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were done in rats at about the same time (Copp et a)., 1947).
Unlike stront-
jum, but like yttrium and cerium, plutonium showed behavior that vas
unaffected by the age of the rats under study or by calcium or phosphorus
levels in the diet.
This suggested that, while strontium followed the
pathways of calcium metabolism, plutonium, yttrium, and cerium did not, and
that they were deposited in the skeleton by other mechanisms.
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A method of protection fran plutonium toxicity was proposed by Copp et al.
(1947), who suggested that where contamination had occured, the diet could be
altered to dimineralize the skeleton.
By then renineralizing the skeleton via
dietary change, a protective layer of new bone would be laid down over the
plutoniun.
Subsequent studies in rats showed the uptake of chronic, orally admintstered plutonium to be 0.003% (Katz et al., 1955; Weeks et al., 1956).
Uptake of plutonium given as a single dosage to pigs wes 0.007% of the
administered anount (Weeks et a)., 1956).
In pigs the metabolism of plutonium after intravenous, intragastric, or
intratracheal administration of plutonium(IV) nitrate was aiso studies.
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liver and skeleton were the principal sites of plutonium deposition, {he quantity absorbed depended on the mode of administration.
Less than) percent of
the administered Pu was in the skeleton and liver up to 2 years after intragastric administration or intratracheal dosing.
After an tntravenous dose, 50
to 77 percent was in skeleton and liver; in this case, however, the plutonium
nitrate solution was buffered with citrate, which may have contributed to the
difference (Bustad et al., 1962).
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Stover et a). (1959; 1962; 1968) studted the long-term metabolism of plutonium fn dogs whose steletal and soft tissue retent:on of injected plutonium