Abstract
Previous
studies of lead metabolism in bone organ culture have defined, in part,
an exchangeable bone lead compartment regulated by the same ions and
hormones that normally control bone cell metabolism. This study was
undertaken to further characterize this subcompartment of exchangeable
lead and to examine possible interactions between lead and calcium in
isolated bone cell populations. Bone cells, derived from mouse calvaria,
were enriched for osteoclasts (OC) and osteoblasts (OB) by a sequential
collagenase digestion. We found that (1) the uptake of 210Pb
by OC cells was rapid, and OC cells had greater avidity for lead,
compared to OB cells, at concurrent time points of incubation, (2) OB
cells showed very little increase in lead uptake as medium lead
concentrations were increased from 6.5 to 65 μm, in contrast, the uptake of lead by OC cells was almost linear, (3) after loading OC cells with 210Pb,
significant release of label (∼ 15 to 30%) occurred within short time
periods (≦2 hr) during incubations in chase medium, (4) parathyroid
hormone (PTH) at physiological concentrations effected a marked increase
in 210Pb and 45Ca uptake in OC cells, after 5 min
of incubation, Pb accumulation into OC cells continued as calcium
uptake markedly decreased, (5) this PTH effect on 210Pb uptake was linear over PTH concentrations of 50 to 250 ng/ml, and (6) rising medium concentrations of lead (≧26 μm)
markedly enhanced/exaggerated calcium uptake by OC cells, far above
that produced by physiological concentrations of PTH. These data
indicate that (1) quantitatively, OC cells are the predominant cell type
in the metabolism of lead in this in vitro system of OC and OB
cell monolayers, (2) mediated incorporation of lead into OC cells
occurs and likely involves changes in membrane permeability effected by
hormonal stimuli, such as PTH, and (3) modulations in cellular calcium
metabolism induced by lead at low concentration may have the potential
of disturbing multiple cell functions of different tissues that depend
upon calcium as a second messenger.
Copyright © 1983 Published by Elsevier Inc.
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