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Cell and bacterial membranes are essential lipid bilayers that define cellular boundaries and maintain the internal environment of all living organisms [6, 14]. In antimicrobial therapy, the bacterial membrane serves as a vital target for drugs like polymyxins and daptomycin, which disrupt its structural integrity or electrical potential [1, 3, 4]. These drugs often distinguish between bacterial and host membranes by targeting specific components like lipopolysaccharides or negatively charged phospholipids that are more prevalent in microbes [3, 4, 12]. Disruption of the membrane leads to the formation of pores, leakage of intracellular ions such as potassium, and eventual cell lysis [3, 5]. Beyond infection, the cell membrane is increasingly recognized as a target in oncology, where differences in membrane fluidity and charge in cancer cells are exploited by therapeutic peptides [6, 12]. However, the high degree of structural similarity between various biological membranes often leads to significant safety concerns, including nephrotoxicity and neurotoxicity [2, 5, 7]. Additionally, the cell membrane acts as a critical reservoir for many lipophilic drugs, influencing their distribution and duration of action [14, 17]. Understanding the biophysical interactions at the membrane interface is therefore crucial for both drug efficacy and the mitigation of adverse effects [7, 11].
Disruption of membrane integrity, pore formation, depolarization of the membrane potential, and alteration of lipid bilayer fluidity, leading to leakage of intracellular contents and cell death.
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