Jay D, Michel B
Arch Inst Cardiol Mex. 1986 May-Jun;56(3):205-10.
In order to establish at subcellular level the biochemical role of cadmium in the etiology of arterial hypertension, we studied the effect of this metal on some mitochondrial functions. The results showed that cadmium inhibits calcium uptake as well as stimulates calcium release in kidney mitochondria. By the same token Cd2+ inhibits the ADP and ATP exchange-reaction and also inhibits succinate oxidation. From these results it is proposed that C d2+ interacts with--SH groups that are important for energy--linked reactions and calcium transport; the above produces metabolic modifications that may result in hypertensive disease.
为了在亚细胞水平确定镉在动脉高血压病因学中的生化作用，我们研究了这种金属对某些线粒体功能的影响。结果表明，镉抑制肾线粒体对钙的摄取并刺激钙的释放。同样，Cd2+抑制ADP与ATP的交换反应，也抑制琥珀酸氧化。从这些结果推测，Cd2+与对能量相关反应和钙转运很重要的-SH基团相互作用；上述情况产生的代谢改变可能导致高血压疾病。
