Multiple reactions in vanadyl-V(IV) oxidation by H2O2

Abstract

Oxidation of vanadyl sulfate by H2O2 involves multiple reactions at neutral pH conditions. The primary reaction was found to be oxidation of V(IV) to V(V) using 0.5 equivalent of H2O2, based on the loss of blue color and the visible spectrum. The loss of V(IV) and formation V(V) compounds were confirmed by ESR and 51V-NMR spectra, respectively. In the presence of excess H2O2 (more than two equivalents), the V(V) was converted into diperoxovanadate, the major end-product of these reactions, identified by changes in absorbance in ultraviolet region and by the specific chemical shift in NMR spectrum. The stoichiometric studies on the H2O2 consumed in this reaction support the occurrence of reactions of two-electron oxidation followed by complexing two molecules of H2O2. Addition of a variety of compounds--Tris, ethanol, mannitol, benzoate, formate (hydroxyl radical quenching), histidine, imidazole (singlet oxygen-consumption that also used V(IV) as the reducing source. This reaction requires concomitant oxidation of vanadyl by H2O2, favoured at low H2O2:V(IV) ratio. Another secondary reaction of oxygen release was found to occur during vanadyl oxidation by H2O2 in acidic medium in which the end-product was not diperoxovanadate but appears to be a mixture of VO3+ (-546 ppm), VO3+ (-531 ppm) and VO2+ (-512 ppm), as shown by the 51V-NMR spectrum. This reaction also occurred in phosphate-buffered medium but only on second addition of vanadyl. The compounds that stimulated the oxygen-consumption reaction were found to inhibit the oxygen-release reaction. A combination of these reactions occur depending on the proportion of the reactants (vanadyl and H2O2), the pH of the medium and the presence of some compounds that affect the secondary reactions.

Reactive Oxygen Species Signaling through Regulation of Protein Tyrosine Phosphorylation in Endothelial Cells

“…Vanadate, a known inhibitor of phosphatases, also interacts with H202 to generate peroxovanadium compounds (11,12). A major product generated by mixing equimolar amounts of H202 and vanadate under neutral pH condition was identified as DPV (18). Our data also indicate that ROS-induced stimulation of PLA2 and PLD was attenuated by genistein, an inhibitor of tyrosine kinases.…”

“…Antiphosphotyrosine antibody (4G10) and EC growth factor were procured from Upstate Biotechnology Inc. (Lake Placid, NY). Diperoxovanadate (potassium salt), a gift from T. Ramasarma (Indian Institute of Science, India), was prepared by bubbling SO2 gas through a solution of triperoxovanadate and characterized as described earlier (18). Enhanced chemiluminescence (ECL) kit for the detection of tyrosine phosphorylated proteins was from Amersham (Arlington Heights, IL).…”

Role of p38 MAP kinase in diperoxovanadate-induced phospholipase D activation in endothelial cells

“…DPV (potassium salt), crystallized and characterized by NMR as described earlier (48), was kindly provided by Dr. T. Ramasarma from the Department of Biochemistry, Indian Institute of Science (Bangalore, India).…”

Lactobacilli and Vaginal Host Defense: Activation of the Human Immunodeficiency Virus Type 1 Long Terminal Repeat, Cytokine Production, and NF‐κB

“…The HIV-1 LTR contains promoter and enhancer sequences required for the initiation of gene transcription and viral replication, and H 2 O 2 is believed to promote gene transcription, at least in part, by activation of the transcription factor NF-kB, which binds to sites in the LTR [14]. Vanadate reacts with H 2 O 2 to form peroxides of vanadate (pervanadate, peroxovanadate) [16,17], which have effects on a number of biologic systems that are considerably greater than the additive effect of H 2 O 2 and vanadate alone. We have described the synergistic effect of H 2 O 2 and vanadate on the activation of the HIV-1 LTR in Jurkat T and THP-1 cells and on the production of intact virions by U-1 cells [15].…”