Gu Lingzhi, Wei Tong, Zhou Mi, Yang Hong, Zhou Yang
Institute of Chemical Materials, China Academy of Engineering and Physics, Mianyang 621900, China.
CAS Key Laboratory of Mechanical Behavior and Design of Materials, Department of Modern Mechanics, University of Science and Technology of China, Hefei 230026, China.
J Phys Chem B. 2021 Sep 30;125(38):10736-10747. doi: 10.1021/acs.jpcb.1c05544. Epub 2021 Sep 15.
The difference between diseased and healthy cellular membranes in response to mechanical stresses is crucial for biology, as well as in the development of medical devices. However, the biomolecular mechanisms by which mechanical stresses interact with diseased cellular components remain largely unknown. In this work, we focus on the response of diseased cellular membranes with lipid peroxidation to high-speed tensile loadings. We find that the critical areal strain (ξ, when the pore forms) is highly sensitive to lipid peroxidation. For example, ξ of a fully oxidized bilayer is only 64 and 69% of the nonoxidized one at the stretching speed of 0.1 and 0.6 m/s, respectively. ξ decreases with the increase in the oxidized lipid ratio, regardless of the speeds. Also, the critical rupture tension of membranes exhibits a similar change. It is obvious that the oxidized membranes are more easily damaged than normal ones by high-speed stretching, which coincides with experimental findings. The reason is that peroxidation introduces a polar group to the tail of lipids, increases the hydrophilicity of tails, and warps the tails to the membrane-water interface, which causes loose accumulation and disorder of lipid tails. This can be deduced from the variation in the area per lipid and order parameter. In addition, the lowering stretching modulus and line tension of membranes (i.e., softening) after lipid peroxidation is also a significant factor. We reveal the difference between the peroxidized (diseased) and normal membrane in response to high-speed stretching, give the ξ value in the pore formation of membranes and analyze the influence of the stretching speed, peroxidation ratio, and molecular structure of phospholipids. We hope that the molecular-level information will be useful for the development of biological and medical devices in the future.
患病细胞膜与健康细胞膜在响应机械应力方面的差异，对生物学以及医疗设备的开发都至关重要。然而，机械应力与患病细胞成分相互作用的生物分子机制在很大程度上仍不为人知。在这项工作中，我们聚焦于脂质过氧化的患病细胞膜对高速拉伸载荷的响应。我们发现临界面应变（ξ，即孔形成时的应变）对脂质过氧化高度敏感。例如，在拉伸速度为0.1和0.6 m/s时，完全氧化双层膜的ξ分别仅为未氧化双层膜的64%和69%。无论速度如何，ξ都随氧化脂质比例的增加而降低。此外，膜的临界破裂张力也呈现类似变化。显然，高速拉伸时氧化膜比正常膜更容易受损，这与实验结果相符。原因是过氧化在脂质尾部引入了极性基团，增加了尾部的亲水性，并使尾部向膜 - 水界面弯曲，这导致脂质尾部堆积松散且无序。这可从每个脂质的面积和序参数的变化推导得出。此外，脂质过氧化后膜的拉伸模量和线张力降低（即软化）也是一个重要因素。我们揭示了过氧化（患病）膜与正常膜在响应高速拉伸方面的差异，给出了膜形成孔时的ξ值，并分析了拉伸速度、过氧化比例和磷脂分子结构的影响。我们希望这些分子层面的信息未来对生物和医疗设备的开发有用。
