Ineffective Hematopoiesis in Folate-Deficient Mice

A folate-free amino acid-based diet provided an opportunity to characterize the effects of folate depletion on growth, tissue folate levels, and hematopoiesis of mice under well-standardized conditions. Weanling mice were fed a folate-free, amino acid-based diet supplemented with either 0 or 2 mg fo...

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Bibliographic Details
Published in:Blood 1992-05, Vol.79 (9), p.2273-2280
Main Authors: Bills, N.D., Koury, M.J., Clifford, A.J., Dessypris, E.N.
Format: Article
Language:English
Subjects:
Anemia, Megaloblastic - etiology
Anemias. Hemoglobinopathies
Animals
Biological and medical sciences
Bone Marrow - pathology
Diseases of red blood cells
Female
Folic Acid Deficiency - blood
Folic Acid Deficiency - pathology
Folic Acid Deficiency - physiopathology
Hematologic and hematopoietic diseases
Hematopoiesis
Medical sciences
Mice
Spleen - pathology
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Summary:A folate-free amino acid-based diet provided an opportunity to characterize the effects of folate depletion on growth, tissue folate levels, and hematopoiesis of mice under well-standardized conditions. Weanling mice were fed a folate-free, amino acid-based diet supplemented with either 0 or 2 mg folic acid/kg diet for 35 to 48 days. Folate concentrations were decreased in liver, kidney, serum, and erythrocytes in mice fed the folate-free diet. The folate-deficient mice had anemia, reticulocytopenia, thrombocytopenia, and leukopenia, all of which reverted to normal after folic acid was reintroduced to the diet. Hematopoietic organs of folate-deficient mice had alterations that were similar to those seen in folate-deficient humans except that in mice, the hyperpla-sia of hematopoietic tissue occurred in the spleen rather than in the marrow. Ferrokinetic studies showed a normal 59Fe-transferrin half-life, but the percentage of 59Fe-incorporation into red blood cells at 48 hours was markedly subnormal. The number of committed hematopoietic progenitors at the stages of erythroid colony-forming units (CFUs), megakaryocyte CFUs, and granulocyte-macrophage CFUs were all increased in folate-deficient mice. However, the progeny of these progenitors was markedly decreased in folate-defi-cient mice. Thus, the folate-deficient mice had “ineffective hematopoiesis” leading to pancytopenia, and they therefore provide a murine model of megaloblastic anemia.
ISSN:0006-4971
1528-0020
DOI:10.1182/blood.V79.9.2273.2273