ABSTRACT
Following intravenous injection into male Sprague-Dawley rats 233Pa, like other elements, deposits predominantly in the skeleton (ca. 70-80 per cent), but unlike Pu and Am the liver deposition of 233Pa is low, about 2-3 per cent between 1 and 7 days. About 99 per cent of the injected 233Pa is lost from the plasma compartment in 3 days, a clearance comparable to that of Pu but much slower than that of Np, Am or Cm. On entering the liver cell cytosol 233Pa is bound rapidly to an unidentified protein of molecular mass 200 kDa and to a protein of 80 kDa, which is probably transferrin. Within a few hours the metal migrates to bind to a protein of greater than 400 kDa which has been tentatively identified as ferritin. Some 233Pa remains bound to small ligands until virtually all the intracellular 233Pa has been deposited in the lysosomes, or to a lesser extent in some other, as yet, unidentified organelles.
Subject(s)
Protactinium/pharmacokinetics , Animals , Injections, Intravenous , Male , Protactinium/administration & dosage , Protactinium/metabolism , Protein Binding , Rats , Tissue DistributionABSTRACT
Protactinium uptake into the normal liver does not exceed 3%, but when the phospholipid levels in the liver are elevated by administration of thioacetamide this uptake increases to 31%. Phosphatidic acid, which is absent from the normal liver, has been shown to extract protactinium into organic solvents. However, phosphatidylserine, a component of normal liver cell membranes, does not extract protactinium. It might be conjectured that this is why so little protactinium is taken up by the normal liver. The hypothesis is advanced that phosphatidylserine, which is known to complex plutonium, americium and curium, may regulate the uptake of these elements by liver.
