NDLI: Mitochondrial Dysfunction in the Pathogenesis of Necrotic and Apoptotic Cell Death

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Cooperation of a “Reactive Oxygen Cycle” with The Q Cycle and The Proton Cycle in the Respiratory Chain—Superoxide Generating and Cycling Mechanisms in Mitochondria

Mitochondrial Genome Mutation in Cell Death and Aging

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Journal of Bioenergetics and Biomembranes : Volume 31, Issue 3, June 1999

Journal of Bioenergetics and Biomembranes : Volume 31, Issue 2, April 1999

Journal of Bioenergetics and Biomembranes : Volume 31, Issue 1, February 1999

Journal of Bioenergetics and Biomembranes : Volume 30

Journal of Bioenergetics and Biomembranes : Volume 29

Mitochondrial Dysfunction in the Pathogenesis of Necrotic and Apoptotic Cell Death

Content Provider	Springer Nature Link
Author	Lemasters, John J. Qian, Ting Bradham, Cynthia A. Brenner, David A. Cascio, Wayne E. Trost, Lawrence C. Nishimura, Yoshiya Nieminen, Anna Liisa Herman, Brian
Copyright Year	1999
Abstract	Mitochondria are frequently the target of injury after stresses leading to necrotic and apoptoticcell death. Inhibition of oxidative phosphorylation progresses to uncoupling when opening ofa high conductance permeability transition (PT) pore in the mitochondrial inner membraneabruptly increases the permeability of the mitochondrial inner membrane to solutes of molecularmass up to 1500 Da. Cyclosporin A (CsA) blocks this mitochondrial permeability transition(MPT) and prevents necrotic cell death from oxidative stress, Ca$^{2+}$ ionophore toxicity,Reye-related drug toxicity, pH-dependent ischemia/reperfusion injury, and other models of cell injury.Confocal fluorescence microscopy directly visualizes onset of the MPT from the movementof green-fluorescing calcein into mitochondria and the simultaneous release from mitochondriaof red-fluorescing tetramethylrhodamine methylester, a membrane potential-indicatingfluorophore. In oxidative stress to hepatocytes induced by tert-butylhydroperoxide, NAD(P)Hoxidation, increased mitochondrial Ca$^{2+}$, and mitochondrial generation of reactive oxygen speciesprecede and contribute to onset of the MPT. Confocal microscopy also shows directly thatthe MPT is a critical event in apoptosis of hepatocytes induced by tumor necrosis factor-α.Progression to necrotic and apoptotic cell killing depends, at least in part, on the effect theMPT has on cellular ATP levels. If ATP levels fall profoundly, necrotic killing ensues. If ATPlevels are at least partially maintained, apoptosis follows the MPT. Cellular features of bothapoptosis and necrosis frequently occur together after death signals and toxic stresses. A newterm, necrapoptosis, describes such death processes that begin with a common stress or deathsignal, progress by shared pathways, but culminate in either cell lysis (necrosis) or programmedcellular resorption (apoptosis) depending on modifying factors such as ATP.
Starting Page	305
Ending Page	319
Page Count	15
File Format	PDF
ISSN	0145479X
Journal	Journal of Bioenergetics and Biomembranes
Volume Number	31
Issue Number	4
e-ISSN	15736881
Language	English
Publisher	Kluwer Academic Publishers-Plenum Publishers
Publisher Date	1999-01-01
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Organic Chemistry Biochemistry Animal Biochemistry Animal Anatomy / Morphology / Histology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Physiology

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