Several investigators have reported experiments which demonstrated biological antagonisms. between certain acridine derivatives and various nucleotides. McIlwain (1) observed the reversal by nucleotides of the inhibition of growth of Escherichia coli and Streptococcus hemolyticus by proflavine and euflavine. Similar results were obtained by Martin and Fisher with Staphylococcus aureus (2). Lewis and Goland reported (3) that the addition of nucleotides to the diet counteracted in part the inhibitory effect of certain acridines upon the growth of sarcomas and carcinomas in mice. Bovarnick et al.(4) observed that the quinacrinel inhibition of oxygen uptake by substrate-depleted Plasmodium lophurae can be prevented partly or completely by adenylic acid (AMP) or adenosinetriphosphate (ATP). Madinaveitia and Raventos (5) demonstrated that quinacrine antagonizes the action of adenosine on guinea pig heart and on the cecum of the hen. Green and Stoner (6, 7) found that quinacrine had considerable effect in counteracting the condition of simulated traumatic shock which can be produced in animals by the injection of AMP or ATP. Several investigators(14) have concluded that the effects of acridine derivatives probably are attributable to a competition of these compounds with AMP or ATP for some essential enzymatic system. However, in two papers (1, 2) the possibility that certain acridines might function, at least in part, by forming complexes with nucleotides was also suggested. Little direct evidence for such complexes was presented other than a report (1) that nucleotides caused partial quenching of the fluorescence of proflavine.

In the present paper evidence for the reversible interaction of quinacrine with nucleotides is presented, and the association exponents are evaluated by partition equilibrium. The data indicate that some of the biological antagonisms between quinacrine and various adenine nucleotides probably cannot be attributed to the formation of complexes between these