MacDonald E, Lihtamo H, Hellevuo K, Komulainen H
Department of Pharmacology University of Kuopio, Finland.
Biol Trace Elem Res. 1988 Aug;16(3):177-88. doi: 10.1007/BF02797134.
Since it has been claimed that vanadate is an endogenous regulator of Na/K-ATPase activity and that it potentiates the toxicity of cardiac glycosides, we were alarmed to discover that certain Finnish physicians were prescribing vanadate in combination with other trace minerals to elderly patients for many different chronic diseases (e.g., cancer, rheumatism). To study the interaction of vanadate and cardiac glycosides, we fed vanadate in the drinking water (25 micrograms/mL) to guinea pigs for 20 d, and studied either their sensitivity to the acute toxicity of the cardiac glycoside ouabain or whether the vanadate would influence the subacute toxicity of ouabain. Vanadate had no influence on the toxicity of ouabain either acute or subchronically administered, nor was there any sign of inhibition of Na/K-ATPase activity as measured by 86Rb-uptake into intact erythrocytes (RBCs), RBC content of sodium or potassium or Na/K-ATPase activity in RBC membranes prepared from the vanadate-treated guinea pigs. Vanadate had been absorbed in substantial quantities from the gastrointestinal tract, since serum, heart, liver, and especially kidney contained measurable amounts of vanadium in contrast to controls, but it is concluded that this vanadate is not in a biologically active form.
由于有人声称钒酸盐是钠钾ATP酶活性的内源性调节剂,并且它会增强强心苷的毒性,所以当我们发现某些芬兰医生给患有多种不同慢性病(如癌症、风湿病)的老年患者开钒酸盐与其他微量矿物质的组合药物时,感到十分震惊。为了研究钒酸盐与强心苷的相互作用,我们给豚鼠饮用含钒酸盐(25微克/毫升)的水20天,然后研究它们对强心苷哇巴因急性毒性的敏感性,或者钒酸盐是否会影响哇巴因的亚急性毒性。无论是急性还是亚慢性给予钒酸盐,它对哇巴因的毒性均无影响,而且用钒酸盐处理过的豚鼠完整红细胞(RBC)对86Rb的摄取、RBC中钠或钾的含量以及RBC膜中钠钾ATP酶活性的测定结果均未显示出有任何抑制钠钾ATP酶活性的迹象。钒酸盐已从胃肠道大量吸收,因为与对照组相比,血清、心脏、肝脏尤其是肾脏中含有可测量的钒量,但可以得出结论,这种钒酸盐不是生物活性形式。