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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  μ M) whereas exhibiting lower inhibition activities for Ca 2+ -ATPase activity (15  μ M) and actin polymerization (17  μ M). 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.

Decavanadate Toxicology and Pharmacological Activities: V10or V1, Both or None?

Decavanadate Toxicology and Pharmacological Activities: V₁₀or V₁, Both or None?