Mitochondrial oxidative stress: implications for cell death.

By S. Orrenius, V. Gogvadze, B. Zhivotovsky. Annual Review of Pharmacology and Toxicology, 2007

1,282 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/31789c7f1ac0984d05d7a92bc3cfebf69b87a922

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Citations in the corpus

Mitochondria in cancer cells: what is so special about them? (2008, positive): “Oxidation of cardiolipin causes the dissociation of cytochrome c [46], which might provide a plausible explanation for the anti-apoptotic effects reported for multiple mitochondrial antioxidant enzymes [ 47 ].”
Role of Bcl-2 family proteins and caspases in the regulation of apoptosis (2011, neutral): “mitochondrial outer membrane permeabilization [74].”
Cytochrome c: functions beyond respiration (2008, background): “Moreover, this increased ROS production can in itself cause lethal cell injur”
Cellular Stress Responses: Cell Survival and Cell Death (2010, background): “Numerous, recent studies have shown that the mode of cell death that occurs depends on the severity of the insult [187– 189].”
Mitochondrial electron transport chain, ROS generation and uncoupling (Review) (2019, background): “A large amount of ROS cause lipid peroxidation, dNA damage, protein oxidation, irreversible impairment of mitochondria, insufficient ATP generation and, eventually, cell death (82).”
Anti-apoptosis and cell survival: a review. (2011, background): “(ROS) also represents a major player in this process [76,77].”
The Warburg effect in tumor progression: Mitochondrial oxidative metabolism as an anti-metastasis mechanism (2014, background): “ROS peroxidate cardiolipin, resulting in the liberation of cytochrome c [34], which may translocate through damaged mitochondrial outer membrane (as a consequence of MOMP) into cytosol, and activate the caspase cascade and apoptosis.”
A Review of the Antioxidant Mechanisms of Polyphenol Compounds Related to Iron Binding (2009, background): “Reactive oxygen species and reactive nitrogen species (RNS), such as hydroxyl radical (OH), hydrogen peroxide (H2O2), superoxide (O2 ), nitric oxide (NO), peroxynitrite (ONOO), and others, are major sources of oxidative stress in cells, damaging proteins, lipids, and DNA [47].”
Molecular mechanisms of necroptosis: an ordered cellular explosion (2010, background): “In mitochondria, the products of lipid peroxidation inhibit oxidative phosphorylation , compromise the permeability of the inner membrane, dissipate the Δ ψ m and reduce the Ca 2+ buffering capacity, thus contributing to necrosi”