Journal ArticleDOI
The Ca2+-induced membrane transition in mitochondria. III. Transitional Ca2+ release.
TLDR
Na2+-induced Ca2+ release was not accompanied by a configurational change; it is concluded that it is not mediated by the Ca2-induced transition.About:
This article is published in Archives of Biochemistry and Biophysics.The article was published on 1979-07-01. It has received 521 citations till now. The article focuses on the topics: NAD+ kinase & Population.read more
Citations
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Mitochondrial Reactive Oxygen Species (ROS) and ROS-Induced ROS Release
TL;DR: The mechanism of mitochondrial RIRR highlights the central role of mitochondria-formed ROS, and all of the known ROS-producing sites and their relevance to the mitochondrial ROS production in vivo are discussed.
Journal ArticleDOI
Calcium, ATP, and ROS: a mitochondrial love-hate triangle
TL;DR: A "two-hit" hypothesis is developed, in which Ca(2+) plus another pathological stimulus can bring about mitochondrial dysfunction, and the delicate balance between the positive and negative effects of Ca( 2+) and the signaling events that perturb this balance is highlighted.
Journal ArticleDOI
Mechanisms by which mitochondria transport calcium.
Thomas E. Gunter,D. R. Pfeiffer +1 more
TL;DR: It has been suggested that the permeability transition and its reversal may also function as a mitochondrial Ca2+ efflux mechanism under some conditions.
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Mitochondrial Transport of Cations: Channels, Exchangers, and Permeability Transition
TL;DR: The review should provide the basic elements needed to understand both earlier mitochondrial literature and current problems associated with mitochondrial transport of cations and hopefully will foster new interest in the molecular definition of mitochondrial cation channels and exchangers as well as their roles in cell physiology.
References
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Journal ArticleDOI
The Ca2+-induced membrane transition in mitochondria: I. The protective mechanisms
TL;DR: It is concluded that mitochondria have a set of protective mechanisms involving endogenous NADH, ADP, and energization which regulate the rate of the Ca2+-induced transition, and that the transition requires neither electron flow nor energy, but rather the mere accessibility of some internal site to Ca2+.
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The Ca2+-induced membrane transition in mitochondria. II. Nature of the Ca2+ trigger site.
TL;DR: It is concluded that the trigger site (by “trigger site” the authors mean the site of binding of Ca2+ which, whenCa2+ is bound, will allow the transition in permeability to occur) is possibly also the site for high-affinity Ca2-induced uptake.
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Relationship between configuration, function, and permeability in calcium-treated mitochondria.
TL;DR: The results of this work indicate that mitochondria have a built-in mechanism which responds to low levels of calcium, phosphate, and fatty acids, resulting in simultaneous changes, including increased permeability, inducation of ATPase, uncoupling of oxidative phosphorylation, and loss of respiratory control.
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Specific inhibition of mitochondrial Ca++ transport by ruthenium red
TL;DR: It is concluded that mucopolysaccharides (in the form of mucoproteins or muco or glycolipids) are at the active center of the sites of mediation of mitochondrial Ca++ transport.
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Studies on the electron transfer system. IV. The electron transfer particle.
TL;DR: The preparation and properties of an electron transfer particle (ETP) obtained from beef heart mitochondria are described and the significance of the fact of the constant composition of ETP for the dynamics of electron transport is discussed.