Abstract
Alterations in outer membrane permeability caused by polycationic antibiotics (e.g. polymyxins) are caused by displacement of divalent cations by competition; on the other hand EDTA removes divalent cations by chelation and thus causes outer membrane perturbation [1]. A wide range of outer membrane permeabilisation events is mediated by polymyxin B: the uptake of hydrophobic fluorescent compounds and nitrocefin respectively is enhanced and rod like projections (i.e. formation of outer membrane blebs) is caused by polymyxin B (2–10). Furthermore polymyxins cause a release of soluble constituents from washed cells of P.aeruginosa; there was an optimum concentration of polymyxin for maximum release of cell constituents, higher concentrations inhibiting the release [11,12]. Interaction of polymyxin B with the divalent cation-binding sites on LPS and permeabilisation of the outer membranes of gram-negative bacteria is reversible upon addition of magnesium or potassium.
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