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Role of Mitochondrial Reverse Electron Transport in ROS Signalling: potential roles in Health and Disease

Lookup NU author(s): Dr Filippo Scialo, Dr Alberto Sanz Montero

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This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).


Abstract

Reactive Oxygen Species (ROS) can cause oxidative damage and have been proposedto be the main cause of aging and age-related diseases including cancer, diabetesand Parkinson’s disease. Accordingly, mitochondria from old individuals have higherlevels of ROS. However, ROS also participate in cellular signaling, are instrumental forseveral physiological processes and boosting ROS levels in model organisms extendslifespan. The current consensus is that low levels of ROS are beneficial, facilitatingadaptation to stress via signaling, whereas high levels of ROS are deleterious becausethey trigger oxidative stress. Based on this model the amount of ROS should determinethe physiological effect. However, recent data suggests that the site at which ROSare generated is also instrumental in determining effects on cellular homeostasis. Thebest example of site-specific ROS signaling is reverse electron transport (RET). RET isproduced when electrons from ubiquinol are transferred back to respiratory complex I,reducing NAD+ to NADH. This process generates a significant amount of ROS. RET hasbeen shown to be instrumental for the activation of macrophages in response to bacterialinfection, re-organization of the electron transport chain in response to changes in energysupply and adaptation of the carotid body to changes in oxygen levels. In Drosophilamelanogaster, stimulating RET extends lifespan. Here, we review what is known aboutRET, as an example of site-specific ROS signaling, and its implications for the field ofredox biology.


Publication metadata

Author(s): Scialo F, Fernandez-Ayala DJ, Sanz A

Publication type: Review

Publication status: Published

Journal: Frontiers in Physiology

Year: 2017

Volume: 8

Online publication date: 27/06/2017

Acceptance date: 02/06/2017

ISSN (electronic): 1664-042X

URL: https://doi.org/10.3389/fphys.2017.00428

DOI: 10.3389/fphys.2017.00428


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