Mitochondrial reactive oxygen species in cell death signaling.
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TLDR
In agreement with this role of ROS in apoptosis signaling, inhibition of apoptosis by anti-apoptotic Bcl-2 and BCl-x(L) is associated with a protection against ROS and/or a shift of the cellular redox potential to a more reduced state.About:
This article is published in Biochimie.The article was published on 2002-02-01 and is currently open access. It has received 958 citations till now. The article focuses on the topics: Intrinsic apoptosis & Programmed cell death.read more
Figures
Figure 2: Effect of antioxidant on Bax and cytochrome c localization in HeLa cells undergoing TNF--induced apoptosis. ![Figure 1: Schematic representation of the formation and the fate of superoxide ions (O2.-) in mitochondria (adapted from Fleury et al. [112]).](/figures/figure-1-schematic-representation-of-the-formation-and-the-h2puz1p2.png)
Figure 1: Schematic representation of the formation and the fate of superoxide ions (O2.-) in mitochondria (adapted from Fleury et al. [112]). 
Figure 4: Schematic model of the roles of mitochondrial ROS in apoptosis 
Figure 3: Effect of Bcl-2 on mitochondrial events occurring during TNF--induced apoptosis of HeLa cells.
![Figure 1: Schematic representation of the formation and the fate of superoxide ions (O2.-) in mitochondria (adapted from Fleury et al. [112]).](/figures/figure-1-schematic-representation-of-the-formation-and-the-h2puz1p2.webp)
Citations
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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.
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Oxidation of biological systems: oxidative stress phenomena, antioxidants, redox reactions, and methods for their quantification.
Ron Kohen,Abraham Nyska +1 more
TL;DR: This review includes different topics essential for understanding oxidative stress phenomena and provides tools for those intending to conduct study and research in this field.
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Molecular and evolutionary basis of the cellular stress response
TL;DR: Functional analysis of the minimal stress proteome yields information about key aspects of the cellular stress response, including physiological mechanisms of sensing membrane lipid, protein, and DNA damage; redox sensing and regulation; cell cycle control; macromolecular stabilization/repair; and control of energy metabolism.
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Mitochondria - Releasing Power for Life and Unleashing the Machineries of Death
TL;DR: A review of promising mechanisms proposed for mitochondrial involvement in cell death are examined, including oxidative phosphorylation, generation of oxygen radicals, dynamic morphological rearrangements, calcium overload, and permeability transition.
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Cellular Stress Responses: Cell Survival and Cell Death
TL;DR: The implications of cellular stress responses to human physiology and diseases are manifold and will be discussed in this review in the context of some major world health issues such as diabetes, Parkinson's disease, myocardial infarction, and cancer.
References
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Journal ArticleDOI
Hydroperoxide metabolism in mammalian organs.
Book ChapterDOI
Role of free radicals and catalytic metal ions in human disease: an overview.
TL;DR: The chapter discusses the metabolism of transition metals, such as iron and copper, and the chelation therapy that is an approach to site-specific antioxidant protection.
Journal ArticleDOI
BCL-2 family members and the mitochondria in apoptosis
TL;DR: As the BCL-2 family members reside upstream of irreversible cellular damage and focus much of their efforts at the level of mitochondria, they play a pivotal role in deciding whether a cell will live or die, and it is argued that the amphipathic a-helical BH3 domain serves as a critical death domain in the pro-apoptotic members.
Journal ArticleDOI
Bcl-2 functions in an antioxidant pathway to prevent apoptosis
TL;DR: A model in which Bcl-2 regulates an antioxidant pathway at sites of free radical generation is proposed in which it protected cells from H2O2- and menadione-induced oxidative deaths and suppressed lipid peroxidation completely.
Journal ArticleDOI
The biology of oxygen radicals
TL;DR: The reactive superoxide radical, O2-, formerly of concern only to radiation chemists and radiobiologists, is now understood to be a normal product of the biological reduction of molecular oxygen.