Decavanadate contribution to vanadium biochemistry: In vitro and in vivo studies

• Decavanadate (V10) interacts with myosin at a specific protein backdoor binding site.
• V10 induces actin cysteine oxidation preventing actin polymerization and myosin-actin interaction.
• In vivo vanadium toxicity is dependent, among others factors, on vanadium ion species such as V10.
• V10 administration induces vanadium accumulation in mitochondria.
• V10 affects several mitochondrial processes at low concentrations (nM).

Although the number of papers about “decavanadate” has increased in the last decade in vivo or/and cellular toxicological studies involving vanadium that takes in account the contribution of decavanadate (V10) ion species to biological responses are scarce. These innovative in vivo studies are supported by the fact that decavanadate interact with major proteins such as myosin, actin and Ca2+-ATPase and affect mitochondria function besides induces changes in several cellular antioxidants markers. These recent findings, that are now briefly reviewed, suggested that the biological responses induced by vanadium, will be dependent on vanadium ion species such as decavanadate. Putting it all together, it is clearly shown that decavanadate can be involved in many cellular processes, and therefore it must be taken in account for the understanding the role of vanadium in biological systems.

Decavanadate interacts with myosin at a specific protein backdoor binding site.Figure optionsDownload as PowerPoint slide