Abstract
The biological fate of plutonium (Pu) introduced as a Pu-standard LICAM(C) complex was investigated in male rats of two strains, in male and female mice and in the baboon. We observed that, whatever the animal species or the entry route, this complex was deposited rapidly in the kidney. In addition, more of the complex accumulated in the rat (16% of injected radioactivity) than in either the mouse (7%) or baboon (5%). This Pu deposit was cleared spontaneously with a half-life of 10 days in the rat and only 5 days in the mouse. We noted that the complex was deposited on bone during this period and that, 10 days after the introduction of Pu, the skeleton became the main organ of retention of Pu (7% of the dose in the rat, 4% in mice and 3% in the baboon). In spite of this, which would indicate that Pu-standard LICAM(C) resembles a weak complex, gut transfer was comparable with that of a strong complex 1.10-3 (f1 = 1.10-3) . Pu deposit seemed to be pH dependent and could be modified be varying the pH balance of urine. Bicarbonate was among the most effective of the different drugs used to affect this balance, as 5 h of continuous perfusion decreased the kidney Pu burden by a factor of 4. Such efficacy was also observed with diethylenetriaminepenta-acetic acid (DTPA) perfusion. The pragmatic consequence of these experiments is the recommendation of mixed therapy: standard LICAM(C) plus bicarbonate or DTPA.
Get full access to this article
View all access options for this article.