金属硫蛋白的生物学功能。六、镉和锌在大鼠体内的代谢相互作用。

Biological function of metallothionein. VI. Metabolic interaction of cadmium and zinc in rats.

机构信息

Department of Agricultural Chemistry, Oregon State University, 97331, Corvallis, Oregon.

出版信息

Biol Trace Elem Res. 1980 Mar;2(1):65-80. doi: 10.1007/BF02789036.

Abstract

The accumulation and depletion of cadmium in liver and kidney metallothionein (MT) and the effects of dietary zinc deficiency on cadmium metabolism were studied in rats. The accumulation of cadmium in liver MT started to plateau after 80 days, but there was a linear accumulation of this element in kidney MT over the entire 300-day experiment. Cadmium in MT fractions was depleted very slowly when rats were changed to a diet without cadmium. The accumulation of cadmium in MT also caused zinc to accumulate in this protein, even in rats fed zinc-deficient diets. However, the reverse situation was found not to be true; zinc did not cause cadmium to accumulate in MT. Dietary zinc deficiency limited the binding of injected(109)Cd to MT of liver, but not of kidneys or testes. However, zinc-deficient rats fed cadmium in their diets metabolized cadmium similarly to zinc-supplemented rats, suggesting that zinc deficiency does not limit the ability of cadmium to stimulate MT synthesis.

摘要

研究了大鼠肝脏和肾脏金属硫蛋白（MT）中镉的积累和消耗，以及膳食锌缺乏对镉代谢的影响。肝脏 MT 中镉的积累在 80 天后开始趋于平稳，但在整个 300 天的实验中，肾脏 MT 中镉的积累呈线性增加。当大鼠改为不含镉的饮食时，MT 中镉的消耗非常缓慢。镉在 MT 中的积累也导致锌在这种蛋白质中积累，即使在喂食缺锌饮食的大鼠中也是如此。然而，情况并非相反；锌不会导致镉在 MT 中积累。膳食锌缺乏限制了注射的(109)Cd 与肝脏 MT 的结合，但不限制肾脏或睾丸 MT 的结合。然而，喂食含镉饮食的缺锌大鼠与补充锌的大鼠一样代谢镉，这表明锌缺乏并不限制镉刺激 MT 合成的能力。