Redox regulation of mitochondrial function with emphasis on cysteine oxidation reactions

Mitochondria have a myriad of essential functions including metabolism and apoptosis. These chief functions are reliant on electron transfer reactions and the production of ATP and reactive oxygen species (ROS). The production of ATP and ROS are intimately linked to the electron transport chain (ETC...

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Main Authors: Ryan J. Mailloux, Xiaolei Jin, William G. Willmore
Format: Article
Language:English
Published: Elsevier 2014-01-01
Series:Redox Biology
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S2213231713000992
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author Ryan J. Mailloux
Xiaolei Jin
William G. Willmore
author_facet Ryan J. Mailloux
Xiaolei Jin
William G. Willmore
author_sort Ryan J. Mailloux
collection DOAJ
description Mitochondria have a myriad of essential functions including metabolism and apoptosis. These chief functions are reliant on electron transfer reactions and the production of ATP and reactive oxygen species (ROS). The production of ATP and ROS are intimately linked to the electron transport chain (ETC). Electrons from nutrients are passed through the ETC via a series of acceptor and donor molecules to the terminal electron acceptor molecular oxygen (O2) which ultimately drives the synthesis of ATP. Electron transfer through the respiratory chain and nutrient oxidation also produces ROS. At high enough concentrations ROS can activate mitochondrial apoptotic machinery which ultimately leads to cell death. However, if maintained at low enough concentrations ROS can serve as important signaling molecules. Various regulatory mechanisms converge upon mitochondria to modulate ATP synthesis and ROS production. Given that mitochondrial function depends on redox reactions, it is important to consider how redox signals modulate mitochondrial processes. Here, we provide the first comprehensive review on how redox signals mediated through cysteine oxidation, namely S-oxidation (sulfenylation, sulfinylation), S-glutathionylation, and S-nitrosylation, regulate key mitochondrial functions including nutrient oxidation, oxidative phosphorylation, ROS production, mitochondrial permeability transition (MPT), apoptosis, and mitochondrial fission and fusion. We also consider the chemistry behind these reactions and how they are modulated in mitochondria. In addition, we also discuss emerging knowledge on disorders and disease states that are associated with deregulated redox signaling in mitochondria and how mitochondria-targeted medicines can be utilized to restore mitochondrial redox signaling.
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spelling doaj.art-b42b4ab86f6148cebad3857557d73ef72022-12-21T21:05:20ZengElsevierRedox Biology2213-23172014-01-012C12313910.1016/j.redox.2013.12.011Redox regulation of mitochondrial function with emphasis on cysteine oxidation reactionsRyan J. Mailloux0Xiaolei Jin1William G. Willmore2Institute of Biochemistry, Carleton University, 1125 Colonel By Drive, Ottawa, Ontario, Canada K1S 5B6Toxicology Research Division, Food Directorate, HPFB, Health Canada, Ottawa, Ontario, Canada K1A 0K9Institute of Biochemistry, Carleton University, 1125 Colonel By Drive, Ottawa, Ontario, Canada K1S 5B6Mitochondria have a myriad of essential functions including metabolism and apoptosis. These chief functions are reliant on electron transfer reactions and the production of ATP and reactive oxygen species (ROS). The production of ATP and ROS are intimately linked to the electron transport chain (ETC). Electrons from nutrients are passed through the ETC via a series of acceptor and donor molecules to the terminal electron acceptor molecular oxygen (O2) which ultimately drives the synthesis of ATP. Electron transfer through the respiratory chain and nutrient oxidation also produces ROS. At high enough concentrations ROS can activate mitochondrial apoptotic machinery which ultimately leads to cell death. However, if maintained at low enough concentrations ROS can serve as important signaling molecules. Various regulatory mechanisms converge upon mitochondria to modulate ATP synthesis and ROS production. Given that mitochondrial function depends on redox reactions, it is important to consider how redox signals modulate mitochondrial processes. Here, we provide the first comprehensive review on how redox signals mediated through cysteine oxidation, namely S-oxidation (sulfenylation, sulfinylation), S-glutathionylation, and S-nitrosylation, regulate key mitochondrial functions including nutrient oxidation, oxidative phosphorylation, ROS production, mitochondrial permeability transition (MPT), apoptosis, and mitochondrial fission and fusion. We also consider the chemistry behind these reactions and how they are modulated in mitochondria. In addition, we also discuss emerging knowledge on disorders and disease states that are associated with deregulated redox signaling in mitochondria and how mitochondria-targeted medicines can be utilized to restore mitochondrial redox signaling.http://www.sciencedirect.com/science/article/pii/S2213231713000992RedoxS-glutathionylationS-oxidationS-nitrosylationMitochondria
spellingShingle Ryan J. Mailloux
Xiaolei Jin
William G. Willmore
Redox regulation of mitochondrial function with emphasis on cysteine oxidation reactions
Redox Biology
Redox
S-glutathionylation
S-oxidation
S-nitrosylation
Mitochondria
title Redox regulation of mitochondrial function with emphasis on cysteine oxidation reactions
title_full Redox regulation of mitochondrial function with emphasis on cysteine oxidation reactions
title_fullStr Redox regulation of mitochondrial function with emphasis on cysteine oxidation reactions
title_full_unstemmed Redox regulation of mitochondrial function with emphasis on cysteine oxidation reactions
title_short Redox regulation of mitochondrial function with emphasis on cysteine oxidation reactions
title_sort redox regulation of mitochondrial function with emphasis on cysteine oxidation reactions
topic Redox
S-glutathionylation
S-oxidation
S-nitrosylation
Mitochondria
url http://www.sciencedirect.com/science/article/pii/S2213231713000992
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AT xiaoleijin redoxregulationofmitochondrialfunctionwithemphasisoncysteineoxidationreactions
AT williamgwillmore redoxregulationofmitochondrialfunctionwithemphasisoncysteineoxidationreactions