Mitochondria as a target for decavanadate toxicity in Sparus aurata heart.

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 IC(50) of 400 nM, while the IC(50) for V1 is 23 microM. V10 also induced mitochondrial depolarization at very low concentrations, with an IC(50) of 196 nM, and 55 microM of V1 was required to induce the same effect. Additionally, up to 5 microM V10 did inhibit neither F(0)F(1)-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.