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A model for p53-induced apoptosis
Examination of transcripts induced by p53 expression before the onset of apoptosis stimulated additional biochemical and pharmacological experiments suggesting that p53 results in apoptosis through a three-step process: the transcriptional induction of redox-related genes; the formation of reactive oxygen species; and the oxidative degradation of mitochondrial components, culminating in cell death. Expand
Reactive Oxygen Species (Ros-Induced) Ros Release: A New Phenomenon Accompanying Induction of the Mitochondrial Permeability Transition in Cardiac Myocytes
We sought to understand the relationship between reactive oxygen species (ROS) and the mitochondrial permeability transition (MPT) in cardiac myocytes based on the observation of increased ROS… Expand
Mitogenic Signaling Mediated by Oxidants in Ras-Transformed Fibroblasts
H-RasV12-induced transformation can lead to the production of ·O2− through one or more pathways involving a flavoprotein and Rac1, suggesting a possible mechanism for the effects of antioxidants against Ras-induced cellular transformation. Expand
MicroRNA-210 controls mitochondrial metabolism during hypoxia by repressing the iron-sulfur cluster assembly proteins ISCU1/2.
- S. Y. Chan, Ying-yi Zhang, C. Hemann, Christopher E Mahoney, J. Zweier, J. Loscalzo
- Biology, Medicine
- Cell metabolism
- 7 October 2009
Important mechanistic connections among microRNA, iron-sulfur cluster biology, hypoxia, and mitochondrial function are identified, with broad implications for cellular metabolism and adaptation to cellular stress. Expand
Superoxide Generation from Endothelial Nitric-oxide Synthase
- Yong Xia, A. Tsai, V. Berka, J. Zweier
- Chemistry, Medicine
- The Journal of Biological Chemistry
- 2 October 1998
Electro paramagnetic resonance spin-trapping experiments have shown that endothelial NOS can also catalyze O⨪2formation, and this appears to occur primarily at the heme center of its oxygenase domain. Expand
Hearts From Rodents Exposed to Intermittent Hypoxia or Erythropoietin Are Protected Against Ischemia‐Reperfusion Injury
Heart isolated from rodents subjected to intermittent hypoxia or EPO administration are protected against postischemic injury, and cardiac protection induced by intermittent Hypoxia is critically dependent on Hif1a gene dosage. Expand
Cardiac Mitochondria and Reactive Oxygen Species Generation
In conclusion, mitochondrial ROS has been linked to mediating the physiological effects of metabolic dilation and preconditioning-like mitochondrial ATP-sensitive potassium channel activation and oxidative post-translational modification by glutathione in complex I and complex II has been shown to affect enzymatic catalysis, protein–protein interactions, and enzyme-mediated ROS production. Expand
Evidence that mitochondrial respiration is a source of potentially toxic oxygen free radicals in intact rabbit hearts subjected to ischemia and reflow.
- G. Ambrosio, J. Zweier, +7 authors M. Chiariello
- Chemistry, Medicine
- The Journal of biological chemistry
- 5 September 1993
The hypothesis that resumption of mitochondrial respiration upon reperfusion might be a mechanism of oxygen radical formation in postischemic hearts, and that treatment with inhibitors of mitochondrialrespiration might prevent this phenomenon is tested, is tested. Expand
The role of oxidants and free radicals in reperfusion injury.
Ischemic preconditioning markedly decreases NO and oxidant generation, and this appears to be an important mechanism contributing to preconditionsing-induced myocardial protection. Expand
Nitric oxide synthase generates superoxide and nitric oxide in arginine-depleted cells leading to peroxynitrite-mediated cellular injury.
- Y. Xia, V. Dawson, T. Dawson, S. Snyder, J. Zweier
- Chemistry, Medicine
- Proceedings of the National Academy of Sciences…
- 25 June 1996
With reduced L-Arg availability NOS elicits cytotoxicity by generating .O2- and NO that interact to form the potent oxidant peroxynitrite and regulating arginine levels may provide a therapeutic approach to disorders involving .O 2-/NO-mediated cellular injury. Expand