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_c, when the pore forms) is highly sensitive to lipid peroxidation. For example, ξ_c 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_c 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_c 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.

中文翻译：

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脂质过氧化对细胞膜对高速等双轴拉伸反应的影响：一项计算研究

对机械应力做出反应时，患病细胞膜和健康细胞膜之间的差异对于生物学以及医疗设备的开发至关重要。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然未知。在这项工作中，我们专注于脂质过氧化的患病细胞膜对高速拉伸载荷的反应。我们发现临界面积应变（ξ _c，当孔形成时）对脂质过氧化高度敏感。例如，在拉伸速度分别为 0.1 和 0.6 m/s 时，完全氧化的双层的ξ _c仅为未氧化双层的 64% 和 69%。ξ _c无论速度如何，都随着氧化脂质比率的增加而降低。此外，膜的临界断裂张力表现出类似的变化。很明显，氧化膜比正常膜更容易被高速拉伸破坏，这与实验结果一致。原因是过氧化作用在脂质尾部引入了极性基团，增加了尾部的亲水性，使尾部翘曲到膜-水界面，导致脂质尾部松散堆积和紊乱。这可以从每个脂质和顺序参数的面积变化中推断出来。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。_c值在膜成孔中的作用，分析拉伸速度、过氧化比和磷脂分子结构的影响。我们希望分子水平的信息对未来生物和医疗器械的发展有用。