanical activities of the guinea-pig ureter were studied. Sodium vanadate at concentrations higher than 10(-5) M induced elevations of basal tension and repetitive twitch-like contractions. The drug depolarized membrane only slightly but induced repetitive action potentials. Sodium vanadate potentiated phasic and tonic contractions of K-contracture. It also increased tension development of high amplitude in K-depolarized preparations. Thus, the change in the resting membrane potential does not seem to play the only role in the initiation of contractions, though sodium vanadate-induced twitch-like contractions were associated by repetitive action potentials. Sodium vanadate-induced twitch-like contractions were blocked by Ca removal or by verapamil, but elevated basal tension was depressed only slightly under these treatments. Sodium vanadate induced tension development in the absence of Ca both in polarized and K-depolarized preparations. These results suggest that sodium vanadate increased mechanical activities by enhancing Ca influx as well as releasing intracellular bound Ca and/or inhibiting Ca extrusion through cell membrane.

Effect of sodium vanadate on deoxyribonucleic acid and protein syntheses in cultured rat calvariae.

Sodium vanadate, an agent known to have multiple cellular actions, was studied for its effects on aspects of bone formation in cultures of 21-day-old fetal rat calvariae. Vanadate (0.1-10 microM) stimulated the incorporation of [3H] thymidine into acid-insoluble residues (DNA); the effect appeared after 3 h and was sustained for 96 h. Vanadate increased the bone DNA content and mitotic index. Treatment with vanadate at 10 microM for 24 h or at 0.3-1 microM for 96 h increased the incorporation of [3H]proline into collagenase-digestible protein (CDP), but the effect was not specific for collagen; vanadate also increased the labeling of noncollagen protein (NCP). Vanadate increased the incorporation of [3H]proline into type I collagen without affecting other collagen types. Vanadate (100 microM) caused a marked and irreversible inhibitory effect on the labeling of DNA, CDP, and NCP. Treatment with vanadate at multiple doses for 3-96 h did not stimulate alkaline phosphatase activity, but this enzyme was inhibited in bones exposed to 1 mM vanadate for 24 h or 10 microM vanadate for 96 h. The stimulatory effect on DNA labeling was primarily observed in the periosteum, while that on CDP labeling was seen only in the periosteum-free bone. These studies indicate that sodium vanadate stimulates bone DNA, collagen, and NCP syntheses in vitro, although high doses of vanadate have an irreversible inhibitory effect.

Effects of sodium vanadate on the smooth muscle of the guinea-pig vas deferens.

Effects of sodium vanadate on electrical and mechanical activities of smooth muscle of the guinea-pig vas deferens were investigated. Sodium vanadate of concentrations higher than 5 X 10(-6) M caused an elevation of basal tension and, at concentrations higher than 5 X 10(-4) M, initiated spontaneous contractions. These effects were not blocked by treatments with reserpine, tetrodotoxin or phentolamine. Treatment with ouabain also did not block the tension development by sodium vanadate. Sodium vanadate caused slight depolarization of membrane and potentiated spike activities. The phasic contraction of potassium contracture was potentiated by sodium vanadate in a similar manner to pretreatment with 15 mM K+ or with ouabain, both treatments occasioning slight depolarization. Sodium vanadate also caused tension development in K-depolarized preparetions. Contrastingly, drug-induced contractions were not significantly affected by sodium vanadate. It is suggested that sodium vanadate acts directly on smooth muscles and causes tension development without relation to Na, K-ATPase activity. Changes in the membrane electrical activities may be part of the cause of contraction. However, it can also initiate tension development without membrane potential changes, presumably acting on intracellular Ca binding sites.

Contraction independent of extracellular Ca by sodium vanadate in guinea-pig vas deferens.

The effects of Ca removal and Ca antagonists on sodium vanadate-induced contractions of the guinea-pig vas deferens were studied. Sodium vanadate-induced tension development could be observed even 120 minutes after the removal of Ca, whereas K-contracture disappeared within 20 minutes. Spontaneous contractions induced by sodium vanadate were abolished by the removal of Ca. Verapamil and nifedipine did not show any effect on sodium vanadate-induced contraction, contrastingly, they blocked spontaneous contractions initiated by sodium vanadate. The effects of sodium vanadate on Ca contracture of depolarized preparations were also studied. Though the drug potentiated phasic contraction, it did not potentiate tonic component of Ca contracture. It was demonstrated that sodium vanadate induced tension development independently of extracellular Ca, presumably by releasing intracellularly bound Ca.

Effects of Sodium Vanadate and Ferric Chloride on Rat Liver Mitochondrial Peroxidation

Effects of Sodium Vanadate and Ferric Chloride on Rat Liver Mitochondrial Peroxidation