Bernardi P, Scorrano L, Colonna R, Petronilli V, Di Lisa F
CNR Unit for the Study of Biomembranes, Department of Biomedical Sciences, University of Padova, Italy.
Eur J Biochem. 1999 Sep;264(3):687-701. doi: 10.1046/j.1432-1327.1999.00725.x.
Mitochondria are involved in cell death for reasons that go beyond ATP supply. A recent advance has been the discovery that mitochondria contain and release proteins that are involved in the apoptotic cascade, like cytochrome c and apoptosis inducing factor. The involvement of mitochondria in cell death, and its being cause or consequence, remain issues that are extremely complex to address in situ. The response of mitochondria may critically depend on the type of stimulus, on its intensity, and on the specific mitochondrial function that has been primarily perturbed. On the other hand, the outcome also depends on the integration of mitochondrial responses that cannot be dissected easily. Here, we try to identify the mechanistic aspects of mitochondrial involvement in cell death as can be derived from our current understanding of mitochondrial physiology, with special emphasis on the permeability transition and its consequences (like onset of swelling, cytochrome c release and respiratory inhibition); and to critically evaluate methods that are widely used to monitor mitochondrial function in situ.
线粒体参与细胞死亡的原因不仅仅在于提供ATP。最近的一项进展是发现线粒体含有并释放参与凋亡级联反应的蛋白质，如细胞色素c和凋亡诱导因子。线粒体在细胞死亡中的参与，以及它是原因还是结果，仍然是原位研究极其复杂的问题。线粒体的反应可能严重依赖于刺激的类型、强度以及最初受到干扰的特定线粒体功能。另一方面，结果还取决于难以剖析的线粒体反应的整合。在这里，我们试图从目前对线粒体生理学的理解中找出线粒体参与细胞死亡的机制方面，特别强调通透性转变及其后果（如肿胀的开始、细胞色素c的释放和呼吸抑制）；并严格评估广泛用于原位监测线粒体功能的方法。
