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Membrane disruption is also thought to be a mechanism for Aβ-mediated cytotoxicity [24], [26].
It is unclear whether subtle membrane disruption is, in itself, a stressful enough event to cause cell death.
Another reason for this selective membrane disruption is the relatively high number of microvilli projections on tumor cells.
For disordered and highly charged peptides membrane disruption is obtained by other mechanisms, e.g., induction of a negative curvature strain, membrane thinning, or local packing defects associated with peptide localization primarily in the phospholipid polar headgroup region[7], [17], [47], [51], [52], [53].
The BPEIs do not cause membrane permeabilization, indicating that membrane disruption is not the primary mechanism of antimicrobial action.
Consistent with this interpretation, the degree of membrane disruption is reportedly dependent on the concentration of peptide adsorbed onto the negatively charged lipid membrane (Ringstad et al. 2007).
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Competent cross-membrane transport and membrane disruption were observed with a strong dependence on dendrimer size (generation), chemical structure, and composition of the model membranes [26, 53].
When both the SH-SY5H and RAW 264.7 cells were incubated with the MNP-PEI-PEG nanoparticles (Figure 6B1, B2), a small but constant (and significant p > 0.05) membrane disruption was evident.
This suggested that membrane disruption was a primary event rather than a consequence of swelling after failure of membrane ion pumps.
Plasma membrane disruption was detected by addition of the cell-impermeable DNA stain SYTOX Blue (5 µM) during or after photosensitization.
Additionally, basement membrane disruption was noted at both early and late stage disease, as shown by the loss of laminin staining in the G93A mice.
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