Feeding of excessive cystine and cysteine enhances defects of dietary copper deficiency in rats by differential mechanisms involving altered iron status.

  title={Feeding of excessive cystine and cysteine enhances defects of dietary copper deficiency in rats by differential mechanisms involving altered iron status.},
  author={Qin Wan and B. S. Yang and Norihisa Kato},
  journal={Journal of nutritional science and vitaminology},
  volume={42 3},
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… 

Contrasting and cooperative effects of copper and iron deficiencies in male rats fed different concentrations of manganese and different sources of sulfur amino acids in an AIN-93G-based diet.

Although the anemia of Cu deficiency was not as pronounced as that reported in rats fed the AIN-76A-based diet, other manifestations of the deficiency were prominent, and many physiologic responses that require Fe were affected by both deficiencies, including lowered blood hemoglobin (Hgb), lower RBC volume and Hgb concentration, and an increased number of reticulocytes.

Silicon deprivation and arginine and cystine supplementation affect bone collagen and bone and plasma trace mineral concentrations in rats

It is indicated that silicon is needed for collagen formation, that high dietary Cys enhances changes induced by Si deprivation in trabecular-rich bone, and that Si nutriture has more impact on trabECular- rich bone than in cortical-richBone.

Heart murmurs, valvular regurgitation and electrical disturbances in copper-deficient genetically hypertensive, hypertrophic cardiomyopathic rats.

The data do not suggest that a copper-deficient diet fed to a strain of rats genetically susceptible to heart disease later in life, hastens or worsens the onset of cardiac disease.

Effects of varying dietary iron on the expression of copper deficiency in the growing rat: anemia, ferroxidase I and II, tissue trace elements, ascorbic acid, and xanthine dehydrogenase.

Results show that copper deficiency may impair liver iron mobilization in the growing rat if dietary iron is low, and possible mechanisms include decreased Fox activity and/or decreased iron reduction by ascorbate or XDH.

Increased hepatic lipid peroxidation with methionine toxicity in the rat.

Methionine supplementation increased hepatic lipid peroxidation, thiobarbituric acid reactive substances, and iron concentrations, indicative of increased oxidative stress resulting from methionine toxicity.

Excess levels of cysteine and homocysteine induce tibial dyschondroplasia in broiler chicks.

The effect of excessive levels of cysteine and homocysteine on tibial dyschondroplasia in broiler chicks was studied and copper supplementation lessened the severity of TD caused by DL-homocystine.

Chronic Treatment With Dimethyl Sulfoxide Protects Against Cardiovascular Defects of Copper Deficiency

  • J. Saari
  • Medicine
    Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine
  • 1989
Dimethyl sulfoxide (DMSO), a highly penetrant antiinflammatory agent and purported hydroxyl radical scavenger, was found to inhibit the cardiac hypertrophy, anemia and depression of heart Cu concentration which occurs with Cu deficiency, suggesting that thehydroxyl free radical may contribute to the cardiovascular defects caused by dietary Cu deficiency.

Differential Effects of Dietary Excessive Cystine and Cysteine on Plasma Ceruloplasmin and Cholesterol in Rats

The result showed that cystine addition depressed plasma ceruloplasmin activity and increased plasma cholesterol, while cysteine addition did not, the first evidence indicating the differencial metabolic responses to dietary addition of 2% Cystine and Cysteine.

Ethane Production in Copper-deficient Rats

  • J. SaariF. DickersonM. Habib
  • Biology
    Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine
  • 1990
Repeated measures analysis of variance indicated that both copper deficiency and breathing 100% O2 enhanced ethane production, with no interaction between treatments, which complements previous evidence that increased lipid peroxidation occurs in copper-deficient rats.

Responses of tissue ascorbic acid and of serum cholesterol, alpha-tocopherol, and ceruloplasmin in rats to dietary level of cystine.

Changes in liver ascorbic acid, serum cholesterol, and serum alpha-tocopherol and in ceruloplasmin activity by dietary cystine correlated with the changes in liver levels of non-protein sulfhydryl.

Excess dietary methionine decreases indices of copper status in the rat.

The results suggest that some of the toxic effects of excess dietary methionine may be mediated through interference with copper metabolism rather than through the previously postulated inhibition of sulfhydryl-sensitive enzymes by metabolites of Methionine.

Effect of dietary mineral composition on nutritional equivalency of amino acid mixtures and casein in rats.

The previous conflicting results concerning nutritional equivalency of amino acid mixtures and protein can be explained by inadequate mineral sources.