Decavanadate interactions with actin: Inhibition of G-actin polymerization and stabilization of decameric vanadate

Ramos, Susana; Manuel, Miguel; Tiago, Teresa; Duarte, Ricardo; Martins, Jorge; Gutiérrez‐Merino, Carlos; Moura, José J. G.; Aureliano, Manuel

doi:10.1016/j.jinorgbio.2006.06.007

Cited by 72 publications

(112 citation statements)

References 38 publications

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“…3A), as described recently [22]. In fact, the concentrations of each vanadate oligomer calculated by integration of the respective areas of the NMR spectra, as a function of total vanadate, exhibit different profiles according to the species.…”

Section: Characterization Of Vanadate Solutionsmentioning

confidence: 87%

“…It has been suggested that V10 decomposition is slow enough to allow studying its effects in biochemical systems [16,17], not only in vitro but also in vivo [16][17][18][19][20][21]. More recently, it was described that V10 can be stabilized upon interaction with cytoskeleton and membrane proteins [22]. Therefore, we cannot exclude the hypothesis that V10 may also occur at physiological conditions for long enough to induce different biological effects in comparison to metavanadate.…”

Section: Introductionmentioning

confidence: 87%

“…This complex oxoanion remains relatively stable at room temperature, allowing studying its effects not only in vitro but also in vivo. Moreover, it was recently described that decameric vanadate stabilization by cytoskeletal and transmembrane proteins can account, at least in part, for decavanadate effects in biological systems [22]. [Decavanadate] total (mM total vanadium) Fig.…”

Section: Characterization Of Vanadate Solutionsmentioning

confidence: 99%

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Vanadium distribution, lipid peroxidation and oxidative stress markers upon decavanadate in vivo administration

Soares

Martins

Duarte

et al. 2007

Journal of Inorganic Biochemistry

110

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The contribution of decameric vanadate species to vanadate toxic effects in cardiac muscle was studied following an intravenous administration of a decavanadate solution (1 mM total vanadium) in Sparus aurata. Although decameric vanadate is unstable in the assay medium, it decomposes with a half-life time of 16 allowing studying its effects not only in vitro but also in vivo. After 1, 6 and 12 h upon decavanadate administration the increase of vanadium in blood plasma, red blood cells and in cardiac mitochondria and cytosol is not affected in comparison to the administration of a metavanadate solution containing labile oxovanadates. Cardiac tissue lipid peroxidation increases up to 20%, 1, 6 and 12 h after metavanadate administration, whilst for decavanadate no effects were observed except 1 h after treatment (+20%). Metavanadate administration clearly differs from decavanadate by enhancing, 12 h after exposure, mitochondrial superoxide dismutase (SOD) activity (+115%) and not affecting catalase (CAT) activity whereas decavanadate increases SOD activity by 20% and decreases (À55%) mitochondrial CAT activity. At early times of exposure, 1 and 6 h, the only effect observed upon decavanadate administration was the increase by 20% of SOD activity. In conclusion, decavanadate has a different response pattern of lipid peroxidation and oxidative stress markers, in spite of the same vanadium distribution in cardiac cells observed after decavanadate and metavanadate administration. It is suggested that once formed decameric vanadate species has a different reactivity than vanadate, thus, pointing out that the differential contribution of vanadium oligomers should be taken into account to rationalize in vivo vanadate toxicity.

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Section: Characterization Of Vanadate Solutionsmentioning

confidence: 87%

Section: Introductionmentioning

confidence: 87%

Section: Characterization Of Vanadate Solutionsmentioning

confidence: 99%

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Vanadium distribution, lipid peroxidation and oxidative stress markers upon decavanadate in vivo administration

Soares

Martins

Duarte

et al. 2007

Journal of Inorganic Biochemistry

110

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“…[4][5][6] In addition, V 10 sition may be prevented through binding to specific proteins, which apparently retard dissociation. Increases in the half-life from 5 to 17 hours in the presence of sarcoplasmic reticulum vesicles, and to 27 hours in the presence of actin were found at room temperature and pH 7.0, 25 whereas no effects were observed with myosin, even though it is known to have a highaffinity V 10 -binding site. 26 Decavanadate was observed to induce protein cysteine oxidation and vanadyl formation in the presence of SR Ca 2+ -ATPase and actin, whereas no effects were observed on incubation with monomeric vanadate.…”

