JAMA. 1944;126(1):31-32. doi:10.1001/jama.1944.02850360033011.
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During the course of the development of sulfonamide chemotherapy many theories have been propounded relative to the fundamental mode of action of these agents. A recent review by Henry1 discusses certain of the existing theories. Early belief that the sulfonamides stimulate the defensive powers of the host or inactivate bacterial toxins are, in light of present knowledge, rather questionable. The primary action of these drugs is now generally agreed to be on the bacteria themselves, and the important manifestation of this action is bacteriostasis. How then do the sulfonamides act on bacteria to inhibit their growth?

The assumption that the sulfonamides are oxidized in the body to their hydroxy derivatives led to the so-called anticatalase theory of their mode of action. This theory assumed that bacteria convert sulfonamides to hydroxy derivatives, which inhibit the enzyme catalase. The absence of this enzyme was supposed to allow the hydrogen peroxide from


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