Deficiency purine nucleotide formation

In muscle, a unique nucleotide reutilization pathway, known as the purine nucleotide cycle, uses three enzymes myoadenylate deaminase, adenylosuccinate synthetase, and adenylosuccinate lyase. In this cycle, AMP is converted to IMP with formation of NH3, and IMP is then reconverted to AMP. Myoadenylate deaminase deficiency produces a relatively benign disorder of muscle... 

The formation of IMP may provide a means by which the intracellular purine nucleotide pool is maintained. AMP deaminase deficiency disrupts the purine... 

Aminobenzamide (SAB), an inhibitor of ADP-ribosyl transferase, also affects de novo purine biosynthesis, demonstrated by an inhibition of incorporation of radiolabel from glucose, methionine and formate into the DNA (1-3). The step(s) affected have not been identified. Mutant ceU lines, deficient in salvage nucleotide synthesis, are no more sensitive to SAB than wild-type (4). Also, there is no effect of SAB on dNTP pool sizes (2, 5). These data indicate that the effect of SAB on de novo purine biosynthesis is not normally rate-limiting. Other effects of SAB include inhibition of cell growth and inhibition of adenosine transport (5). 

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