Abstract
Several participants in this conference will discuss the physiological regulatory roles that adenosine (Ado) may serve, beyond its status as an intermediate in the interconversion of purine compounds. Along with others at this symposium, I have been primarily concerned with the nonphysiologic, cytotoxic effects of Ado and 2′-deoxy Ado (dAdo) that occur in vivo when their major route of metabolism, deamination, is blocked. Interest in the cytotoxic, and particularly the lymphocytotoxic, effects of these nucleosides stems from the discovery, made 10 years ago by Giblett and her colleagues [1], that genetic deficiency of Ado deaminase (ADA) is associated with selective depletion of lymphoid tissue, manifest clinically as severe combined immunodeficiency disease (SCID). In addition, there is now also considerable interest in the use of inhibitors of ADA, alone and in combination with Ado analogues such as adenine arabinoside (Ara-A), as rational therapies for lymphoproliferative diseases and as immunosuppressive agents.
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© 1983 Martinus Nijhoff Publishers, The Hague
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Hershfield, M.S. (1983). S-Adenosylhomocysteine Hydrolase as a Target in Genetic and Drug-Induced Deficiency of Adenosine Deaminase. In: Berne, R.M., Rall, T.W., Rubio, R. (eds) Regulatory Function of Adenosine. Developments in Pharmacology, vol 2. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-3909-0_11
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DOI: https://doi.org/10.1007/978-1-4613-3909-0_11
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