Pancreatic lithostathine inhibitor of calcium carbonate precipitation: structure-function relationship
Bernard, J.P.; Takacs, T.; de Reggi, M.; Sarles, H.; Dagorn, J.C.
Nephrologie 14(6): 257-259
1993
ISSN/ISBN: 0250-4960 PMID: 8145882 Document Number: 422170
Pancreatic juice is naturally supersatured in calcium and bicarbonate ions. A mechanism controlling CaCO3 crystal formation and growth is therefore necessary to prevent duct clogging. Lithostathine, a glycoprotein synthesized by acinar cells and secreted in pancreatic juice, could be involved in such a control. Lithostathine significantly delayed crystal nucleation and inhibited growth of CaCO3 crystals from supersatured solutions. Lithostathine adsorbed to sites specifically inhibiting crystal growth with a dissociation constant Kd = 0.9 x 10(-6) mol/L. The glycosylated N-terminal undecapeptide generated by limited trypsin hydrolysis of lithostathine, inhibited CaCO3 crystal growth with a Kd = 3.4 x 10(-6) mol/L similar to that of lithostathine. On the contrary, the carboxy-terminal polypeptide (lithostathine H) was inactive. The N-terminal undecapeptide of lithostathine is therefore essential to the inhibitory activity of the protein on CaCO3 crystal growth.