Reduced Coupling of Oxidative Phosphorylation In Vivo Precedes Electron Transport Chain Defects Due to Mild Oxidative Stress in Mice

Siegel, Michael; Kruse, Shane E.; Knowels, Gary; Salmon, Adam B.; Beyer, Richard P.; Xie, Hui; Remmen, Holly Van; Smith, Steven R.; Marcinek, David J.

doi:10.1371/journal.pone.0026963

Cited by 43 publications

(53 citation statements)

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“…These have the potential to cause oxidative stress, which might mediate the trade-off between reproduction and lifespan (Dowling and Simmons, 2009;Monaghan et al, 2009). Although this is still a topic of great debate, several hypotheses have tried to link mitochondrial activity and ROS production (Brand, 2000;Balaban et al, 2005;Speakman, 2008;Neretti et al, 2009;Siegel et al, 2011). Two different hypotheses can be put forward to relate our results to ROS production.…”

Section: Discussionmentioning

confidence: 97%

“…ROS have long been considered a by-product of mitochondrial respiration, which cause damage to macromolecules and cellular dysfunction. However, more recent studies have now demonstrated that ROS are potential regulators of a number of intracellular pathways (St-Pierre et al, 2006;Han et al, 2008;Rasbach and Schnellmann, 2007;Siegel et al, 2011;Finkel, 2012;Ray et al, 2012). Recently, using the same set of mice, we demonstrated that livers of reproductive females showed higher activity of superoxide dismutase (SOD) relative to non-reproductive females, as well as decreased protein oxidation (Garratt et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

“…Although their role in cellular function is most commonly associated with damage to macromolecules, ROS are also involved in the regulation of several cellular processes such as mitochondrial biogenesis and increased activation of antioxidant defences (StPierre et al, 2006;Rasbach and Schnellmann, 2007;Han et al, 2008;Siegel et al, 2011). Several studies have predicted that oxidative stress could be an unavoidable consequence of reproduction (Costantini, 2008;Speakman, 2008;Dowling and Simmons, 2009;Monaghan et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

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Physiological adaptations to reproduction II. Mitochondrial adjustments in livers of lactating mice

Pichaud

Garratt

Ballard

et al. 2013

Journal of Experimental Biology

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SUMMARYReproduction imposes significant costs and is characterized by an increased energy demand. As a consequence, individuals adjust their cellular structure and function in response to this physiological constraint. Because mitochondria are central to energy production, changes in their functional properties are likely to occur during reproduction. Such changes could cause adjustments in reactive oxygen species (ROS) production and consequently in oxidative stress levels. In this study, we investigated several mechanisms involved in energy production, including mitochondrial respiration at different steps of the electron transport system (ETS) and related the results to citrate synthase activity in the liver of non-reproductive and reproductive (two and eight pups) female house mice at peak lactation. Whereas we did not find differences between females having different litter sizes, liver mitochondria of reproductive females showed lower ETS activity and an increase in mitochondrial density when compared with the non-reproductive females. Although it is possible that these changes were due to combined processes involved in reproduction and not to the relative investment in lactation, we propose that the mitochondrial adjustment in liver might help to spare substrates and therefore energy for milk production in the mammary gland. Moreover, our results suggest that these changes lead to an increase in ROS production that subsequently upregulates antioxidant defence activity and decreases oxidative stress.

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Physiological adaptations to reproduction II. Mitochondrial adjustments in livers of lactating mice

Pichaud

Garratt

Ballard

et al. 2013

Journal of Experimental Biology

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“…EDL and SOL muscles were dissected, and either flash‐frozen in liquid nitrogen or a mitochondrial extract derived from equivalent muscle weight/buffer volume was prepared as previously described (Siegel et al ., 2011). Briefly, muscle tissue was mechanically disrupted in phosphate buffer, and mitochondria were enriched by dual‐step differential centrifugation and resuspended in appropriate buffer.…”

