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Microbial cell membranes and proteins serve as the primary targets for the antiseptic povidone-iodine (PVP-I), which exhibits broad-spectrum activity against bacteria, fungi, viruses, and protozoa (Bigliardi et al., 2017). The mechanism involves the slow release of free iodine from the povidone polymer, which then acts as a powerful oxidizing agent that penetrates the microbial cell wall (McDonnell & Russell, 1999). Once internalized, iodine reacts with the thiol groups of amino acids like cysteine and methionine, as well as with nucleotides and fatty acids, leading to the denaturation of essential enzymes and structural proteins (Barreto et al., 2014). This non-specific, multi-targeted disruption of the cell membrane and internal metabolic machinery results in rapid microbial death and prevents the development of resistance (Eggers, 2019). PVP-I is a cornerstone in clinical practice for surgical site preparation, wound management, and infection control due to its efficacy and safety profile (StatPearls, 2023). However, clinicians must monitor for potential systemic iodine absorption, which can lead to thyroid dysfunction or metabolic disturbances in susceptible populations (NIH PubChem).
Povidone-iodine acts by releasing free iodine, which serves as a powerful oxidizing agent that penetrates microbial cell walls. It reacts with functional groups of proteins (specifically thiol groups in cysteine and methionine), nucleotides, and fatty acids, leading to protein denaturation, inhibition of essential enzymes, and loss of membrane integrity, ultimately resulting in rapid microbial death (McDonnell & Russell, 1999; Bigliardi et al., 2017).
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