Abstract
Myeloperoxidase and activated granulocytes effect nucleic acid binding of a series of arylamines. Studies on the inhibition of such binding by azide has led to the proposal that arylamine activation in granulocytes occurs through multiple pathways, and that myeloperoxidase is not the principal cause. On the other hand, the phenolic substrate, acetaminophen, is activated primarily by this enzyme. The extensive nucleic acid binding of aniline approaches that seen for the potent carcinogen, 2-aminofluorene, which raises an important question concerning current methods for the prediction of chemical carcinogenicity.