Orrenius S, Nicotera P
Klin Wochenschr. 1986;64 Suppl 7:138-41.
Molecular mechanisms involved in the development of toxic cell injury have attracted increased interest in recent years. In particular, the possible existence of a final common pathway in toxic cell killing has been addressed in a number of studies. Recent work from our laboratory suggests that a disruption of intracellular Ca2+ homeostasis may represent a common step in the development of toxic damage to hepatocytes, and that activation of Ca2+-dependent, neutral proteases by a sustained increase in cytosolic free Ca2+ concentration represents one mechanism by which toxic agents can kill hepatocytes.
近年来,毒性细胞损伤发生过程中涉及的分子机制已引起越来越多的关注。特别是,许多研究探讨了毒性细胞杀伤中可能存在最终共同途径的问题。我们实验室最近的研究表明,细胞内钙离子稳态的破坏可能是肝细胞毒性损伤发生过程中的一个共同步骤,而胞质游离钙离子浓度持续升高激活钙离子依赖性中性蛋白酶是毒性剂杀死肝细胞的一种机制。