The role of vanadium in biochemistry has attracted attention for the last three decades. It could be used as inhibitor for nucleases and phosphatases [6]. Cantley and coworkers revealed a potent inhibitor of Na+/K+ – ATPase, widely used to study the mechanism of the sodium-potassium pump [7,8]. This pump is necessary for proper transport of materials across cell membranes to maintain ionic equilibrium.
Vanadium(V) (H2VO4−) enters into cells probably through the phosphate transport mechanism and reduced to vanadium(IV) through one-electron reduction in the gastrointestinal tract. VO2+ undergoes auto oxidation to vanadate in the presence of oxygen, whereas glutathione, ascorbate, cysteine and similar reducing agents can reduce vanadate. Thus, endogenous reducing agents and dissolved oxygen ensure that both vanadium(V) and vanadium(IV) species are present in serum. Vanadium has been found in its +IV oxidation state in mammalian lung and heart tissues [9] whereas +V oxidation state is common in kidney, liver and erythrocytes. It has also been suggested that extra cellular vanadium exists primarily as vanadium(V) and exclusively vanadium(IV) inside the cells [10]. The processes of interactions between vanadium species and serum albumin are still a challenge for scientists. However, the deposition of the vanadium in different tissue, obtained from in vitro experiments performed in different laboratories on several animals, follows the order: bone > kidney > liver > spleen > intestine stomach, blood, muscle, testes, lungs and brain. The excretion of the small fraction of ingested and not retained vanadium occurs mainly through urine, as low molecular weight VO2+ complexes. Biliar excretion seems to be a secondary route [11–14].
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