Journal
FREE RADICAL BIOLOGY AND MEDICINE
Volume 48, Issue 6, Pages 749-762Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2009.12.022
Keywords
ROS and apoptosis; GSH and thioredoxin redox systems; GSH redox signaling and apoptosis; Pyridine nucleotide redox couples and apoptosis; Mitochondria and apoptosis; Redox control of caspases
Funding
- National Institutes of Health [DK44510]
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Reactive oxygen species (ROS) are products of normal metabolism and xenobiotic exposure, and depending on their concentration, ROS can be beneficial or harmful to cells and tissues. At physiological low levels, ROS function as redox messengers in intracellular signaling and regulation, whereas 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-and the 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 this review, we focus on several key aspects of ROS and redox mechanisms in apoptotic signaling and highlight the gaps in knowledge and potential avenues for further investigation. 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. (c) 2010 Elsevier Inc. All rights reserved.
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