scholarly journals Reactive Oxygen Species in Skeletal Muscle Signaling

2012 ◽  
Vol 2012 ◽  
pp. 1-17 ◽  
Author(s):  
Elena Barbieri ◽  
Piero Sestili
Keyword(s):  
Reactive Oxygen Species ◽  
Skeletal Muscle ◽  
Signaling Pathways ◽  
Contractile Activity ◽  
Reactive Oxygen ