Mitochondrial ROS produced via reverse electron transport extend animal lifespan

A1 Journal article (refereed)


Internal Authors/Editors


Publication Details

List of Authors: Filippo Scialò, Ashwin Sriram, Daniel Fernández-Ayala, Nina Gubina, Madis Lõhmus, Glyn Nelson, Angela Logan, Helen M. Cooper, Plácido Navas, Jose Antonio Enríquez, Michael P. Murphy, Alberto Sanz
Publisher: CELL PRESS
Publication year: 2016
Journal: Cell Metabolism
Journal acronym: CELL METAB
Volume number: 23
Issue number: 4
Start page: 725
End page: 734
Number of pages: 10
ISSN: 1550-4131
eISSN: 1932-7420


Abstract

Increased production of reactive oxygen species (ROS) has long been considered a cause of aging. However, recent studies have implicated ROS as essential secondary messengers. Here we show that the site of ROS production significantly contributes to their apparent dual nature. We report that ROS increase with age as mitochondrial function deteriorates. However, we also demonstrate that increasing ROS production specifically through respiratory complex I reverse electron transport extends Drosophila lifespan. Reverse electron transport rescued pathogenesis induced by severe oxidative stress, highlighting the importance of the site of ROS production in signaling. Furthermore, preventing ubiquinone reduction, through knockdown of PINK1, shortens lifespan and accelerates aging; phenotypes that are rescued by increasing reverse electron transport. These results illustrate that the source of a ROS signal is vital in determining its effects on cellular physiology and establish that manipulation of ubiquinone redox state is a valid strategy to delay aging.

Last updated on 2019-19-10 at 04:36