Shaikh Z A
Dev Toxicol Environ Sci. 1982;9:69-76.
Upon exposure to cadmium, the biosynthesis of metallothionein is increased in liver and kidneys. The protein sequesters a large fraction of the tissue cadmium, thereby making it less available for excretion. The primary function of the protein in cadmium metabolism, therefore, appears to be storage of the metal in a less toxic form. Low levels of metallothionein are found in plasma and urine upon cadmium exposure. The protein is cleared from the circulation and is reabsorbed by kidney. There it is rapidly degraded, releasing Cd2+ ions which are the probable cause of the proximal tubular damage. Circulating metallothionein can also induce the autoimmune response, resulting in the formation of soluble immune complexes which may deposit in glomeruli and affect their function as well. Therefore, due to its release into the circulation, the metallothionein-bound storage form of cadmium may in fact be responsible for both tubular and glomerular dysfunction observed after chronic cadmium exposure.
接触镉后，肝脏和肾脏中金属硫蛋白的生物合成会增加。该蛋白质会螯合大部分组织中的镉，从而使其较少可用于排泄。因此，该蛋白质在镉代谢中的主要功能似乎是以毒性较小的形式储存金属。镉暴露后，血浆和尿液中会发现低水平的金属硫蛋白。该蛋白质从循环中清除并被肾脏重新吸收。在那里它会迅速降解，释放出Cd2+离子，这可能是近端肾小管损伤的原因。循环中的金属硫蛋白还可诱导自身免疫反应，导致可溶性免疫复合物的形成，这些复合物可能沉积在肾小球中并影响其功能。因此，由于其释放到循环中，镉与金属硫蛋白结合的储存形式实际上可能是慢性镉暴露后观察到的肾小管和肾小球功能障碍的原因。
