Walker H L, Moses H A
J Natl Med Assoc. 1979 Dec;71(12):1187-9.
In recent years interest has increased in the study of the metabolism of cadmium because of its presence in the environment as a toxic agent. Having no known essential bodily functions and possibly altering the action of various other trace metals, eg, lead and zinc, cadmium has been suspect as a causative factor in certain pathological alterations, such as hypertension. A study of this association was undertaken by the authors.Female Sprague-Dawley rats were fed laboratory chow and given cadmium nitrate ad libitum. Systolic pressure was monitored and weights were recorded at weekly intervals. Cadmium and lead were determined in kidney and liver tissues of the sacrificed animals by using a trace metal analyzer and by atomic absorption spectrophotometer. After 36 weeks on the experimental regimen, the cadmium-treated animals had higher systolic pressures than the control group (155 ± 10 mmHg compared to 96 ± 5 mmHg). Increased levels of cadmium reflective of the cadmium consumed were found to occur in liver and kidney tissues. The urinary excretion of deltaaminolevulenic acid by the experimental animals was higher than that of the control animals. This suggests that the supplemented cadmium induced lead to leave the kidney and become metabolically active.
近年来，由于镉作为一种有毒物质存在于环境中，对其代谢的研究兴趣有所增加。镉在人体中没有已知的基本生理功能，并且可能改变其他各种微量元素（例如铅和锌）的作用，因此镉被怀疑是某些病理改变（如高血压）的致病因素。作者进行了一项关于这种关联的研究。给雌性斯普拉格-道利大鼠喂食实验室饲料，并随意给予硝酸镉。每周监测收缩压并记录体重。使用痕量金属分析仪和原子吸收分光光度计测定处死动物的肾脏和肝脏组织中的镉和铅。在实验方案实施36周后，镉处理组动物的收缩压高于对照组（分别为155±10 mmHg和96±5 mmHg）。在肝脏和肾脏组织中发现，镉水平的升高反映了所摄入的镉量。实验动物的δ-氨基乙酰丙酸尿排泄量高于对照动物。这表明补充的镉会导致铅离开肾脏并变得具有代谢活性。
