We postulate that the susceptibility of the flgE mutant to SP-A-mediated membrane permeabilization is due to its inability to assemble a flagellum.
Functional cellular studies with outer membrane-, cytoplasmembranerane vitality- and redox-specific fluorescence dyes revealed that the lethal effect of the isolated antimicrobial peptides is due to membrane permeabilization and inhibition of redox-driven bacterial respiration.
Plasma membrane permeabilization also triggers cell volume changes due to the so-called colloid osmotic mechanism [45], [48].
A very recent study suggests that the increased levels of sphingomyelin observed in Niemann Pick disease type A, cause lysosomal dysfunction due to lysosomal membrane permeabilization [ 65].
Importantly, our data show that killerFLIP-induced cell death is mostly due to direct plasma membrane permeabilization, not activation of apoptosis or necroptosis.
This may be due to amyloid forming peptides inducing membrane permeabilization by altering bilayer structure [21], [24], [25], [26], [27] or by forming unregulated pore-like structures [28].
Despite its somewhat lower membrane affinity, θp100 exhibited higher membrane permeabilization activity, a greater flip-flop rate, as well as more antimicrobial activity due to a higher pore formation rate compared with θp180.
Membrane studies using propidium iodide and bis- 1,3-dibutylbarbituric acid) trimethine oxonol [Dibis- 1,3-dibutylbarbituriche antifungal effect of l- and d-CopA3 was due to the membis- 1,3-dibutylbarbituric contracidwitrimethinen poxonoling apoptotic mechanism without membrane permeabilization.
On the other hand, viscotoxins A1, A2, A3, and 1-PS were cytotoxic to human lymphocytes, due the fact that they induce the production of reactive oxygen species (ROS) and cell membrane permeabilization [ 26].
