Hydrogen peroxide (H2O2) is membrane-permeable and relatively stable, so it can diffuse away from the site of production (Winterbourn CC et al. 2006). Though H2O2 can permeate bacteria, it is unlikely to be directly bactericidal at the concentrations achieved in the phagosome. The derivatives of H2O2 such as hydroxyl radical (OH.) are far more reactive (Root RK & Metcalf JA 1977; Winterbourn CC et al. 2006). Hydroxyl radical is produced by interaction of free ferrous iron (Fe2+) with hydrogen peroxide (Fenton-like reaction). The increase of free Fe2+ concentration within the bacterial cell is associated with superoxide (O2.-) that oxidatively attacks iron-sulfur [4Fe-4S] clusters of dehydratases such that they release ferrous iron, which can then rapidly react with H2O2 (Liochev SI & Fridovich I 1994). Thus, H2O2 may damage dehydratases and kill bacteria by mechanisms in which site-directed Fenton chemistry targets vulnerable molecules in the bacterial cytosol and the bacterial DNA (Keyer K & Imlay JA 1996; Jang S & Imlay JA 2007).