Oxidation of NADH by vanadium: Kinetics, effects of ligands and role of H2O2 or O2

Stankiewicz, Paul J.; Stern, Arnold; Davison, Allan J.

doi:10.1016/0003-9861(91)90381-r

Cited by 25 publications

(6 citation statements)

References 42 publications

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“…Our analysis of 2.5 mM peroxovanadate in either OR2 or nRP showed the five vanadium species reported by Stankiewicz et al (1991): V1 (16%), V, (4%), V4 (4%), monoperoxovanadate (8%), and diperoxovanadate (68%). For present purposes, NMR analysis of peroxovanadate solutions presents some difficulties.…”

Section: V Nmr Analysissupporting

confidence: 56%

“…Addition of H,Oz to vanadate solutions results in the formation of mono and diperoxovanadates (Stankiewicz et al, 1991;Posner et al, 1994; present study). The enhanced biological activity of PV solutions cannot be due to the presence of H,O,, since this compound is at best a weak insulin mimetic, active at concentrations of -0.5 mM (Barnes et al, unpub.…”

Section: Xenopus Oocytes As Vanadateipv-sensitive Cellssupporting

confidence: 50%

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Multiple sites of vanadate and peroxovanadate action in Xenopus oocytes

Barnes

Sykes

Shechter

et al. 1995

Journal Cellular Physiology

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In Xenopus laevis oocytes, the insulin mimics, vanadate and peroxovanadates (PV), stimulated the uptake of 3H-2-deoxyglucose and incorporation of 35S-methionine into protein. For both hexose transport and protein synthesis, peroxovanadates (produced by reacting vanadate and H2O2) were at least as potent as vanadate. Microinjection of peroxovanadates into the oocytes stimulated 2-deoxyglucose uptake. However, methionine incorporation was not stimulated by microinjection of peroxovanadate or vanadate solutions. Consistent with these results and with the possibility that vanadate and peroxovanadates enter the cell on a phosphate transporter, raising the medium phosphate concentration from 1 mM to 10 mM blocked vanadate-stimulated hexose transport and partially reduced peroxovanadates stimulation of hexose transport. Increased medium phosphate did not reduce stimulation of protein synthesis by either effector. Taken together, these data indicate that vanadate/peroxovanadates act at both intracellular and extracellular sites. Action at the former stimulates hexose uptake and action at the latter, protein synthesis.

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Section: V Nmr Analysissupporting

confidence: 56%

Section: Xenopus Oocytes As Vanadateipv-sensitive Cellssupporting

confidence: 50%

Multiple sites of vanadate and peroxovanadate action in Xenopus oocytes

Barnes

Sykes

Shechter

et al. 1995

Journal Cellular Physiology

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“…This is supported by the observation that NADH is oxidized, albeit at a slower rate, even in the absence of another reductant for vanadate. The chemical reactions by which aluminum augments the reduction of vanadate are not obvious, but several possibilities can be considered [23], At equilibrium, the chemical species of aluminum in aqueous solution at pH 7.4 include the follow ing: …”

Section: ]mentioning

confidence: 99%

The Effect of Aluminum on the Vanadium-Mediated Oxidation of NADH

Adler

Caruso²,

Berlyne³

1995

Nephron

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Aluminum catalyzes the oxidation of NADH by vanadate both in the presence and absence of a reducing sugar. The effect of aluminum is concentration dependent and inhibitable with superoxide dismutase but not catalase. The fructose-6-phosphate-free reaction is characterized by an initial lag phase which can be eliminated by preincubating aluminum with NADH, but is not altered by preincubating aluminum with vanadate, suggesting that the effect of aluminum is not directly on vanadate. Aluminum also catalyzes vanadyl-mediated oxidation of NADH, and this effect is similarly inhibitable by superoxide dismutase as well as catalase. It is suggested that aluminum catalyzes the oxidation of NADH by vanadium though enhancing the production of superoxide radicals and that this effect may account in part of the biological toxicity associated with aluminum, particularly when associated with the accumulation of other trace elements such as vanadium..

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“…Lastly, because V III easily complexes sulfate (Meier et al, 1992), it is possible V III enters cells in a manner akin to iron polysulfates. While the exact description of how V III enters cells is still lacking, once inside, V III could react with O 2 to be oxidized to V IV (Stern et al, 1992); under very rare circumstances, V III complexes (i.e., with superoxide [Stankiewicz et al, 1991]) acts as an oxidant, though the metal is not reduced to V II .…”

Section: Introductionmentioning

confidence: 99%

Pulmonary Immunotoxic Potentials of Metals Are Governed by Select Physicochemical Properties: Vanadium Agents

Cohen

Sisco

Prophete

et al. 2007

Journal of Immunotoxicology

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The in situ reactions of metal ions/complexes are important in understanding the mechanisms by which environmental and occupational metal particles alter lung immune responses. A better understanding of these reactions in situ will also allow for the improved specificity and controlled toxicity of novel metallocompounds to be used as inhaled diagnostics or therapeutics. Our previous work showed that inhalation of metals (e.g., chromium, vanadium, nickel) caused altered lung immune cell function and host resistance. The data also suggested that the degree of immunomodulation induced depended not only on the amount of metal deposited, but also the compound used. If specificity governs pulmonary immunomodulatory potential, it follows that physicochemical properties inherent to the metal have a role in the elicited effects. We hypothe-size that major determinants of any metal compound's potential are its redox behavior, valency (generally referred to as oxidation state and considered speciation in chemical literature), and/or solubility. In accord with the extensive work carried out with vanadium (chemical symbol V) compounds showing the importance of form used, differences in potential for a range of V agents (pentavalent [V(V)] insoluble vanadium pentoxide and soluble sodium metavanadate, tetravalent [V(IV)] vanadyl dipicolinate, and trivalent [V(III)] bis(dipicolinato)vanadium) were quantified based on induced changes in local bacterial resistance after host inhalation of each agent at 100 mu g V/m(3) (5 hr/d for 5 d). Differences in effect between V(V) forms indicated that solubility was a critical property in in situ pulmonary immunotoxicity. Among the soluble forms, oxidizing vanadate had the greatest impact on resistance; reducing V(III) altered resistance to a lesser extent. Both the V(IV) and insoluble V(V) had no effect. When data was analyzed in the context of pre-infection lung V burdens, soluble V agents with different oxidation states induced varying responses, supporting the hypothesis that differences in immunomodulatory potential might be attributed to redox behavior or valency. Our findings both provide a basis for understanding why some metals could be a greater health risk than others (when encountered in equal amounts) and will assist in the design of inhalable metallopharmaceuticals by allowing researchers to preempt selection of certain metal ions or complexes for use in such products.

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Oxidation of NADH by vanadium: Kinetics, effects of ligands and role of H2O2 or O2

Cited by 25 publications

References 42 publications

Multiple sites of vanadate and peroxovanadate action in Xenopus oocytes

Multiple sites of vanadate and peroxovanadate action in Xenopus oocytes

The Effect of Aluminum on the Vanadium-Mediated Oxidation of NADH

Pulmonary Immunotoxic Potentials of Metals Are Governed by Select Physicochemical Properties: Vanadium Agents

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