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首页> 外文会议>Energy-based treatment of tissue and assessment VII >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：高温下凋亡细胞死亡中胱天蛋白酶级联反应热激活的假说

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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: (e)k/(e)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：细胞凋亡是一个特别重要的过程，会影响从HIV / AIDS到自身免疫疾病再到癌症的疾病状态。引发剂和execution子糖酶功能蛋白的级联反应是细胞凋亡的标志。当被激活时，各种半胱天冬酶激活其他半胱天冬酶或切割细胞骨架的结构蛋白，导致质膜“起泡”，形成凋亡体，该凋亡体完全包围分解的细胞成分。凋亡小体中包含的胞质成分可将细胞凋亡与坏死病和坏死区分开，两者均将碎片化的胞浆和其他细胞成分释放到细胞内空间。 caspase激活的生化模型揭示了凋亡的广泛反馈回路。他们清楚地解释了Arrhenius模型的失败，无法给出高温加热方案中细胞存活曲线的准确预测。但是，可以合理地假定每个单独的反应速度都遵循Arrhenius动力学。如果是这样，则反应速度对温度升高的热敏感性为：（e）k /（e）T = E_a [k / RT〜2]。由较高的活化能E_a描述的特定反应步骤可能比较低能量的反应对热更敏感，并且在不存在其他应激信号的情况下可能引发凋亡。此外，虽然经典的不可逆Arrhenius公式无法准确表示许多细胞存活和/或染料吸收曲线（显示早期肩部区域的曲线），但扩展的可逆质量作用方程模型似乎证明是有效的，并且是直接基于在坚实的理论热力学基础上。

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