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Previous Volume 341:1986-1995 December 23, 1999 Number 26 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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Iron has the capacity to accept and donate electrons readily, interconverting between ferric (Fe²⁺) and ferrous (Fe³⁺) forms. This capability makes it a useful component of cytochromes, oxygen-binding molecules (i.e., hemoglobin and myoglobin), and many enzymes. However, iron can also damage tissues by catalyzing the conversion of hydrogen peroxide to free-radical ions that attack cellular membranes, proteins, and DNA. Proteins sequester iron to reduce this threat. Iron ions circulate bound to plasma transferrin and accumulate within cells in the form of ferritin. Iron protoporphyrin (heme) and iron–sulfur clusters serve as enzyme cofactors. Under normal circumstances, only trace amounts . . . [Full Text of this Article]

Physiology of Iron Transport

Distribution of Iron

Regulation of Iron Absorption

Diseases of Iron Deficiency

Iron-Deficiency Anemia

Anemia of Chronic Inflammation

Diseases of Iron Overload

Hereditary Hemochromatosis

Hemochromatosis Not Attributable to Mutations in HFE

African Iron Overload

Juvenile Hemochromatosis

Neonatal Hemochromatosis

Aceruloplasminemia

Transfusional Siderosis

Source Information

From the Howard Hughes Medical Institute, Department of Pediatrics, Harvard Medical School, and the Division of Hematology and Oncology, Children's Hospital — both in Boston.

Address reprint requests to Dr. Andrews at Children's Hospital, Enders 720, 300 Longwood Ave., Boston, MA 02115, or at nandrews@rascal.med.harvard.edu.

References

Related Letters:

Disorders of Iron Metabolism
Andrews P. A., Green R., Conrad M. E., Umbreit J. N., Andrews N. C.
Extract | Full Text  
N Engl J Med 2000; 342:1293-1294, Apr 27, 2000. Correspondence

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