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Biochemical Basis for Deoxyadenosine and 2-Chlorodeoxyadenosine Toxicity to Resting Human Lymphocytes

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Purine and Pyrimidine Metabolism in Man V

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 195B))

Abstract

An Inherited deficiency of adenosine deaminase (ADA; adenosine aminohydrolase EC 3, 5, 4, 4) results in a combined immunodeficiency disease (1). The selective lymphopenia seen in ADA deficient children has been attributed to the toxic effects of deoxyadenosine (dAdo) metabolites (2). Micromolar concentrations of dAdo are toxic in vitro to ADA-inhibited human resting peripheral blood lymphocytes (PBL). The ADA-resistent dAdo congener, 2-chlorodeoxyadenosine (CdA) is similarly cytotoxic to resting human T cells (3). Since the toxic mechanisms of dAdo have not been clearly elucidated, we have examined the metabolic changes that follow exposure of PBL to dAdo plus deoxycoformycin (dCF), as well as to CdA (4).

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© 1986 Plenum Press, New York

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Seto, S., Carrera, C.J., Wasson, D.B., Carson, D.A. (1986). Biochemical Basis for Deoxyadenosine and 2-Chlorodeoxyadenosine Toxicity to Resting Human Lymphocytes. In: Nyhan, W.L., Thompson, L.F., Watts, R.W.E. (eds) Purine and Pyrimidine Metabolism in Man V. Advances in Experimental Medicine and Biology, vol 195B. Springer, New York, NY. https://doi.org/10.1007/978-1-4684-1248-2_90

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  • DOI: https://doi.org/10.1007/978-1-4684-1248-2_90

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