The cellular energy crisis: Mitochondria and cell death

Medicine and Science in Sports and Exercise

Volumn 35, Issue 1, 2003, Pages 105-110

  Waterhouse, Nigel J ^a  

^a PETER MACCALLUM CANCER CENTRE   (Australia)

Author keywords

ATP; BCL 2; Cytochrome c; Mitochondrial membrane potential; Outer membrane permeabilization; Review

Indexed keywords

ADENOSINE TRIPHOSPHATE; CYTOCHROME C; PROTEIN BCL 2;

APOPTOSIS; CELL DEATH; CONFERENCE PAPER; ENERGY BALANCE; HUMAN; MEMBRANE PERMEABILITY; MEMBRANE POTENTIAL; MITOCHONDRIAL MEMBRANE; MITOCHONDRIAL RESPIRATION; MOLECULAR DYNAMICS; NONHUMAN; OXIDATIVE PHOSPHORYLATION; SIGNAL TRANSDUCTION;

ANIMALS; APOPTOSIS; BCL-2 HOMOLOGOUS ANTAGONIST-KILLER PROTEIN; BCL-2-ASSOCIATED X PROTEIN; CASPASES; CYTOCHROME C GROUP; ENERGY METABOLISM; HUMANS; MEMBRANE PROTEINS; MITOCHONDRIA; MITOCHONDRIAL PROTEINS; PROTO-ONCOGENE PROTEINS; PROTO-ONCOGENE PROTEINS C-BCL-2;

EID: 0037232688     PISSN: 01959131     EISSN: None     Source Type: Journal    
DOI: 10.1097/00005768-200301000-00017     Document Type: Conference Paper

References (53)

