Decavanadate Toxicology and Pharmacological Activities: V(10) or V(1), Both or None?

This review covers recent advances in the understanding of decavanadate toxicology and pharmacological applications. Toxicological in vivo studies point out that V(10) induces several changes in several oxidative stress parameters, different from the ones observed for vanadate (V(1)). In in vitro studies with mitochondria, a particularly potent V(10) effect, in comparison with V(1), was observed in the mitochondrial depolarization (IC(50) = 40 nM) and oxygen consumption (99 nM). It is suggested that mitochondrial membrane depolarization is a key event in decavanadate induction of necrotic cardiomyocytes death. Furthermore, only decavanadate species and not V(1) potently inhibited myosin ATPase activity stimulated by actin (IC(50) = 0.75 μM) whereas exhibiting lower inhibition activities for Ca(2+)-ATPase activity (15 μM) and actin polymerization (17 μM). Because both calcium pump and actin decavanadate interactions lead to its stabilization, it is likely that V(10) interacts at specific locations with these proteins that protect against hydrolysis but, on the other hand, it may induce V(10) reduction to oxidovanadium(IV). Putting it all together, it is suggested that the pharmacological applications of V(10) species and compounds whose mechanism of action is still to be clarified might involve besides V(10) and V(1) also vanadium(IV) species.