Journal ArticleDOI
Protein S-glutathionylation alters superoxide/hydrogen peroxide emission from pyruvate dehydrogenase complex
TLDR
It is reported that O2•‐/ H2O2 emission from pyruvate dehydrogenase (Pdh) is altered by S‐glutathionylation, which alters the amount of ROS formed by the enzyme complex and confirmed that Ogdh is controlled in a similar manner.About:
This article is published in Free Radical Biology and Medicine.The article was published on 2017-05-01. It has received 61 citations till now. The article focuses on the topics: OGDH & Pyruvate decarboxylation.read more
Citations
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Journal ArticleDOI
Reactive Oxygen Species in Metabolic and Inflammatory Signaling.
TL;DR: The role of ROS in the regulation metabolic/inflammatory diseases including atherosclerosis, diabetes mellitus, and stroke is highlighted and the balance ROS signaling plays in both physiology and pathophysiology is understood.
Journal ArticleDOI
Lipoic acid metabolism and mitochondrial redox regulation
TL;DR: Collectively, its functions explain why lipoic acid is required for cell growth, mitochondrial activity, and coordination of fuel metabolism.
Journal ArticleDOI
Redox crosstalk at endoplasmic reticulum (ER) membrane contact sites (MCS) uses toxic waste to deliver messages
TL;DR: Interestingly, important components of the redoxosome are ER chaperones and oxidoreductases, identifying ER oxidative protein folding as a key ROS producer and controller of the tri-organellar membrane contact sites (MCS) formed at the red ox triangle.
Journal ArticleDOI
An evolving understanding of the S-glutathionylation cycle in pathways of redox regulation.
TL;DR: A number of human diseases with associated aberrant S‐glutathionylation have been identified and the existence of human polymorphisms of enzymes involved in the cycle (particularly glutathione S‐transferase P) create a scenario for inter‐individual variance in response to oxidative stress.
Journal ArticleDOI
Mitochondrial Uncoupling Proteins: Subtle Regulators of Cellular Redox Signaling.
TL;DR: The mitochondria are the energetic, metabolic, redox, and information signaling centers of the cell and are the energy and metabolic, metabolic and redox centers of a cell as mentioned in this paper.
References
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Journal ArticleDOI
Ischaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS.
Edward T. Chouchani,Edward T. Chouchani,Victoria R. Pell,Edoardo Gaude,Dunja Aksentijevic,Stephanie Y. Sundier,Ellen L. Robb,Angela Logan,Sergiy M. Nadtochiy,Emily N.J. Ord,Anthony C. Smith,Filmon Eyassu,Rachel Shirley,Chou Hui Hu,Anna J. Dare,Andrew M. James,Sebastian Rogatti,Richard C. Hartley,Simon Eaton,Ana S. H. Costa,Paul S. Brookes,Sean M. Davidson,Michael R. Duchen,Kourosh Saeb-Parsy,Michael J. Shattock,Alan J. Robinson,Lorraine M. Work,Christian Frezza,Thomas Krieg,Michael P. Murphy +29 more
TL;DR: In this article, a comparative in vivo metabolomic analysis was conducted to identify widely conserved metabolic pathways responsible for mitochondrial reactive oxygen species (ROS) production during ischaemia reperfusion.
Journal ArticleDOI
High protonic potential actuates a mechanism of production of reactive oxygen species in mitochondria.
TL;DR: Inhibition of H2O2 formation by uncoupler, malonate and ADP+Pi is shown to be proportional to the ΔΨ decrease by these compounds, which is in line with the concept that a high proton motive force in state 4 is potentially dangerous for the cell due to an increase in the probability of superoxide formation.
Ischaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS
EE Chouchani,Pell,Edoardo Gaude,Dunja Aksentijevic,Stephanie Y. Sundier,Michael R. Duchen,Michael J. Shattock,Christian Frezza,Thomas Krieg,Michael P. Murphy +9 more
TL;DR: It is shown that selective accumulation of the citric acid cycle intermediate succinate is a universal metabolic signature of ischaemia in a range of tissues and is responsible for mitochondrial ROS production during reperfusion, and a new pathway for metabolic control of ROS production in vivo is revealed.
Journal ArticleDOI
Mitochondrial generation of superoxide and hydrogen peroxide as the source of mitochondrial redox signaling
TL;DR: This review examines the generation of reactive oxygen species by mammalian mitochondria, and the status of different sites of production in redox signaling and pathology, and identifies specific suppressors of two sites that allow the cellular roles of mitochondrial superoxide/hydrogen peroxide production to be investigated without catastrophic confounding bioenergetic effects.
Journal ArticleDOI
Mitochondrial α-Ketoglutarate Dehydrogenase Complex Generates Reactive Oxygen Species
Anatoly A. Starkov,Gary Fiskum,Christos Chinopoulos,Beverly J. Lorenzo,Susan E. Browne,Mulchand S. Patel,M. Flint Beal +6 more
TL;DR: The data strongly indicate that KGDHC is a primary site of ROS production in normally functioning mitochondria, and NAD+ inhibited ROS production by the isolated enzymes and by permeabilized mitochondria.