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Article
October 5, 1970

Aggravation or Initiation of Megaloblastosis by Amino Acids in the Diet

Author Affiliations

From the Department of Medicine, Mount Sinai School of Medicine, New York, Veterans Administration Hospital, Bronx, NY, and the Department of Pathology, College of Physicians and Surgeons, Columbia University, New York.

JAMA. 1970;214(1):101-104. doi:10.1001/jama.1970.03180010043009
Abstract

Megaloblastosis is characterized morphologically by delayed nuclear maturation1 and biochemically by defective DNA synthesis.2 The megaloblast has a "young" nucleus apparently due to a reduction in the ability to double the amount of nuclear DNA (DNA synthesis phase) in order for the cell to divide. The lesion in DNA synthesis usually results from deficiency of vitamin B12 or folic acid or both. One pathway affected is concerned with the de novo synthesis of DNA thymine from deoxyuridylate (dUMP) (Fig 1).2,3 This involves the methylation of dUMP to thymidylate (dTMP) and requires 5,10-methylene-tetrahydrofolic acid, one of the reduced coenzymes of folate.4,5 In this pathway (Fig 1) there is interaction of vitamin B12, folic acid, and pyridoxine, each of which may correct megaloblastic anemia. Since the dietary amino acids methionine, homocysteine, serine, and glycine are involved in production of DNA thymine, derangements in the availability of

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