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

Abstract

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.

Decavanadate interactions with actin: cysteine oxidation and vanadyl formation

“…Decavanadate solutions were obtained by adjusting the pH of the metavanadate solution to 4.0. 14, 29 The presence of decameric vanadate species was revealed by a characteristic orange color. Decavanadate solutions were always adjusted to pH 7.5 immediately before using.…”

“…The kinetics were followed for 120 min at different temperatures. Since the V 10 dissociation follows a firstorder reaction kinetics, 29 it was possible to determine the activation energy (E a ) for the dissociation.…”

“…As it has been described in previous studies, the 51 V-NMR spectroscopy of meta-and decavanadate solutions allows precise quantification of the amount of each vanadate species in the assays. 14,15, 29 In fact, for the decavanadate concentration used in the NMR studies (5 mM total vanadate), the spectrum obtained ( Fig. 2A) shows the characteristic signals of decameric (V 10A at -516 ppm; V 10B at -502 ppm; V 10C at -424 ppm) and monomeric species (V 1 at -561 ppm), containing approximately 480 mM V 10 and 200 mM V 1 (decameric vanadate is about 2.5-fold more concentrated than monomeric vanadate).…”

Decavanadate induces mitochondrial membrane depolarization and inhibits oxygen consumption

“…Decameric vanadate, composed by fused V(V) octahedra, has an ellipsoid like structure with a major and minor axis of approximately 7 and 6 Å , respectively [1]. 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].…”

DNA cleavage activity of VIVO(acac)2 and derivatives

“…When pH and V concentration are changed from the thermodynamically favourable ones it decomposes with a very slow kinetics [34,47]. Like the monomeric species, decavanadate (V10) does not show any activity in the absence of an activating agent (Fig.…”