NEW YORK (Reuters) -- The identification of a protein essential to iron uptake may help solve the scientific mystery surrounding iron metabolism, researchers say.
"This finding allows us to take a major step forward in our understanding of iron metabolism," said Dr. Michael Garrick, a researcher at the State University of New York Buffalo, and co-author of the study, which is published in the current issue of the Proceedings of the National Academy of Sciences.
Iron is essential to the transport of oxygen by blood cells. Iron deficiency, especially prevalent in the underdeveloped world, can cause fatigue, headaches, and breathlessness.
On the other hand, a condition known as hemochromatosis is due to excess iron in the blood, and is often treated through periodic bleeding of patients.
Scientists had long puzzled over just how iron is absorbed into, and transported within, body cells.
The Buffalo researchers studied the DNA of rats specially-bred to be iron-deficient. They discovered a mutation in a gene involved in the manufacture of a cellular protein called Nramp2.
Remarkably, study co-authors at Children's Hospital in Boston, Massachusetts, found an identical mutation in a species of mice, also bred for their tendency to anemia.
Inter-species coincidences like these are rare in genetics, leading the scientists to speculate that the mutation might occur in many mammals, and "human patients with congenital anemia might also harbor mutations in Nramp2."
Nramp2 is "the first known mammalian iron transporter to be characterized on a molecular level," the researchers say. They believe that the protein helps deliver iron to mitochondria, the cell's metabolic "power-plants." Nramp2 may also play a role in reducing the excess buildup of iron within the body, a condition that can lead to cirrhosis of the liver and heart damage.
The researchers say a previous study suggests that Nramp2 may also aid in the intracellular transport of other elements, including manganese, cobalt, and zinc.
SOURCE: Proceedings of the National Academy of Sciences (1998;95:1148-1153)
