Mitochondria as a target for decavanadate toxicity in Sparus aurata heart

摘要: Abstract In a previous in vivo study we have reported that vanadium distribution, antioxidant enzymes activity and lipid peroxidation Sparus aurata heart are strongly dependent on the oligomeric vanadate species being administered. Moreover, it was suggested is accumulated mitochondria, particular when V10 intravenously injected. this work done comparative of effects monomeric (V1) cardiac mitochondria from S. . inhibits mitochondrial oxygen consumption with an IC 50 400 nM, while for V1 23 μM. also induced depolarization at very low concentrations, 196 nM, 55 μM required to induce same effect. Additionally, up 5 μM did inhibit neither F 0 1 -ATPase nor NADH levels not affect respiratory complexes I II, but changes redox steady-state complex III. It concluded induces membrane more than V1, pointing out toxicological target importance take into account contribution toxic effects.