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The peroxidase–H₂O₂–iodide system is a critical antimicrobial mechanism of the innate immune system, primarily mediated by heme-containing peroxidases such as myeloperoxidase (MPO) and lactoperoxidase (LPO). This system functions by utilizing hydrogen peroxide (H₂O₂) to catalyze the oxidation of iodide ions (I⁻) into highly reactive iodine species, most notably hypoiodous acid (HOI) (Klebanoff, 1967). These reactive intermediates are potent oxidants that target and destroy a wide array of microbial cellular components, including membrane lipids, essential enzymes, and nucleic acids, providing broad-spectrum defense against bacteria, viruses, and fungi (Thomas & Fishman, 1986). In clinical contexts, this system is exploited in topical antiseptic formulations and is a subject of study in the management of infections in the oral cavity and respiratory tract. However, excessive or chronic activation of the system can lead to host tissue damage, linking it to the pathogenesis of inflammatory conditions such as atherosclerosis and cystic fibrosis (Klebanoff, 1999). Consequently, therapeutic strategies involve both the enhancement of this system for antimicrobial purposes and the use of specific peroxidase inhibitors to prevent collateral damage in chronic inflammatory diseases (Davies, 2011).
The system catalyzes the oxidation of iodide by hydrogen peroxide to produce hypoiodous acid and other reactive iodine species, which then non-specifically oxidize microbial proteins, lipids, and DNA, leading to cell death (Klebanoff, 1967; Thomas & Fishman, 1986).
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