Abstract
Tissue copper levels of brindled ( Mo br) mice and normal litter-mates after single and repeated dosing with CuCl 2 and/or D-penicillamine are examined, together with a study of the cytosol distribution of copper after CuCl 2 treatment. The results confirm that the mutant mouse kidney is capable of extensive copper accumulation in association with the low MW copper-binding protein. Deficient tissues such as brain, heart and spleen are able to sequester sufficient of the exogenous copper to raise their levels to the normal control level, whereas mutant liver levels, even after copper treatment, remain below normal, indicating that the Mo gene affects the ability of the liver to retain copper.
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