Abstract

Previous data in bone organ culture have demonstrated a mobile compartment of Pb regulated like bone mineral. To test for its existence in vivo, after 7mg/kg of Pb plus 25μCi 203Pb were given IV, TPTX rats were placed in metabolism cages; and 4 days later, EDTA or PTH was infused via a catheterized tall vein for 6 hours. Measurements were made of stable Pb and 203Pb from aliquots of total organs, urinary Pb/creatinine (Pb-U), and blood Pb (Pb-B), μg/dl. 3 days later the rats were sacrificed and the cpm of 203Pb from bone (B), liver (L), and kidney (K) were expressed as the % change vs saline-infused controls. The results (* = p < .01;** = < .001) were: PTH infusion period: Pb-U = 2.29 ± .04*; Pb-B = 34± 2**; PTH 72-H after infusion: Pb-U = .56 ± .10; Pb-B = 9.0 ± 2; EDTA infusion period: Pb-U = 20.28 ± 5.16**; Pb-B = 33 ± 2**; EDTA 72-H after infusion: Pb-U = 1.35 ± .04*; Pb-B = 8 ± 2. In EDTA-treated rats, 203Pb decreased from B, L, K by 22 ± 1**, 46 ± 4**, and 40 ± 6**, respectively. In PTH-treated rats, 203Pb decreased from B.L.K by 11 ± 2*. 29 ± 4** and 30 ± 2**. Similar increases in the urinary excretion of calcium, phosphate and hydroxyproline were produced by both agents.These in vivo data are consistent with previous in vitro observations. Moreover, PTH's dramatic effects on the redistribution of Pb in soft and hard tissues may well modify the toxic activities of Pb and thereby be of considerable clinical importance.

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