American Journal of Clinical Nutrition, Vol 26, 657-672, Copyright © 1973 by The American Society for Clinical Nutrition, Inc.

Proposed role of copper-molybdenum interaction in iron-deficiency and iron-storage diseases

¹ Adjunct Associate Professor of Pharmacology, New York Medical College, New York, N.Y.; Research Associate in Pediatrics, Maimonides Medical Center, Brooklyn, N.Y.; and Physician in Charge: Nutrition Metabolism, Goldwater Memorial Hospital, New York University Medical Center, New York, N.Y. 10017

Iron-deficiency anemias that are associated with high plasma levels of copper include the anemias of pregnancy, rheumatoid arthritis, or infection. Iron-deficiency anemias that are associated with high hepatic levels of copper include the anemias of prematurity, cirrhosis, or hemochromatosis. Such conditions are associated with shortened erythrocyte survival time, as in sickle cell anemia, in which the erythrocytes have also been shown to have elevated copper levels. Other hemolytic disorders associated with copper poisoning, or with metabolic abnormalities, have similar erythrocyte dysfunctions.

There are animal studies that show that hepatic levels of molybdenum and xanthine oxidase are low in fetal and neonatal liver, and clinical evidence that patients with iron-deficiency anemia have low blood levels of molybdenum. Patients with cirrhosis or hemochromatosis have been shown to have low hepatic levels of xanthine oxidase. The available evidence thus points toward a high Cu/Mo ratio in diseases of iron deficiency and storage. The foregoing are speculations requiring experimental investigation.