The deposition and retention of plutonium and americium in the mammalian liver after administration of about 5 μCi/kg or less are briefly reviewed. Inferences are drawn regarding physiological mechanisms and radiotoxic consequences. The initial deposition patterns, but not the retention patterns, of plutonium and americium in the liver are generally similar in a variety of species. The major biological process responsible for the variable and non-uniform hepatic deposition appears to be phagocytosis. The amount of radionuclide phagocytized is dependent upon the extent of hydrolysis and polymerization of the adminis-tered actinide. The different biological half times of plutonium and americium in the liver of different species suggest that there may be species differences in phagocytic function, protein binding, etc. The main route of elimination of plutonium (and probably americium) is via the bile and feces. There is a gradual aggregation of radionuclide by Kupffer cells and, at least in the mouse, also by parenchyma) cells. This aggregation is believed to result from a repeated sequence of phagocytosis, irradiation death of the phagocyte, and rephagocytosis. In the mouse and dog, 20 nCi of 239Pu or 241Am per gram of liver appears to be the threshold concentration that results in sufficient radiation-induced tissue damage to produce accelerated radionuclide loss into the blood, and translocation to the skeleton. In man it is postulated that progressive aggregation of low levels of actinide in the liver could also lead to radiation damage and subsequent translocation to critical osteogenic bone surfaces.
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