Copper-iron metabolism interaction in rats

Iron deficiency anemia can be due to copper deficiency, even when iron intake is adequate. The objective of this study was to evaluate the interaction of copper with iron metabolism in anemic rats, using standard (copper and iron sulfate) or rice and beans diets containing the same iron concentratio...

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Published inNutrition research (New York, N.Y.) Vol. 25; no. 1; pp. 79 - 92
Main Authors Ramírez-Cárdenas, Lucía, Costa, Neuza Maria Brunoro, Reis, Fernando Pinheiro
Format Journal Article
LanguageEnglish
Published New York, NY Elsevier Inc 2005
Elsevier Science
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ISSN0271-5317
1879-0739
DOI10.1016/j.nutres.2004.07.003

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Abstract Iron deficiency anemia can be due to copper deficiency, even when iron intake is adequate. The objective of this study was to evaluate the interaction of copper with iron metabolism in anemic rats, using standard (copper and iron sulfate) or rice and beans diets containing the same iron concentration (24 ppm) but different levels of copper (2, 4, 6, or 12 ppm). A factorial model (2 × 4) was used together with a control treatment (0 ppm Cu, 24 ppm Fe), and the 9 treatments were randomly assigned to 8 blocks. The copper-iron interaction was evaluated by regression analysis. An increase in the levels of hemoglobin, hematocrit, and serum iron was observed with increased copper concentration, reaching a maximum value of about 6 ppm. Low hematological levels were probably due to deficiency of ceruloplasmin and cytochrome c oxidase, which are copper-dependent enzymes required for iron metabolism. Both copper deficiency and excess result in anemia. However, an excess of up to 12 ppm was less harmful than the absence of copper in the diet. As copper concentration in the control diet increases, nonenzymatic hemoglobin glycosylation decreases to about 6 ppm. An opposite effect is observed as copper concentration increases in the diet. A significant difference ( P < .05) between the two diets was observed in the hemoglobin and glycosylated hemoglobin levels. This suggests lower bioavailability of these minerals in a rice and beans diet.
AbstractList Iron deficiency anemia can be due to copper deficiency, even when iron intake is adequate. The objective of this study was to evaluate the interaction of copper with iron metabolism in anemic rats, using standard (copper and iron sulfate) or rice and beans diets containing the same iron concentration (24 ppm) but different levels of copper (2, 4, 6, or 12 ppm). A factorial model (2 x 4) was used together with a control treatment (0 ppm Cu, 24 ppm Fe), and the 9 treatments were randomly assigned to 8 blocks. The copper-iron interaction was evaluated by regression analysis. An increase in the levels of hemoglobin, hematocrit, and serum iron was observed with increased copper concentration, reaching a maximum value of about 6 ppm. Low hematological levels were probably due to deficiency of ceruloplasmin and cytochrome c oxidase, which are copper-dependent enzymes required for iron metabolism. Both copper deficiency and excess result in anemia. However, an excess of up to 12 ppm was less harmful than the absence of copper in the diet. As copper concentration in the control diet increases, nonenzymatic hemoglobin glycosylation decreases to about 6 ppm. An opposite effect is observed as copper concentration increases in the diet. A significant difference (P < .05) between the two diets was observed in the hemoglobin and glycosylated hemoglobin levels. This suggests lower bioavailability of these minerals in a rice and beans diet.
Iron deficiency anemia can be due to copper deficiency, even when iron intake is adequate. The objective of this study was to evaluate the interaction of copper with iron metabolism in anemic rats, using standard (copper and iron sulfate) or rice and beans diets containing the same iron concentration (24 ppm) but different levels of copper (2, 4, 6, or 12 ppm). A factorial model (2 × 4) was used together with a control treatment (0 ppm Cu, 24 ppm Fe), and the 9 treatments were randomly assigned to 8 blocks. The copper-iron interaction was evaluated by regression analysis. An increase in the levels of hemoglobin, hematocrit, and serum iron was observed with increased copper concentration, reaching a maximum value of about 6 ppm. Low hematological levels were probably due to deficiency of ceruloplasmin and cytochrome c oxidase, which are copper-dependent enzymes required for iron metabolism. Both copper deficiency and excess result in anemia. However, an excess of up to 12 ppm was less harmful than the absence of copper in the diet. As copper concentration in the control diet increases, nonenzymatic hemoglobin glycosylation decreases to about 6 ppm. An opposite effect is observed as copper concentration increases in the diet. A significant difference ( P < .05) between the two diets was observed in the hemoglobin and glycosylated hemoglobin levels. This suggests lower bioavailability of these minerals in a rice and beans diet.
Author Ramírez-Cárdenas, Lucía
Reis, Fernando Pinheiro
Costa, Neuza Maria Brunoro
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Issue 1
Keywords Rats
Iron
Bioavailability
Copper
Anemia
Vertebrata
Mammalia
Rat
Animal
Interaction
Rodentia
Metabolism
Language English
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Snippet Iron deficiency anemia can be due to copper deficiency, even when iron intake is adequate. The objective of this study was to evaluate the interaction of...
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SubjectTerms Anemia
animal models
Bioavailability
Biological and medical sciences
Copper
dietary minerals
enzyme activity
Feeding. Feeding behavior
ferroxidase
Fundamental and applied biological sciences. Psychology
hematocrit
heme iron
hemoglobin
Iron
iron deficiency anemia
NADH dehydrogenase
nutrient availability
nutrient deficiencies
nutrient-nutrient interactions
Rats
Vertebrates: anatomy and physiology, studies on body, several organs or systems
Title Copper-iron metabolism interaction in rats
URI https://www.clinicalkey.com/#!/content/1-s2.0-S0271531704001307
https://dx.doi.org/10.1016/j.nutres.2004.07.003
https://www.proquest.com/docview/47353514
Volume 25
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