Section: Introductionmentioning

confidence: 88%

Characterization of decavanadate and decaniobate solutions by Raman spectroscopy

et al. 2016

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The decaniobate ion, (Nb 10 = [Nb 10 O 28 ] 6− ) being isoelectronic and isostructural with the decavanadate ion (V 10 = [V 10 O 28 ] 6− ), but chemically and electrochemically more inert, has been useful in advancing the understanding of V 10 toxicology and pharmacological activities. In the present study, the solution chemistry of Nb 10 and V 10 between pH 4 and 12 is studied by Raman spectroscopy. The Raman spectra of V 10show that this vanadate species dominates up to pH 6.45 whereas it remains detectable until pH 8.59, which is an important range for biochemistry. Similarly, Nb 10 is present between pH 5.49 and 9.90 and this species remains detectable in solution up to pH 10.80. V 10 dissociates at most pH values into smaller tetrahedral vanadate oligomers such as V 1 and V 2 , whereas Nb 10 dissociates into Nb 6 under mildly (10 > pH > 7.6) or highly alkaline conditions. Solutions of V 10 and Nb 10 are both kinetically stable under basic pH conditions for at least two weeks and at moderate temperature. The Raman method provides a means of establishing speciation in the difficult niobate system and these findings have important consequences for toxicology activities and pharmacological applications of vanadate and niobate polyoxometalates.

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“…In previous studies [2][3][4][5][6][7][8], we have demonstrated that once formed in aqueous solutions decameric vanadate decomposition is slow enough to allow studying differential effects between decameric and monomeric vanadate not only in vitro but also in vivo. Furthermore, decameric vanadate is stabilized upon interaction with cytoskeleton and membrane proteins, while it affects calcium translocation by the sarcoplasmic reticulum calcium pump and it prevents actin polymerization [9].…”

Section: Introductionmentioning

confidence: 99%

Decavanadate induces mitochondrial membrane depolarization and inhibits oxygen consumption

Soares¹,

Gutiérrez‐Merino²,

Aureliano³

2007

Journal of Inorganic Biochemistry

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Decavanadate induced rat liver mitochondrial depolarization at very low concentrations, half-depolarization with 39 nM decavanadate, while it was needed a 130-fold higher concentration of monomeric vanadate (5 lM) to induce the same effect. Decavanadate also inhibits mitochondrial repolarization induced by reduced glutathione in vitro, with an inhibition constant of 1 lM, whereas no effect was observed up to 100 lM of monomeric vanadate. The oxygen consumption by mitochondria is also inhibited by lower decavanadate than monomeric vanadate concentrations, i.e. 50% inhibition is attained with 99 nM decavanadate and 10 lM monomeric vanadate. Thus, decavanadate is stronger as mitochondrial depolarization agent than as inhibitor of mitochondrial oxygen consumption. Up to 5 lM, decavanadate does not alter mitochondrial NADH levels nor inhibit neither F O F 1 -ATPase nor cytochrome c oxidase activity, but it induces changes in the redox steady-state of mitochondrial b-type cytochromes (complex III). NMR spectra showed that decameric vanadate is the predominant vanadate species in decavanadate solutions. It is concluded that decavanadate is much more potent mitochondrial depolarization agent and a more potent inhibitor of mitochondrial oxygen consumption than monomeric vanadate, pointing out the importance to take into account the contribution of higher oligomeric species of vanadium for the biological effects of vanadate solutions.

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Decavanadate interactions with actin: Inhibition of G-actin polymerization and stabilization of decameric vanadate

Cited by 72 publications

References 38 publications

Vanadium distribution, lipid peroxidation and oxidative stress markers upon decavanadate in vivo administration

Vanadium distribution, lipid peroxidation and oxidative stress markers upon decavanadate in vivo administration

Characterization of decavanadate and decaniobate solutions by Raman spectroscopy

Decavanadate induces mitochondrial membrane depolarization and inhibits oxygen consumption

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