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- Vanadium distribution, lipid peroxidation and oxidative stress markers upon decavanadate in vivo administrationPublication . S. Soares, Sandra; Martins, H.; Duarte, Rui O.; Moura, JosƩ J. G.; Coucelo, Josefina; GutiƩrrez-Merino, Carlos; Aureliano, M.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 ( 55%) 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.
- Mitochondria as a target for decavanadate toxicity in Sparus aurata heartPublication . S. Soares, Sandra; GutiƩrrez-Merino, Carlos; Aureliano, M.In a previous in vivo study we have reported that vanadium distribution, antioxidant enzymes activity and lipid peroxidation in Sparus aurata heart are strongly dependent on the oligomeric vanadate species being administered. Moreover, it was suggested that vanadium is accumulated in mitochondria, in particular when V10 was intravenously injected. In this work we have done a comparative study of the effects of V10 and monomeric vanadate (V1) on cardiac mitochondria from S. aurata. V10 inhibits mitochondrial oxygen consumption with an IC50 of 400 nM, while the IC50 for V1 is 23 M. V10 also induced mitochondrial depolarization at very low concentrations, with an IC50 of 196 nM, and 55 Mof V1was required to induce the same effect. Additionally, up to 5 M V10 did inhibit neither F0F1-ATPase activity nor NADH levels and it did not affect respiratory complexes I and II, but it induced changes in the redox steady-state of complex III. It is concluded that V10 inhibits mitochondrial oxygen consumption and induces membrane depolarization more strongly than V1, pointing out that mitochondria is a toxicological target for V10 and the importance to take into account the contribution of V10 to the vanadate toxic effects.