Role of mitochondrial reverse electron transport in ROS signaling: potential roles in health and disease

Scialò, F., Fernández-Ayala, D. J. and Sanz, A. (2017) Role of mitochondrial reverse electron transport in ROS signaling: potential roles in health and disease. Frontiers in Physiology, 8, 428. (doi: 10.3389/fphys.2017.00428) (PMID:28701960) (PMCID:PMC548615)

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Reactive Oxygen Species (ROS) can cause oxidative damage and have been proposed to be the main cause of aging and age-related diseases including cancer, diabetes and Parkinson's disease. Accordingly, mitochondria from old individuals have higher levels of ROS. However, ROS also participate in cellular signaling, are instrumental for several physiological processes and boosting ROS levels in model organisms extends lifespan. The current consensus is that low levels of ROS are beneficial, facilitating adaptation to stress via signaling, whereas high levels of ROS are deleterious because they trigger oxidative stress. Based on this model the amount of ROS should determine the physiological effect. However, recent data suggests that the site at which ROS are generated is also instrumental in determining effects on cellular homeostasis. The best example of site-specific ROS signaling is reverse electron transport (RET). RET is produced when electrons from ubiquinol are transferred back to respiratory complex I, reducing NAD+ to NADH. This process generates a significant amount of ROS. RET has been shown to be instrumental for the activation of macrophages in response to bacterial infection, re-organization of the electron transport chain in response to changes in energy supply and adaptation of the carotid body to changes in oxygen levels. In Drosophila melanogaster, stimulating RET extends lifespan. Here, we review what is known about RET, as an example of site-specific ROS signaling, and its implications for the field of redox biology.

Item Type:Articles
Additional Information:The authors thank the European Research Council (ComplexIandAging No 260632) and the BBSRC (BB/M023311/1) for the support given to our research that is partially summarized in this review.
Glasgow Author(s) Enlighten ID:Sanz Montero, Professor Alberto
Authors: Scialò, F., Fernández-Ayala, D. J., and Sanz, A.
College/School:College of Medical Veterinary and Life Sciences > Institute of Molecular Cell and Systems Biology
Journal Name:Frontiers in Physiology
Publisher:Frontiers Media
ISSN (Online):1664-042X
Copyright Holders:Copyright © 2017 Scialò, Fernández-Ayala and Sanz.
First Published:First published in Frontiers in Physiology 8:428
Publisher Policy:Reproduced under a Creative Commons License

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