1. AMARANTE-MENDES, G. P., D. M. FINUCANE, S. J. MARTIN, T. G. COTTER, G. S. SALVESEN, and D. R. GREEN. Anti-apoptotic oncogenes prevent caspase-dependent and independent commitment for cell death. Cell Death Differ. 5:298-306, 1998.
2. BEERE, H. M., B. B. WOLF, K. CAIN, et al. Heat-shock protein 70 inhibits apoptosis by preventing recruitment of procaspase-9 to the Apaf-1 apoptosome. Nat. Cell Biol. 2:469-475, 2000.
3. BOSSY-WETZEL, E., D. D. NEWMEYER, and D. R. GREEN. Mitochondrial cytochrome c release in apoptosis occurs upstream of DEVD- specific caspase activation and independently of mitochondrial transmembrane depolarization. EMBO J. 17:37-49, 1998.
4. BROWN, D. G., X. M. SUN, and G. M. COHEN. Dexamethasone- induced apoptosis involves cleavage of DNA to large fragments prior to internucleosomal fragmentation. J. Biol. Chem. 268:3037-3039, 1993.
5. DARMON, A. J., T. J. LEY, D. W. NICHOLSON, and R. C. BLEACKLEY. Cleavage of CPP32 by granzyme B represents a critical role for granzyme B in the induction of target cell DNA fragmentation. J. Biol. Chem. 271:21709-21712, 1996.
6. DAVIS, J. E., V. R. SUTTON, M. J. SMYTH, and J. A. TRAPANI. Dependence of granzyme B-mediated cell death on a pathway regulated by Bcl-2 or its viral homolog, BHRF1. Cell Death Differ. 7:973-983, 2000.
7. DE GIORGI, F., L. LARTIGUE, and F. ICHAS. Electrical coupling and plasticity of the mitochondrial network. Cell Calcium 28:365-370, 2000.
8. DESHMUKH, M., K. KUIDA, and E. M. JOHNSON, JR. Caspase inhibition extends the commitment to neuronal death beyond cytochrome c release to the point of mitochondrial depolarization. J. Cell Biol. 150:131-143, 2000.
9. DU, C., M. FANG, Y. LI, L. LI, and X. WANG, SMAC, a mitochondrial protein that promotes cytochrome c-dependent caspase activation by eliminating IAP inhibition. Cell 102:33-42, 2000.
10. EKERT, P. G., J. SILKE, and D. L. VAUX. Caspase inhibitors. Cell Death Differ. 6:1081-1086, 1999.
11. FADOK, V. A., D. L. BRATTON, D. M. ROSE, A. PEARSON, R. A. EZEKEWITZ, and P. M. HENSON. A receptor for phosphatidylserine- specific clearance of apoptotic cells. Nature 405:85-90, 2000.
12. FEHRENBACH, E., and H. NORTHOFF. Free radicals, exercise, apoptosis, and heat shock proteins. Exerc. Immunol. Rev. 7:66-89, 2001.
13. FINUCANE, D. M., E. BOSSY-WETZEL, N. J. WATERHOUSE, T. G. COTTER, and D. R. GREEN. Bax-induced caspase activation and apoptosis via cytochrome c release from mitochondria is inhibitable by Bcl-xL. J. Biol Chem. 274:2225-2233, 1999.
14. GOLDSTEIN, J. C., N. J. WATERHOUSE, P. JUIN, G. I. EVAN, and D. R. GREEN. The coordinate release of cytochrome c during apoptosis is rapid, complete and kinetically invariant. Nat. Cell Biol. 2:156-162, 2000.
15. GREIDINGER, E. L., D. K. MILLER, T. T. YAMIN, L. CASCIOLA-ROSEN, and A. ROSEN. Sequential activation of three distinct ICE-like activities in Fas-ligated Jurkat cells. FEBS Lett. 390:299-303, 1996.
16. HEIBEIN, J. A., M. BARRY, B. MOTYKA, and R. C. BLEACKLEY. Granzyme B-induced loss of mitochondrial inner membrane potential (Delta Psi m) and cytochrome c release are caspase independent. J. Immunol. 163:4683-4693, 1999.
17. HONARPOUR, N., C. Du, J. A. RICHARDSON, R. E. HAMMER, X. WANG, and J. HERZ, Adult Apaf-1-deficient mice exhibit male infertility. Dev. Biol. 218:248-258, 2000.
18. KORSMEYER, S. J., M. C. WEI, M. SAITO, S. WEILER, K. J. OH, and P. H. SCHLESINGER. Pro-apoptotic cascade activates BID, which oligomerizes BAK or BAX into pores that result in the release of cytochrome c. Cell Death Differ. 7:1166-1173, 2000.
19. LEIST, M., B. SINGLE, A. F. CASTOLDI, S. KUHNLE, and P. NICOTERA. Intracellular adenosine triphosphate (ATP) concentration: a switch in the decision between apoptosis and necrosis. J. Exp. Med. 185:1481-1486, 1997.
20. LI, H., H. ZHU, C. J. XU, and J. YUAN. Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway of apoptosis. Cell 94:491-501, 1998.
21. LIM, M. L., T. MINAMIKAWA, and P. NAGLEY. The protonophore CCCP induces mitochondrial permeability transition without cytochrome c release in human osteosarcoma cells. FEBS Lett. 503:69-74, 2001.
22. LIN, Y. S., H. L. Kuo, C. F. Kuo, S. T. WANG, B. C. YANG, and H. I. CHEN. Antioxidant administration inhibits exercise-induced thymocyte apoptosis in rats. Med. Sci. Sports Exerc. 31:1594-1598, 1999.
23. LINDSTEN, T., A. J. Ross, A. KING, et al. The combined functions of proapoptotic Bcl-2 family members bak and bax are essential for normal development of multiple tissues. Mol. Cell. 6:1389-1399, 2000.
24. MARCHETTI, P., M. CASTEDO, S. A. SUSIN, et al. Mitochondrial permeability transition is a central coordinating event of apoptosis. J. Exp. Med. 184:1155-1160, 1996.
25. MARTIN, S. J., D. M. FINUCANE, G. P. AMARANTE-MENDES, G. A. O'BRIEN, and D. R. GREEN. Phosphatidylserine externalization during CD95-induced apoptosis of cells and cytoplasts requires ICE/CED-3 protease activity. J. Biol. Chem. 271:28753-28756, 1996.
26. MARTINOU, I., S. DESAGHER, R. ESKES, et al. The release of cytochrome c from mitochondria during apoptosis of NGF-deprived sympathetic neurons is a reversible event. J. Cell Biol. 144:883-889, 1999.
