Difference between revisions of "Scialo 2016 Cell Metab"
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|journal=Cell Metab | |journal=Cell Metab | ||
|abstract=[[Image:O2k-Publications.jpg|80px|link=O2k-Publications: Topics|O2k-Publications: Topics]][http://wiki.oroboros.at/images/7/7d/Scialo_2016_Cell_Metab_O2k-brief.pdf O2k-in brief] | |abstract=[[Image:O2k-Publications.jpg|80px|link=O2k-Publications: Topics|O2k-Publications: Topics]][http://wiki.oroboros.at/images/7/7d/Scialo_2016_Cell_Metab_O2k-brief.pdf O2k-''in brief''] | ||
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. | 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. | ||
Revision as of 17:15, 10 July 2018
| Scialò F, Sriram A, Fernández-Ayala D, Gubina N, Lõhmus M, Nelson G, Logan A, Cooper HM, Navas P, Enríquez JA, Murphy MP, Sanz A (2016) Mitochondrial ROS produced via reverse electron transport extend animal lifespan. Cell Metab 23:725-34. |
Scialo F, Sriram A, Fernandez-Ayala D, Gubina N, Lohmus M, Nelson G, Logan A, Cooper HM, Navas P, Enriquez JA, Murphy MP, Sanz A (2016) Cell Metab
Abstract: 
O2k-in brief
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.
Copyright © 2016 The Authors. Published by Elsevier Inc. All rights reserved. • Keywords: Aging, Coenzyme Q, Electron transport chain, Mitochondria, Reactive oxygen species
• O2k-Network Lab: UK Newcastle Sanz A
Labels: MiParea: Respiration
Pathology: Aging;senescence
Stress:Oxidative stress;RONS
Organism: Drosophila
Preparation: Homogenate
Coupling state: LEAK, OXPHOS
Pathway: N, Gp, CIV, Other combinations, ROX
HRR: Oxygraph-2k
2016-06
