Abstract:
Pathological calcifications may consist of calcium oxalate (CaOx), hydroxyapatite (HAP), and brushite (BRU). The objective of this study was to evaluate the effect of phytate (inositol hexakisphosphate, InsP6), InsP6 hydrolysates, and individual lower InsPs (InsP5, InsP4, InsP3, and InsP2) on the crystallization of CaOx, HAP and BRU in artificial urine. All of the lower InsPs seem to inhibit the crystallization of calcium salts in biological fluids, although our in vitro results showed that InsP6 and InsP5 were stronger inhibitors of CaOx crystallization, and InsP5 and InsP4 were stronger inhibitors of BRU crystallization. For the specific in vitro experimental conditions we examined, the InsPs had very weak effects on HAP crystallization, although it is likely that a different mechanism is responsible for HAP crystallization in vivo. For example, calciprotein particles seem to have an important role in the formation of cardiovascular calcifications in vivo. The experimental conditions that we examined partially reproduced the in vivo conditions of CaOx and BRU crystallization, but not the in vivo conditions of HAP crystallization.
摘要:
病理性钙化可能由草酸钙(CaOx)组成,羟基磷灰石(HAP),和笔刷(BRU)。本研究的目的是评估植酸(肌醇六磷酸,InsP6),InsP6水解产物,和单个较低的InsPs(InsP5,InsP4,InsP3和InsP2)对CaOx的结晶,人工尿液中的HAP和BRU。所有较低的InsP似乎都抑制了生物流体中钙盐的结晶,尽管我们的体外研究结果表明InsP6和InsP5是CaOx结晶的更强抑制剂,InsP5和InsP4是BRU结晶的更强抑制剂。对于我们检查的特定体外实验条件,InsPs对HAP结晶的影响非常弱,尽管可能是不同的机制导致体内HAP结晶。例如,钙蛋白颗粒似乎在体内心血管钙化的形成中起重要作用。我们检查的实验条件部分再现了CaOx和BRU结晶的体内条件,但不是HAP结晶的体内条件。