Control of apoptosis by the cellular ATP level

被引:450
作者
Richter, C [1 ]
Schweizer, M [1 ]
Cossarizza, A [1 ]
Franceschi, C [1 ]
机构
[1] UNIV MODENA,DEPT BIOMED SCI,I-41100 MODENA,ITALY
关键词
mitochondria; reactive oxygen; nitric oxide; calcium; adenosine triphosphate; apoptosis;
D O I
10.1016/0014-5793(95)01431-4
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
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(Delta psi), which is the driving force for mitochondrial ATP synthesis, declines during apoptosis, and maintenance of Delta psi 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.
引用
收藏
页码:107 / 110
页数:4
相关论文
共 62 条
[41]   ALTERATIONS IN MITOCHONDRIAL STRUCTURE AND FUNCTION ARE EARLY EVENTS OF DEXAMETHASONE-INDUCED THYMOCYTE APOPTOSIS [J].
PETIT, PX ;
LECOEUR, H ;
ZORN, E ;
DAUGUET, C ;
MIGNOTTE, B ;
GOUGEON, ML .
JOURNAL OF CELL BIOLOGY, 1995, 130 (01) :157-167
[42]   APOPTOSIS INDUCED BY IL-2 WITHDRAWAL IS ASSOCIATED WITH AN INTRACELLULAR ACIDIFICATION [J].
REBOLLO, A ;
GOMEZ, J ;
DEARAGON, AM ;
LASTRES, P ;
SILVA, A ;
PEREZSALA, D .
EXPERIMENTAL CELL RESEARCH, 1995, 218 (02) :581-585
[43]   PRO-OXIDANTS AND MITOCHONDRIAL CA2+ - THEIR RELATIONSHIP TO APOPTOSIS AND ONCOGENESIS [J].
RICHTER, C .
FEBS LETTERS, 1993, 325 (1-2) :104-107
[44]   OXIDATIVE STRESS IN MITOCHONDRIA - ITS RELATIONSHIP TO CELLULAR CA-2+ HOMEOSTASIS, CELL-DEATH, PROLIFERATION, AND DIFFERENTIATION [J].
RICHTER, C ;
KASS, GEN .
CHEMICO-BIOLOGICAL INTERACTIONS, 1991, 77 (01) :1-23
[45]   NITRIC-OXIDE KILLS HEPATOCYTES BY MOBILIZING MITOCHONDRIAL CALCIUM [J].
RICHTER, C ;
GOGVADZE, V ;
SCHLAPBACH, R ;
SCHWEIZER, M ;
SCHLEGEL, J .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1994, 205 (02) :1143-1150
[46]  
SCHANNE FA, 1979, SCIENCE, V206, P699
[47]   SENSITIVITY OF MITOCHONDRIAL PEPTIDYL-PROLYL CIS-TRANS-ISOMERASE, PYRIDINE-NUCLEOTIDE HYDROLYSIS AND CA2+ RELEASE TO CYCLOSPORINE-A AND RELATED-COMPOUNDS [J].
SCHWEIZER, M ;
SCHLEGEL, J ;
BAUMGARTNER, D ;
RICHTER, C .
BIOCHEMICAL PHARMACOLOGY, 1993, 45 (03) :641-646
[48]   NITRIC-OXIDE POTENTLY AND REVERSIBLY DEENERGIZES MITOCHONDRIA AT LOW-OXYGEN TENSION [J].
SCHWEIZER, M ;
RICHTER, C .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1994, 204 (01) :169-175
[49]  
SHAPIRO HM, 1995, PRACTICAL FLOW CYTOM, P329
[50]   PREVENTION OF HYPOXIA-INDUCED CELL-DEATH BY BCL-2 AND BCL-XL [J].
SHIMIZU, S ;
EGUCHI, Y ;
KOSAKA, H ;
KAMIIKE, W ;
MATSUDA, H ;
TSUJIMOTO, Y .
NATURE, 1995, 374 (6525) :811-813