Journal of Lipid Research, Vol 35, 279-290, Copyright © 1994 by Lipid Research, Inc.
Inhibition of calcium phosphate precipitation by bile salts: a test of the Ca(2+)-buffering hypothesis
RS Crowther and M Okido
Department of Internal Medicine, University of Texas Medical Branch, Galveston 77555.
The ability of bile salts to inhibit the precipitation of either calcium
hydroxyapatite or its precursor, amorphous calcium phosphate, by reducing
Ca2+ activity or poisoning nascent crystals was determined. When apatite
precipitated rapidly (1-4 h), glycocholate and taurine- conjugated bile
salts (up to 100 mM) had little effect on apatite formation, but prevented
amorphous calcium phosphate precipitation by lowering Ca2+ activity. In
contrast, glycodeoxycholate and glycochenodeoxycholate (2-3 mM) inhibited
apatite formation for at least 24 h by poisoning embryonic apatite. When
apatite precipitated slowly (> 24 h), all the dihydroxy bile salts
prevented apatite formation for at least 4 days. At constant initial
supersaturation, the phosphate concentration determined the degree of
inhibition caused by the six bile salts mixed together in physiologic
proportion. At low phosphate concentrations (1.2 mM) total inhibition was
achieved by poisoning embryos (approximately -5 mM total bile salt), but
with 4.0 mM phosphate only approximately 60% inhibition was attained (150
mM bile salt) by a combination of poisoning and Ca(2+)-buffering. Thus, at
low supersaturation all dihydroxy bile salts can prevent apatite formation
by reducing free Ca2+ (taurine and glycine conjugates) or poisoning embryos
(glycine conjugates). With mixtures of bile salts at higher
supersaturation, inhibition of apatite depends on a combination of
poisoning and reduction of free Ca2+, mainly caused by glycodeoxycholate
and glycochenodeoxycholate.
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