Rubinacci A, Boniforti F, De Ponti A
Sezione Fisiopatologia dell'Osso e del Metabolismo Minerale, Istituto Scientifico H San Raffaele, Milano.
Minerva Endocrinol. 1992 Jul-Sep;17(3):95-101.
Controversies surround the view that the blood-bone ionic equilibrium is controlled by ionic changes at a so called "bone membrane" that display a pump-leak mechanism able to maintain a concentration gradient for chloride in addition to that for calcium, sodium and potassium. On the other hand it is known that a chloride-bicarbonate transport is active at bone cells membrane to control cytosolic pH. We tested the hypothesis that a modification of the chloride concentration of the culture medium, as well as a block of the chloride-bicarbonate transport by an anionic channels blocker, in an experimental model that keeps intact the bone membrane, may influence the bone cells activity and that the influence may be quantitatively different to that previously observed in isolated bone cells. The experimental model is the intact fetal rat limb bone, cultured for 24 hours in a simplified medium at different chloride concentrations obtained by substituting chloride with isethionate. Alkaline phosphatase activity released in the medium was measured as a marker of osteoblasts activity. By progressively reducing the chloride concentration from 117 mM to 29 mM, alkaline phosphatase activity was found unchanged. By dramatically reducing the medium chloride concentration to the range 14-0 mM, alkaline phosphatase activity was significantly (p = 0.0002) inhibited by 31.58%.(ABSTRACT TRUNCATED AT 250 WORDS)
血骨离子平衡由所谓“骨膜”处的离子变化控制,该骨膜呈现出一种泵-漏机制,除了能维持钙、钠和钾的浓度梯度外,还能维持氯离子的浓度梯度。另一方面,已知氯离子-碳酸氢根转运在骨细胞膜处活跃,以控制胞质pH值。我们测试了以下假设:在保持骨膜完整的实验模型中,培养基中氯离子浓度的改变以及阴离子通道阻滞剂对氯离子-碳酸氢根转运的阻断,可能会影响骨细胞活性,且这种影响在数量上可能与先前在分离的骨细胞中观察到的不同。实验模型是完整的胎鼠肢体骨,在简化培养基中于不同氯离子浓度下培养24小时,通过用羟乙基磺酸替代氯离子来获得不同浓度。测量培养基中释放的碱性磷酸酶活性作为成骨细胞活性的标志物。将氯离子浓度从117 mM逐步降低至29 mM时,发现碱性磷酸酶活性未发生变化。当将培养基氯离子浓度大幅降低至14 - 0 mM范围时,碱性磷酸酶活性显著(p = 0.0002)受到抑制,抑制率为31.58%。(摘要截断于250字)