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Bacterial and keratinocyte macromolecules and cell membranes represent a composite target for broad-spectrum, non-specific antiseptic agents such as povidone-iodine and chlorhexidine. These agents do not bind to a single specific receptor but instead interact with a wide array of cellular components, including proteins, enzymes, nucleic acids, and lipid bilayers (StatPearls, 2023). In pathogens, this non-specific attack leads to the denaturation of essential proteins and the disruption of the cell membrane, resulting in rapid microbial death and a low likelihood of resistance development (NCBI, 2022). However, because these agents lack specificity, they also interact with the macromolecules and membranes of host cells, such as keratinocytes and fibroblasts in the wound bed. This interaction can lead to host cell cytotoxicity, which may paradoxically delay the wound healing process by inhibiting re-epithelialization (PubMed, 2021). Consequently, while effective for antisepsis, the non-specific nature of these interactions requires a careful balance between antimicrobial efficacy and the preservation of regenerating host tissue.
The mechanism involves the non-specific oxidation of functional groups in proteins and nucleic acids, alongside the physical disruption of lipid bilayers, leading to the leakage of cellular contents and the cessation of metabolic activity (StatPearls, 2023; NCBI, 2022).
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