Centre for Molecular Nanoscience, School of Chemistry, University of Leeds, Leeds, U.K.
Langmuir. 2012 Sep 4;28(35):12831-7. doi: 10.1021/la301771b. Epub 2012 Jul 17.
Understanding the interactions between nanoparticles (NPs) and biological matter is a high-priority research area because of the importance of elucidating the physical mechanisms underlying the interactions leading to NP potential toxicity as well as NP viability as therapeutic vectors in nanomedicine. Here, we use two model membrane systems, giant unilamellar vesicles (GUVs) and supported monolayers, to demonstrate the competition between adhesion and elastic energy at the nanobio interface, leading to different mechanisms of NP-membrane interaction relating to NP size. Small NPs (18 nm) cause a "freeze effect" of otherwise fluid phospholipids, significantly decreasing the phospholipid lateral mobility. The release of tension through stress-induced fracture mechanics results in a single microsize hole in the GUVs after interaction. Large particles (>78 nm) promote membrane wrapping, which leads to increased lipid lateral mobility and the eventual collapse of the vesicles. Electrochemical impedance spectroscopy on the supported monolayer model confirms that differently sized NPs interact differently with the phospholipids in close proximity to the electrode during the lipid desorption process. The time scale of these processes is in accordance with the proposed NP/GUV interaction mechanism.
理解纳米颗粒 (NPs) 和生物物质之间的相互作用是一个高度优先的研究领域,因为阐明导致 NP 潜在毒性的相互作用的物理机制以及 NPs 作为纳米医学中治疗载体的可行性至关重要。在这里,我们使用两种模型膜系统,即巨大的单分子层囊泡 (GUVs) 和支撑单层膜,来证明纳米生物界面处粘附和弹性能之间的竞争,导致与 NP 尺寸相关的不同 NP-膜相互作用机制。小 NPs(18nm)导致原本为流体的磷脂发生“冻结效应”,显著降低磷脂的侧向流动性。通过应力诱导的断裂力学释放张力会导致 GUV 中出现单个微尺寸孔。大颗粒(>78nm)促进膜包裹,导致脂质侧向流动性增加,最终导致囊泡崩溃。在支撑单层模型上的电化学阻抗谱证实,在脂质解吸过程中,不同尺寸的 NPs 以不同的方式与靠近电极的磷脂相互作用。这些过程的时间尺度与所提出的 NP/GUV 相互作用机制一致。