Influence of phospholipid on bile salt binding to calcium hydroxyapatite and on the poisoning of nascent hydroxyapatite crystals

Authors

  • Masayuki Okido,

    1. Department of Surgery I, Kyushu University, Fukuoka, Japan
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  • Roger D. Soloway,

    1. Division of Gastroenterology, Department of Internal Medicine, University of Texas Medical Branch, Galveston, TX, USA
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  • Roger S. Crowther

    Corresponding author
    1. Division of Gastroenterology, Department of Internal Medicine, University of Texas Medical Branch, Galveston, TX, USA
      Division of Gastroenterology, University of Texas Medical Branch, 301 University Blvd., Galveston, TX 77555–0764, USA
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Division of Gastroenterology, University of Texas Medical Branch, 301 University Blvd., Galveston, TX 77555–0764, USA

Abstract

Abstract: Glycine-conjugated, dihydroxy bile salts inhibit calcium hydroxyapatite (HAP) formation by binding to and poisoning nascent crystal embryos. Their taurine-conjugated counterparts bind less well to hydroxyapatite and do not inhibit its formation; but more hydrophobic, synthetic analogs of the taurine conjugated bile salts are inhibitors of hydroxyapatite formation. Because hydrophobicity is an important determinant of the ability of bile salts to inhibit hydroxyapatite crystal growth, experiments were performed to study the effect of the physiologically important mixed micelles of bile salt and phospholipid. Taurodeoxycholate/phosphatidylcholine (10:1) mixed micelles bound to HAP at lower total lipid concentrations than did pure taurodeoxycholate. At low total lipid concentrations, phosphatidylcholine (PC) binding appeared to predominate, suggesting that PC had a higher affinity than did taurodeoxycholate (TDC) for the HAP surface. Although glycodeoxycholate (3 mM) significantly (>95%) inhibited hydroxyapatite precipitation, higher concentrations of taurodeoxycholate, either alone or mixed with phosphatidylcholine, did not affect hydroxyapatite formation. These results suggest that biliary phospholipids do not modulate the ability of bile salts to inhibit hydroxyapatite crystal growth.

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