2’-deoxyadenosine inhibits the growth of human colon-carcinoma cell lines and is found to be associated with purine nucleoside phosphorylase (PNP) deficiency.
In the absence of deoxycoformycin, 2’-deoxyadenosine is primarily deaminated to 2’-deoxyinosine and then converted into hypoxanthine. In the presence of the inhibitor, the deoxynucleoside, in addition to a phosphorylation process, undergoes phosphorolytic cleavage giving rise to adenine. The conversion of 2’-deoxyadenosine to adenine might represent a protective device, emerging when the activity of adenosine deaminase is reduced or inhibited. There is much evidence to indicate that the enzyme catalyzing this processs may be distinct from methylthioadenosine phosphorylase and S-adenosyl homocysteine hydrolase, which are the enzymes reported to be responsible for the formation of adenine from 28-deoxyadenosine in mammals[1].
References:
[1]. Bemi V, et al. Deoxyadenosine metabolism in a human colon-carcinoma cell line (LoVo) in relation to its cytotoxic effect in combination with deoxycoformycin. Int J Cancer. 1998 Mar 2;75(5):713-20.