The potential for generation of H₂O₂ (a key component of the iodinating system) of all the normal cells studied, gauged by their content of cyanide-insensitive NADH oxidase, seemed comparable. Peroxidase levels varied widely, and were highest in PMN and almost undetectable in MAC. Catalase was at negligible levels in all the cell types obtained from mice. The fixation of ¹³¹I by phagocytes ingesting ¹⁴C-labeled dead tubercle bacilli appeared to be primarily a function of the cellular peroxidase content. Thus, mouse macrophages, with virtually no peroxidase, displayed no fixation of iodide. PMN proved far more able to fix ¹³¹I during phagocytosis than did MN. In experiments comparing PMN from normal human subjects and from children with chronic granulomatous disease (CGD), a sex-linked condition characterized by a deficiency of H₂O₂ production during phagocytosis and low microbicidal activity, the iodination ratio of CGD cells was dramatically less than that of normal PMN (by about two orders of magnitude). Capacity for iodination was correlated with bactericidal activity toward E. coli.

At low bacterial loads (ca. 5:1), phagocytes killed efficiently, and little discrepancy in ability among cell types was apparent. Under the stress of higher loads of ¹⁴C-labeled E. coli (ca. 100:1), differences in bactericidal activity were exaggerated, and a substantial disparity between MN and PMN was observed in favor of the latter. The hierarchy for killing efficiencies therefore agreed with that for iodination, with one notable exception: mouse MAC were consistently competent in their killing activity, more so than MN, even though they virtually lack peroxidase and the ability to iodinate ingested bacteria.