Exposure to bis(maltolato)oxovanadium(IV) increases levels of hepcidin mRNA and impairs the homeostasis of iron but not that of manganese.

The aim of this study was to examine whether alterations in iron homeostasis, caused by exposure to vanadium, are related to changes in the gene expression of hepatic hepcidin. Two groups of rats were examined: control and vanadium-exposed. Vanadium, as bis(maltolato)oxovanadium(IV) was supplied in the drinking water. The experiment had a duration of five weeks. Iron and manganese were measured in excreta, serum and tissues. Leptin, ferritin, IL-1β, IL-6, TNF-α, red blood cells, haemoglobin and haematocrit were determined. Protein carbonyl group levels and hepcidin gene expression were determined in the liver. In the vanadium-exposed rats, iron absorption, serum iron and leptin and all haematological parameters decreased. Levels of IL-6, TNF-α and ferritin in serum and of iron in the liver, spleen and heart increased. In the liver, levels of protein carbonyl groups and hepcidin mRNA were also higher in the vanadium-exposed group. Exposure to vanadium did not modify manganese homeostasis. The results obtained from this study provide the first evidence that bis(maltolato)oxovanadium(IV) produces an increase in the gene expression of the hepcidin, possibly caused by an inflammatory process. Both factors could be the cause of alterations in Fe homeostasis and the appearance of anaemia. However, Mn homeostasis was not affected.