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首页> 外文会议>SPIE Conference on Energy-based Treatment of Tissue and Assessment >Hypothesis for thermal activation of the caspase cascade in apoptotic cell death at elevated temperatures
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Hypothesis for thermal activation of the caspase cascade in apoptotic cell death at elevated temperatures

机译：升高温度下凋亡细胞死亡中胱天蛋白酶级联热活化的假设

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Apoptosis is an especially important process affecting disease states from HIV-AIDS to auto-immune disease to cancer. A cascade of initiator and executioner capsase functional proteins is the hallmark of apoptosis. When activated the various caspases activate other caspases or cleave structural proteins of the cytoskeleton, resulting in "blebbing" of the plasma membrane forming apoptotic bodies that completely enclose the disassembled cellular components. Containment of the cytosolic components within the apoptotic bodies differentiates apoptosis from necroptosis and necrosis, both of which release fragmented cytosol and other cellular constituents into the intracellular space. Biochemical models of caspase activation reveal the extensive feedback loops characteristic of apoptosis. They clearly explain the failure of Arrhenius models to give accurate predictions of cell survival curves in hyperthermic heating protocols. Nevertheless, each of the individual reaction velocities can reasonably be assumed to follow Arrhenius kinetics. If so, the thermal sensitivity of the reaction velocity to temperature elevation is: ?k/?T = E_a [k/RT~2]. Particular reaction steps described by higher activation energies, E_a, are likely more thermally-sensitive than lower energy reactions and may initiate apoptosis in the absence of other stress signals. Additionally, while the classical irreversible Arrhenius formulation fails to accurately represent many cell survival and/or dye uptake curves - those that display an early stage shoulder region - an expanded reversible model of the law of mass action equation seems to prove effective and is directly based on a firm theoretical thermodynamic foundation.
机译：细胞凋亡是影响从艾滋病毒艾滋病疾病状态对癌症的疾病状态的重要过程。级联的引发剂和刽子手胶囊官能蛋白是细胞凋亡的标志。当激活各种胱天蛋糖时，激活胞胎骨架的其他胱糖或切割结构蛋白，导致质膜的“Blebbing”形成完全包围拆卸细胞组分的凋亡体。凋亡体内的细胞溶质组分区分凋亡和坏死的细胞凋亡，其中两者均匀释放碎裂的细胞溶质和其他细胞成分进入细胞内空间。 Caspase激活的生化模型揭示了细胞凋亡的广泛反馈循环特征。它们清楚地解释了阿列尼斯模型的失败，以便在高温加热方案中提供对细胞存活曲线的准确预测。然而，可以合理地假设每个单独的反应速度跟随Arhenius动力学。如果是，则反应速度与温度升高的热敏激素是：αk/Δt= e_a [k / rt〜2]。通过较高的活化能量，E_A描述的特定反应步骤，比较低的能量反应更热敏，并且可以在不存在其他应力信号时引发细胞凋亡。此外，虽然经典的不可抗拒的Arrhenius配方未能准确地代表许多细胞存活和/或染料吸收曲线 - 展示早期肩部区域的那些 - 大规模行动方程规律的扩展可逆模型似乎证明是有效的，直接基于论坚定的理论热力学基础。

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