Section: Methodsmentioning

confidence: 99%

Age modifies respiratory complex I and protein homeostasis in a muscle type‐specific manner

et al. 2015

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SummaryChanges in mitochondrial function with age vary between different muscle types, and mechanisms underlying this variation remain poorly defined. We examined whether the rate of mitochondrial protein turnover contributes to this variation. Using heavy label proteomics, we measured mitochondrial protein turnover and abundance in slow‐twitch soleus (SOL) and fast‐twitch extensor digitorum longus (EDL) from young and aged mice. We found that mitochondrial proteins were longer lived in EDL than SOL at both ages. Proteomic analyses revealed that age‐induced changes in protein abundance differed between EDL and SOL with the largest change being increased mitochondrial respiratory protein content in EDL. To determine how altered mitochondrial proteomics affect function, we measured respiratory capacity in permeabilized SOL and EDL. The increased mitochondrial protein content in aged EDL resulted in reduced complex I respiratory efficiency in addition to increased complex I‐derived H2O2 production. In contrast, SOL maintained mitochondrial quality, but demonstrated reduced respiratory capacity with age. Thus, the decline in mitochondrial quality with age in EDL was associated with slower protein turnover throughout life that may contribute to the greater decline in mitochondrial dysfunction in this muscle. Furthermore, mitochondrial‐targeted catalase protected respiratory function with age suggesting a causal role of oxidative stress. Our data clearly indicate divergent effects of age between different skeletal muscles on mitochondrial protein homeostasis and function with the greatest differences related to complex I. These results show the importance of tissue‐specific changes in the interaction between dysregulation of respiratory protein expression, oxidative stress, and mitochondrial function with age.

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“…Furthermore, the process Novel Prospects in Oxidative and Nitrosative Stressof peroxidation can inhibit the activity of protein transporters and ion channels [89,91]. The increase of the permeability also seems to occur in internal mitochondrial membrane, uncoupling respiratory-chain phosphorylation [93]. Finally, the lipid peroxidation leads the severe damages: modification of membrane permeability, enzymatic inhibitions, inactivation of transporters [37,92].…”

Section: Effects On Biological Membranesmentioning

confidence: 99%

Oxidative Stress: Noxious but Also Vital

Bagatini¹,

Jaques²,

Oliveira³

et al. 2018

Novel Prospects in Oxidative and Nitrosative Stress

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The imbalance between reactive oxygen species (ROS) production and antioxidant defenses determines the condition called oxidative stress. When there is an increase in ROS production or a decrease in the antioxidant defenses, this systemic antioxidant/pro-oxidant imbalance may lead to the accumulation of oxidative damage, which, in turn, may lead to a modification of biomolecules. These consist of reactions resulting in protein adducts, DNA oxidation, and formation of lipid peroxides, which, in turn, reduce the cellular functional capacity and increase the risk of disease development. The body has natural scavenging systems against free radicals and other reactive species. However, sometimes the endogenous antioxidant capacity is exceeded by the production of ROS. When this occurs, exogenous antioxidants exert important function for the human health. These bioactive compounds act preventing and neutralizing the formation of new reactive species and free radical s .I ns o m ec a s e s ,a n increase of ROS can help the host to resolve an infection or even to control the tumor growth. Finally, the levels of ROS can be perceived by signal transduction pathways involving known targets(i.e.,p53,Ras,andNF-κB) and regulate physiopathological events such as the cellular cycle, apoptosis, and inflammation.Keywords: reactive species, cellular oxidation, antioxidant system, health, disease © 2018 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Cellular respiration and generation of reactive species in the mitochondria: implications in cell viability and agingOxidative phosphorylation is the center of energy metabolism in plants, animals and several microbial life forms [1]. In eukaryotes, this process occurs in mitochondria. The mitochondria is a cytoplasmic organelle surrounded by two membranes, outer and inner membrane, which main function is the production of most of the phosphate compounds necessary for the energetic balance of the cell. In addition, other functions such as the regulation of the body'sheatgeneration [2][3][4] programmed cell death [5][6][7], reactive oxygen species (ROS) generation and cell signaling [8] is also associated with mitochondria. Cellular vitality is directly related to mitochondria, and mitochondrial dysfunctions are frequent causes of accidental cell death [5,[9][10][11], cancer [12, 13], diabetes [14][15][16] and neurodegenerative diseases [17][18][19], among others.The characterization of the respiratory electron chain could be performed in studies using the fractionation of its components by certain detergents that at low concentrations break the interactions between proteins and lipids in the membranes, leaving associations between proteins intact [20]. In electron transport chain, through this process, four protein complexes were found....

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Reduced Coupling of Oxidative Phosphorylation In Vivo Precedes Electron Transport Chain Defects Due to Mild Oxidative Stress in Mice

Cited by 43 publications

References 53 publications

Physiological adaptations to reproduction II. Mitochondrial adjustments in livers of lactating mice

Physiological adaptations to reproduction II. Mitochondrial adjustments in livers of lactating mice

Age modifies respiratory complex I and protein homeostasis in a muscle type‐specific manner

Oxidative Stress: Noxious but Also Vital

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