Abstract
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.
Highlights
The ability of bile salts to inhibit the precipitation of either calcium hydroxyapatite or its precursor, amorphous calcium phosphate, by reducing CaZ+activity or poisoning nascent crystals was determined
Any reduction of Ca2+activity may alter the kinetics of salt formation (Le., alter the onset of precipitation), but longterm, thermodynamic prevention of precipitation requires that the bile salt concentration and its Ca2+binding affinity must together be sufficient to make bile unsaturated with respect to the target Ca2+salt
We recently showed that glycochenodeoxycholate (GCDC) inhibited calcium phosphate precipitation by “poisoning” calcium hydroxyapatite (HAP) embryos, which prevented the transformation of amorphous calcium phosphate (ACP) into HAP [18]
Summary
The ability of bile salts to inhibit the precipitation of either calcium hydroxyapatite or its precursor, amorphous calcium phosphate, by reducing CaZ+activity or poisoning nascent crystals was determined. B at low supersaturation all dihydroxy bile salts can prevent apatite formation by reducing free Ca2+ (taurine and glycine conjugates) or poisoning embryos (glycine conjugates). Seminal work by Williamson and Percy-Robb [3, 4], subsequently confirmed by others [5,6,7,8,9,10,11,12,13], showed that bile salts bind Ca2+ions and lower Ca2+activity This observation led Moore, Celic, and Ostrow ( 6 ) to propose the "Ca2+-buffering"hypothesis: inhibiting Ca2+-sensitiveanion precipitation in bile by reducing Ca2+activity is a major physiological function of bile salts.
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