Aluminum action on mouse bone cell metabolism and response to PTH and 1,25(OH)2D3

Lieberherr, M.; Grosse, B.; Cournot-Witmer, G.; Hermann-Erlee, M. P. M.; Balsan, S.
March 1987
Kidney International;Mar1987, Vol. 31 Issue 3, p736
Academic Journal
Aluminum (Al) accumulation in bone is associated with low bone formation and mineralization rates: resorption may also be reduced. The mechanism of these Al-induced changes was investigated using cultured mouse osteoblast-like (OB) and osteoclast-like (OC) cells. The AI effect on bone resorption was measured by the in vitro release of 45Ca and β-glucuronidase from mouse fetal limb-bones. AI had a biphasic effect, High concentrations (>1.5 × 10-6 M) of Al inhibited collagen and DNA synthesis, ornithine decarboxylase and alkaline phosphatase activity in OB, and depressed tartrate-resistant acid phosphatase activity in OC. Lower AI concentrations stimulated these cellular activities and 45Ca and β-glucuronidase release from fetal bones. A1 had no effect on basal cAMP levels in OB but inhibited the stimulating effect of bPTH on cAMP content. Al also altered the 1,25(OH)2D3 effects on the ornithine decarboxylase activity of OB cells. These data suggest that: (i) the low bone formation observed in vivo during AI intoxication may be due to the inhibition of collagen synthesis and to depressed cell proliferation; and (ii) AI may indirectly influence bone remodeling by interfering with the actions of bPTH and 1,25(OH)2D3 on bone cells.


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