Biochemical Consequences of Treatment with the Adenosine Deaminase Inhibitor 2′-Deoxycoformycin
A congenital absence of the enzyme adenosine deaminase (ADA, EC 220.127.116.11) has been associated with profound T and B cell deficiencies in children, leading to immune dysfunction (1). Cohen et al (2) have demonstrated that ADA deficient children have elevated levels of 2′-deoxyadenosine triphosphate (dATP) in their erythrocytes. dATP is a known negative effector of the enzyme ribonucleotide reductase (3). In view of the finding that ADA activity is high in the blast cells of patients with T-cell acute lymphocytic leukaemia (4), an ADA inhibitor might well induce a selectively toxic event in the lymphoblast.
KeywordsAdenosine Deaminase Adenosine Deaminase Activity Triplicate Assay Adenosine Deaminase Deficiency Deoxyadenosine Triphosphate
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- 5.A. Boyum, Separation of leukocytes from blood and bone marrow, Scand. J. Clin. Lab. Investig. 21, supp. 97: 77 (1968).Google Scholar
- 10.K.R. Harrap and R.M. Paine, Use of a regulatory effector as a potential antitumour agent, Excerpta Medica, Characterisation and Treatment of Human Tumours 4: 239 (1978).Google Scholar