Benzalkonium chloride accelerates the formation of the amyloid fibrils of corneal dystrophy-associated peptides.

摘要: Corneal dystrophies are genetic disorders resulting in progressive corneal clouding due to the deposition of amyloid fibrils derived from keratoepithelin, also called transforming growth factor β-induced protein (TGFBI). The formation is often accelerated by surfactants such as sodium dodecyl sulfate (SDS). Most eye drops contain benzalkonium chloride (BAC), a cationic surfactant, preservative substance. In present study, we aimed reveal role BAC fibrillation keratoepithelin-derived peptides vitro. We used three types 22-residue synthetic covering Leu110-Glu131 keratoepithelin sequence: an R-type peptide with wild-type R124, C-type C124 associated lattice dystrophy type I, and H-type H124 granular II. time courses spontaneous seed-dependent fibril elongation were monitored presence various concentrations or SDS using thioflavin T fluorescence. all absence seeds. Optimal acceleration occurred near CMC, which suggests that unstable dynamic interactions amphipathic led fibrils. These results suggest containing may deteriorate those without preferred especially for patients dystrophies.