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Metallothionein as a storage protein for cadmium: its toxicological implications.

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.