Feeding of Excessive Cystine and Cysteine Enhances Defects of Dietary Copper Deficiency in Rats by Differential Mechanisms Involving Altered Iron Status.

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Abstract
We have reported that excess cystine feeding exaggerates the defects of dietary copper deficiency in rats by a mechanism not involving oxidative stress and altered copper status. This study was conducted to examine whether this exacerbation is caused by a mechanism involving altered iron status and to compare the influences of cystine and cysteine feeding on the defects of copper deficiency. Male Wistar rats were fed copper-adequate or copper-deficient diet with supplementation of L-cystine or L-cysteine (2%) for 10 days or 21 days. Copper-deficient diet increased heart weight, caused anemia, reduced plasma iron and elevated liver iron. These defects were exacerbated by supplemental cystine. Cysteine feeding also exacerbated the defects of dietary copper deficiency including anemia, increased heart weight, and reduced plasma iron, although cysteine feeding had no influence on liver iron concentration. Supplemental cysteine reduced apparent absorption of iron, while supplemental cystine did not. These results suggest that cystine feeding enhances the defects of copper deficiency by a mechanism involving impaired mobilization of iron from liver into blood, and that cysteine feeding enhances the defects of copper deficiency by a mechanism involving reduced intestinal absorption of iron.

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