The influence of combined magnesium and vanadate administration on the level of some elements in selected rat organs: V-Mg interactions and the role of iron-essential protein (DMT-1) in the mechanism underlying altered tissues iron level.

The effect of 12 week co-administration of sodium metavanadate (SMV) and magnesium sulfate (MS) on the levels of some elements in selected rats' organs and an attempt to elucidate a role of divalent metal transporter 1 (DMT-1) in the mechanism(s) of the SMV-induced disorders in some tissue Fe homeostasis were studied. SMV taken up separately or in combination with MS may pose a risk of the rise and shortage of the total hepatic and splenic Fe and Cu contents, respectively, cerebral Fe deficiency, splenic Ca deposition, and the hepatic, renal, and cerebral DMT-1 down-regulation. When administered alone, SMV may also cause the decrease in the total renal Fe and Cu contents. A visible protective effect of Mg against the renal and cerebral V accumulation and the decrease in the renal Fe and Cu contents during the SMV-MS co-administration together with our previous findings suggest a beneficial role of Mg at SMV exposure. Further, the SMV-induced fall in total iron binding capacity (TIBC), reported previously, and its correlations with the hepatic, splenic, and cerebral Fe levels allow us to suggest that diminished TIBC could be partly involved in the mechanism(s) responsible for the dramatic redistribution of Fe in those tissues. Finally, DMT-1, which potentially could participate in the hepatic non-transferrin Fe-bound uptake, does not play a significant role in this process indicating the need for studying other Fe transporters to more precisely elucidate molecular mechanism(s) underlying the hepatic Fe loading in our experimental conditions.