Control of apoptosis by the cellular ATP level

FEBS Letters

Franceschi, Claudio²  Schweizer, Matthias¹  Cossarizza, Andrea²  Richter, Christoph¹ 

[1] Laboratory of Biochemistry I, Swiss Federal Institute of Technology (ETH), Universitätstr. 16, CH-8092 Zürich, Switzerland;Department of Biomedical Sciences, University of Modena, I-41100 Modena, Italy

关键词: Mitochondria;    Reactive oxygen;    Nitric oxide;    Calcium;    Adenosine triphosphate;    Apoptosis;    ΔΨ;    mitochondrial membrane potential;    negative inside;    NAC;    N-acetylcysteine;    ROS;    reactive oxygen species;    TNF-α;    tumour necrosis factor-α;   

DOI  :  10.1016/0014-5793(95)01431-4

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Apoptosis is a physiological form of cell death. Its causes and execution mechanisms are not clearly understood. Oxidative stress, nitric oxide and its congeners, Ca²⁺, proteases, nucleases, and mitochondria are considered mediators of apoptosis. At present their importance and exact role are elusive but it is clear that mitochondria are both the target and the source of oxidative stress, nitric oxide, and Ca²⁺. The mitochondrial membrane potential (ΔΨ), which is the driving force for mitochondrial ATP synthesis, declines during apoptosis, and maintenance of ΔΨ prevents apoptosis. Since apoptosis is highly regulated and involves the activity of hydrolytic enzymes, chromatin condensation and vesicle formation apoptosis is likely to have a high energy demand. We propose that the cellular ATP level is an important determinant for cell death. This hypothesis is supported by circumstantial evidence, is consistent with the available data, has a corrolary in aging, and is amenable to direct experimental testing particularly with flow cytometry as a promising tool.

【 授权许可】

Unknown