Abstract

Aluminium oxide nanoparticles (Al2O3 NPs) potentially cause health hazards after their release into the environment. The crystalline phase of Al2O3 NPs determines their surface structure and the number of functional groups. The adsorption of natural organic matter (NOM) or biomolecules on the surface Al2O3 NPs also alters their surface properties and subsequent interactions with organisms. In this study, the roles of the Al2O3 crystalline phase and the surface coating of the nanoparticles on the membrane integrity and fluidity were investigated. Giant and small unilamellar vesicles (GUVs and SUVs) were prepared as model cell membranes to detect membrane disruption after exposure to Al2O3 NPs. Due to amorphous structure and high surface activity of γ-Al2O3 NPs, they had a stronger affinity with the membrane and caused more serious membrane rupture than that of α-Al2O3 NPs. The deposition of Al2O3 NPs on the membrane and the induced membrane disruption were monitored by a quartz crystal microbalance with dissipation (QCM-D) method. HA-coated Al2O3 NPs disrupted the SUV layer on the QCM-D sensor, while BSA-coated Al2O3 NPs only adhered to the membrane and induced unremarkable vesicle disruption. In addition, untreated γ-Al2O3 NPs induced remarkable gelation of a negatively charged membrane, but other types of Al2O3 NPs caused negligible membrane phase changes. The outcomes of this study demonstrate that the crystalline phase of the Al2O3 NPs affects the integrity and fluidity of cell membranes. The protein coatings on the NPs weaken the NP-membrane interaction, while HA coatings increase the damage of the NP-induced interaction.

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