Reactive oxygen species, cellular redox systems and apoptosis
Magdalena L. Circu,Tak Yee Aw +1 more
TLDR
A full understanding of the redox control of apoptotic initiation and execution could underpin the development of therapeutic interventions targeted at oxidative stress-associated disorders.About:
This article is published in Free Radical Biology and Medicine.The article was published on 2010-03-15 and is currently open access. It has received 2834 citations till now. The article focuses on the topics: Thioredoxin & Intracellular.read more
Citations
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Reactive Oxygen Species in Inflammation and Tissue Injury
TL;DR: The current review compiles the past and current research in the area of inflammation with particular emphasis on oxidative stress-mediated signaling mechanisms that are involved in inflammation and tissue injury.
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Activation of Apoptosis Signalling Pathways by Reactive Oxygen Species
TL;DR: ROS play a central role in cell signalling as well as in regulation of the main pathways of apoptosis mediated by mitochondria, death receptors and the endoplasmic reticulum, and current understanding of the role of ROS in each of these three main pathways is focused on.
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The importance of antioxidants which play the role in cellular response against oxidative/nitrosative stress: current state
TL;DR: The aim of this review is to emphasize with current information the importance of antioxidants which play the role in cellular responce against oxidative/nitrosative stress, which would be helpful in enhancing the knowledge of any biochemist, pathophysiologist, or medical personnel regarding this important issue.
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Oxidative stress: the mitochondria-dependent and mitochondria-independent pathways of apoptosis
TL;DR: This review highlights the basic mechanisms of ROS production and their sites of formation; detail mechanism of both mitochondria-dependent and mitochondrial-independent pathways of apoptosis as well as their regulation by ROS and describes the involvement of oxidative stress under various environmental toxin- and drug-induced organ pathophysiology and diabetes-mediated apoptosis.
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ATM Activation by Oxidative Stress
TL;DR: It is shown that oxidation of ATM directly induces ATM activation in the absence of DNA DSBs and the MRN complex, and that ATM is an important sensor of reactive oxygen species in human cells.
References
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Oxidants, antioxidants, and the degenerative diseases of aging
TL;DR: It is argued that this damage to DNA, protein, and lipid is a major contributor to aging and to degenerative diseases of aging such as cancer, cardiovascular disease, immune-system decline, brain dysfunction, and cataracts.
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The NOX Family of ROS-Generating NADPH Oxidases: Physiology and Pathophysiology
Karen Bedard,Karl-Heinz Krause +1 more
TL;DR: This review summarizes the current state of knowledge of the functions of NOX enzymes in physiology and pathology.
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Mitochondrial formation of reactive oxygen species.
TL;DR: This review describes the main mitochondrial sources of reactive species and the antioxidant defences that evolved to prevent oxidative damage in all the mitochondrial compartments and discusses various physiological and pathological scenarios resulting from an increased steady state concentration of mitochondrial oxidants.
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Redox environment of the cell as viewed through the redox state of the glutathione disulfide/glutathione couple.
TL;DR: Estimates can be used to more fully understand the redox biochemistry that results from oxidative stress, which hopefully will provide a rationale and understanding of the cellular mechanisms associated with cell growth and development, signaling, and reductive or oxidative stress.
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Molecular characterization of mitochondrial apoptosis-inducing factor
Santos A. Susin,Hans K. Lorenzo,Naoufal Zamzami,Isabel Marzo,Bryan E. Snow,Joan Mangion,Etienne Jacotot,Paola Costantini,Markus Loeffler,Nathanael Larochette,David R. Goodlett,Ruedi Aebersold,David P. Siderovski,Josef M. Penninger,Guido Kroemer +14 more
TL;DR: The identification and cloning of an apoptosis-inducing factor, AIF, which is sufficient to induce apoptosis of isolated nuclei is reported, indicating that AIF is a mitochondrial effector of apoptotic cell death.