四硼酸钠对氟致肾损伤的拮抗作用及机理

Protection and its Mechanism of Sodium Tetraborate on the Kidneys and Cultured Renal Cells from Fluoride Damage

本文研究了四硼酸钠对氟化钠所致实验动物肾脏和离体肾细胞损伤的拮抗作用,并探讨了其机理。亚急性和慢性氟暴露家兔尿中γ-GT活性增加,肾组织AKP、SDH和AcP活性减低,小管细胞内多种细胞器出现损伤。大鼠离体肾细胞的蛋白质、RNA和DNA合成代谢不同程度地受到含氟培养液的影响。四硼酸钠对氟的上述不良效应具有较全面的拮抗作用。其机理可能是:①硼与氟在体内形成氟硼酸根,改变了氟在体内的存在形式,并促使氟随尿排出;②硼降低了细胞膜对氟离子的通透性,使细胞内的氟含量减少。

The paper first reported the protection andits mechanism of sodium tetraborate on thekidneys and the cultured renal cells from so-dium fluoride damage. Under subacute and ch-ronic fluomde exposures, the rabbits urinaryr-GT excretion increased renal AKP, SDH,and AcP activities decreased, various organel-les of renal tubular cells were damaged. Theanabolisms of protein, RNA and DNA in thecultured rat renal cells were also affected byfluoride. Boron could eliminate or reduce allabove adverse effects of fluoride. The possibleprotection mechanism of boron was that boroncould integrate itself with fluorine to formBF_(4^-), and that probably boron reduced thepermeability of the cellular membrane forfluorine.