Ermakova I P, Sokolova T Iu, Pronchenko I A
Biull Eksp Biol Med. 1990 Nov;110(11):493-5.
The kinetics of calcium binding to plasma proteins in hypo- and hypercalcaemia, induced in vitro, were studied in 60 patients after renal transplantation. Langmuir and Scatchard analysis revealed the normal binding of calcium to plasma proteins in 10 patients (cooperative mechanism of calcium-protein interaction in hypocalcaemic state and existence of one or several sets of calcium binding independent sites in hypercalcaemic state). Cooperative binding with the decreased values of effective Ka, effective n. molar binding ratio (CaPr/A) and specific buffer capacity (beta sp.) were observed in 1/3 patients. Cooperative mechanism of calcium-proteins interaction has not been observed in more than 1/2 patients and the values of n. CaPr/A, beta sp, decreased in most of the patients. The observed changes may be caused by a proteins metabolism deterioration and may result in deterioration of calcium homeostasis.
在60例肾移植患者中，研究了体外诱导的低钙血症和高钙血症状态下钙与血浆蛋白结合的动力学。朗缪尔和斯卡查德分析显示，10例患者钙与血浆蛋白的结合正常（低钙血症状态下钙 - 蛋白相互作用的协同机制以及高钙血症状态下存在一组或几组独立的钙结合位点）。1/3的患者观察到有效Ka值、有效n、摩尔结合比（CaPr/A）和比缓冲容量（βsp.）降低的协同结合。超过1/2的患者未观察到钙 - 蛋白相互作用的协同机制，并且大多数患者的n、CaPr/A、βsp值降低。观察到的变化可能是由蛋白质代谢恶化引起的，并且可能导致钙稳态的恶化。
