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Increased Level of Ribonucleotide Reductase in Deoxyadenosine Resistant Adenosine Deaminase Deficient Human Histiocytic Lymphoma Cells

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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))

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Abstract

Inherited deficiencies of the two enzymes of purine metabolism, adenosine deaminase and purine nucleoside Phosphorylase, cause severe immunodeficiency disease in humans (1). The mechanisms by which deoxynucleosides exert their cytotoxic effects are not fully understood but the importance of the conversion of deoxyribonucleosides to their corresponding nucleotides stems from the observation that it is the deoxyribonucleoside triphosphates that are cytotoxic. The harmful effects of deoxyadenosine, deoxyguanosine and thymidine are apparently caused by inhibition of ribonucleotide reductase (2-5). The accumulation of high intracellular pools of one of the effector substances, i.e. dATP, dGTP and dTTP, will lead to interference with the de novo synthesis of the other deoxyribonucleotides, essential for DNA-synthesis.

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© 1986 Plenum Press, New York

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Dahbo, Y., Carson, D., Eriksson, S. (1986). Increased Level of Ribonucleotide Reductase in Deoxyadenosine Resistant Adenosine Deaminase Deficient Human Histiocytic Lymphoma Cells. 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_35

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  • DOI: https://doi.org/10.1007/978-1-4684-1248-2_35

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  • Publisher Name: Springer, New York, NY

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  • Online ISBN: 978-1-4684-1248-2

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