27. MARZO, I., C. BRENNER, N. ZAMZAMI, et al. The permeability transition pore complex: a target for apoptosis regulation by caspases and bcl-2-related proteins. J. Exp. Med. 187:1261-1271, 1998.
28. MATSUYAMA, S., J. LLOPIS, Q. L. DEVERAUX, R. Y. TSIEN, and J. C. REED. Changes in intramitochondrial and cytosolic pH: early events that modulate caspase activation during apoptosis. Nat. Cell Biol. 2:318-325, 2000.
29. MINAMIKAWA, T., D, A. WILLIAMS, D. N. BOWSER, and P. NAGLEY. Mitochondrial permeability transition and swelling can occur reversibly without inducing cell death in intact human cells. Exp. Cell Res, 246:26-37, 1999.
30. MUCHMORE, S. W., M. SATTLER, H. LIANG, et al. X-ray and NMR structure of human Bcl-xL, an inhibitor of programmed cell death. Nature 381:335-341, 1996.
31. NECHUSHTAN, A., C. L. SMITH, I. LAMENSDORF, S. H. YOON, and R. J. YOULE. Bax and Bak coalesce into novel mitochondria-associated clusters during apoptosis. J. Cell Biol. 153:1265-1276, 2001.
32. PINKOSKI, M. J., N. J. WATERHOUSE, J. A. HEIBEIN, et al. Granzyme B-mediated apoptosis proceeds predominantly through a Bcl-2-inhibitable mitochondrial pathway. J. Biol. Chem. 276:12060-12067, 2001.
33. SARIN, A., M. S. WILLIAMS, M. A. ALEXANDER-MILLER, J. A. BERZOFSKY, C. M. ZACHARCHUK, and P. A. HENKART. Target cell lysis by CTL granule exocytosis is independent of ICE/Ced-3 family proteases. Immunity 6:209-215, 1997.
34. SCAFFIDI, C., S. FULDA, A. SRINIVASAN, et al. Two CD95 (APO-1/ Fas) signaling pathways. EMBO J. 17:1675-1687, 1998.
35. SCHENDEL, S. L., R. AZIMOV, K. PAWLOWSKI, A. GODZIK, B. L. KAGAN, and J. C. REED. Ion channel activity of the BH3 only Bcl-2 family member, BID. J. Biol. Chem. 274:21932-21936, 1999.
36. SCHENDEL, S. L., M. MONTAL, and J. C. REED. Bcl-2 family proteins as ion-channels. Cell Death Differ. 5:372-380, 1998.
37. SCHLESINGER, P. H., A. GROSS, X. M. YIN, et al. Comparison of the ion channel characteristics of proapoptotic BAX and antiapoptotic BCL-2. Proc. Natl, Acad. Sci. USA 94:11357-11362, 1997.
38. SHIMIZU, S., T. IDE, T. YANAGIDA, and Y. TSUJIMOTO. Electrophysiological study of a novel large pore formed by Bax and the voltage-dependent anion channel that is permeable to cytochrome c. J. Biol. Chem, 275:12321-12325, 2000.
39. SHIMIZU, S., M. NARITA, and Y. TSUJIMOTO. Bcl-2 family proteins regulate the release of apoptogenic cytochrome c by the mitochondrial channel VDAC. Nature 399:483-487, 1999.
40. SLEE, E. A., M. T. HARTE, R. M. KLUCK, et al. Ordering the cytochrome c-initiated caspase cascade: hierarchical activation of caspases-2, -3, -6, -7, -8, and -10 i, and -10 in a caspase-9- dependent manner. J. Cell Biol. 144:281-292, 1999.
41. SUSIN, S. A., N. ZAMZAMI, M. CASTEDO, et al. Bcl-2 inhibits the mitochondrial release of an apoptogenic protease. J. Exp. Med. 184:1331-1341, 1996.
42. VAN DE CRAEN, M., I. VAN DEN BRANDE, W. DECLERCQ, et al. Cleavage of caspase family members by granzyme B: a comparative study in vitro. Eur. J. Immunol. 27:1296-1299, 1997.
43. VANDER HEIDEN, M. G., N. S. CHANDEL, P. T. SCHUMACKER, and C. B, THOMPSON. Bcl-xl prevents cell death following growth factor withdrawal by facilitating mitochondrial ATP/ADP exchange. Mol. Cell 3:159-167, 1999.
44. VANDER HEIDEN, M. G., N. S. CHANDEL, E. K. WILLIAMSON, P. T. SCHUMACKER, and C. B. THOMPSON. Bcl-xl regulates the membrane potential and volume homeostasis of mitochondria. Cell 91:627-637, 1997.
45. VANDER HEIDEN, M. G., X. X. LI, E. GOTTLIEB, R. B. HILL, C. B. THOMPSON, and M. COLOMBINI. Bcl-xl promotes the open configuration of the voltage-dependent anion channel and metabolite passage through the outer mitochondrial membrane. J. Biol. Chem. 276:19414-19419, 2001.
46. VERHAGEN, A. M., P. G. EKERT, M. PAKUSCH, et al. Identification of Diablo, a mammalian protein that promotes apoptosis by binding to and antagonizing IAP proteins. Cell 102:43-53, 2000.
47. VERHAGEN, A. M., J. SILKE, P. G. EKERT, et al. HtrA2 promotes cell death through its serine protease activity and its ability to antagonise inhibitor of apoptosis proteins. J. Biol. Chem. 277:445-454, 2002.
48. WATERHOUSE, N. J., J. C. GOLDSTEIN, O. VON AHSEN, M. SCHULER, D. D. NEWMEYER, and D. R. GREEN. Cytochrome c maintains mitochondrial transmembrane potential and ATP generation after outer mitochondrial membrane permeabilization during the apoptotic process. J. Cell Biol. 153:319-328, 2001.
49. WEI, M. C., T. LINDSTEN, V. K. MOOTHA, et al. tBID, a membrane-targeted death ligand, oligomerizes BAK to release cytochrome c. Genes Dev. 14:2060-2071, 2000.
50. WEI, M. C., W. X. ZONG, E. H. CHENG, et al. Proapoptotic BAX and BAK: a requisite gateway to mitochondrial dysfunction and death. Science 292:727-730, 2001.
51. YOSHIDA, H., Y. Y. KONG, R. YOSHIDA, et al. Apaf1 is required for mitochondrial pathways of apoptosis and brain development. Cell 94:739-750, 1998.
52. ZAMZAMI, N., P. MARCHETTI, M. CASTEDO, et al. Sequential reduction of mitochondrial transmembrane potential and generation of reactive oxygen species in early programmed cell death. J. Exp. Med. 182:367-377, 1995.
53. Zou, H., Y. LI, X. LIU, and X. WANG. An APAF-1 cytochrome c multimeric complex is a functional apoptosome that activates procaspase-9. J. Biol. Chem. 274:11549-11556, 1999.