Whanger P D
Environ Health Perspect. 1979 Feb;28:115-21. doi: 10.1289/ehp.7928115.
Exposure of rats to cadmium causes a marked depletion of iron in liver and kidney. Selenium neither counteracts or intensifies the influence of cadmium on tissue iron levels. Selenium injections protect against cadmium-induced testicular damage but cause this element to accumulate in the testes at higher concentration than in animals exposed to cadmium without selenium. Selenium injection diverts the binding of cadmium from low molecular weight proteins to high molecular weight ones. Dosing rats with selenium and cadmium or inclusion of Se or Cd in the diet did not result in altered cadmium binding in tissues, raising some questions concerning the environmental significance of these injection experiments. Addition of selenium to a diet containing cadmium decreased the accumulation of cadmium in liver and kidney, but increased its deposition in testes. The metabolism of cadmium bound to metallothionein was markedly different as compared to the inorganic salt of this element. Dietary ascorbate, but not citrate or cysteine, decreased the deposition of cadmium in rat tissues. In some low-level exposure experiments with cadmium (1 to 1000 ppb), no differences were found in the percentage of dose absorbed or rate of cadmium accumulation when provided in food versus water. Female rats tended to absorb more cadmium than males. The binding of cadmium to cytosolic proteins was found to be different between rats fed low levels of cadmium (up to 1 ppm) as compared to those fed high levels of this element (100 ppm). Cadmium was not found to contribute to hypertension in rats, and a summary of results by various investigators is presented. Blood and hair cadmium levels in Oregon residents were found to be highest in employees of a mine, and hair cadmium was found to be respectively higher in smokers than nonsmokers and in metal workers than office workers. No relationships were observed in humans between blood or hair cadmium levels and blood pressure.
大鼠接触镉会导致肝脏和肾脏中铁的显著减少。硒既不会抵消也不会增强镉对组织铁水平的影响。注射硒可预防镉诱导的睾丸损伤,但会使该元素在睾丸中的积累浓度高于未注射硒而接触镉的动物。注射硒会使镉从低分子量蛋白质的结合转向高分子量蛋白质的结合。给大鼠注射硒和镉或在饮食中添加硒或镉并不会导致组织中镉结合的改变,这引发了一些关于这些注射实验环境意义的问题。在含镉的饮食中添加硒会减少镉在肝脏和肾脏中的积累,但会增加其在睾丸中的沉积。与该元素的无机盐相比,与金属硫蛋白结合的镉的代谢明显不同。饮食中的抗坏血酸(而非柠檬酸或半胱氨酸)会减少镉在大鼠组织中的沉积。在一些低水平镉暴露实验(1至1000 ppb)中,当镉通过食物或水提供时,在吸收剂量百分比或镉积累速率方面未发现差异。雌性大鼠往往比雄性大鼠吸收更多的镉。发现喂食低水平镉(高达1 ppm)的大鼠与喂食高水平镉(100 ppm)的大鼠相比,镉与细胞溶质蛋白的结合有所不同。未发现镉会导致大鼠高血压,并呈现了不同研究者的结果总结。俄勒冈州居民血液和头发中的镉水平在一家矿山的员工中最高,且发现吸烟者头发中的镉含量高于不吸烟者,金属工人头发中的镉含量高于办公室工作人员。在人类中未观察到血液或头发镉水平与血压之间的关系。