REACTIVE OXYGEN SPECIES, CELLULAR REDOX SYSTEMS AND APOPTOSIS

By M. Circu, T. Aw. Free Radical Biology & Medicine, 2010

3,220 citations recorded by the source corpus.

Reactive oxygen species (ROS) are products of normal metabolism and xenobiotic exposure, and depending on concentrations, ROS can be beneficial or harmful to cells and tissues. At physiological low levels, ROS function as “redox messengers” in intracellular signaling and regulation while excess ROS induce oxidative modification of cellular macromolecules, inhibit protein function and promote cell death. Additionally, various redox systems, such as the glutathione, thioredoxin, and pyridine nucleotide redox couples, participate in cell signaling and modulation of cell function, including apoptotic cell death. Cell apoptosis is initiated by extracellular and intracellular signals via two main pathways, the death receptor- or mitochondria-mediated pathways. Various pathologies can result from oxidative stress induced apoptotic signaling that is consequent to ROS increases and/or antioxidant decreases, disruption of intracellular redox homeostasis, and irreversible oxidative modifications of lipid, protein or DNA. In the current review, we focused on several key aspects of ROS and redox mechanisms in apoptotic signaling, and highlighted the gaps in knowledge and potential avenues for further investigation. A full understanding of redox control of apoptotic initiation and execution could underpin the development of therapeutic interventions targeted at oxidative stress associated disorders.

Subfields: Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/0b8fc40f3bf7fed441521360d2f87e805f644aae

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In Immunology

1. W. Dichtl
2. T. Senoner
3. E. Kurutaş

In Molecular Biology

1. W. Dichtl
2. T. Senoner
3. T. Vlachogianni
4. A. Valavanidis
5. E. Kurutaş

Citations in the corpus

• The importance of antioxidants which play the role in cellular response against oxidative/nitrosative stress: current state (2015, background): “However, this increases the oxidative state in the cell, and resulting in a homeostatic disruption of the redox balance, cell damage, and apoptosis [117, 118].”
• Reactive Oxygen Species in Inflammation and Tissue Injury (2014, neutral): “Release of endosomal DISC to the cytosol further recruits initiator procaspase-8, resulting in its activation (64).”
• Oxidative stress in bone remodeling: role of antioxidants. (2017, background): “ROS are produced during normal metabolism following the activation of various enzymes such as NADPH oxidase (membrane enzyme), superoxide dismutase (cytoplasmic enzyme) and various mitochondrial oxidases (3, 4).”
• Mitochondrial electron transport chain, ROS generation and uncoupling (Review) (2019, neutral): “Apoptosis i) death receptor pathway: ROS-death receptors (FasL, TNF-α, TRAIL)-caspase-8-caspase-3 (87-91)”
• Oxidative Stress in Cardiovascular Diseases: Still a Therapeutic Target? (2019, background): “Decreasing the amount of free radicals in our organism may impede some essential defense mechanisms such as apoptosis, phagocytosis, and detoxification [157,158].”
• Pulmonary Oxidative Stress, Inflammation and Cancer: Respirable Particulate Matter, Fibrous Dusts and Ozone as Major Causes of Lung Carcinogenesis through Reactive Oxygen Species Mechanisms (2013, background): “neoplasms, diabetes mellitus, atherosclerosis and various neurodegenerative diseases [24–28].”
• The Cystine/Glutamate Antiporter System xc − in Health and Disease: From Molecular Mechanisms to Novel Therapeutic Opportunities (2013, neutral): “GSH is not uniformly distributed in cells, but rather different subcellular compartments have distinct GSH levels and GSH/GSSG ratios (42).”