Molybdenum uptake through the anion exchanger in human erythrocytes.

Human red blood cells were incubated in the presence of Na2MoO4 and the initial rate of molybdenum uptake was measured by using inductively coupled plasma emission spectroscopy. About 99% of molybdenum uptake was inhibited by DIDS or by SITS. DIDS-sensitive molybdenum uptake was inhibited by external chloride, bicarbonate, sulphate and phosphate in the range of concentrations previously described for anion carrier fluxes. Trace elements, previously described to be translocated by the anion carrier, i.e. copper, zinc and cadmium, slightly inhibited molybdenum uptake. Molybdenum uptake was strongly stimulated by acidification, suggesting that the monovalent HMoO4- anion species, which is formed in acidic media (pK approximately 4.1), can be more rapidly translocated than the divalent anion complex MoO4(2-), which is the predominant form at physiological pH. In conclusion, the anion carrier can catalyse rapid molybdenum movements across red cells membranes. This supports previous reports of an enterohepatic circulation of molybdenum, with red blood cells acting as molybdenum carrier between the intestine and the liver.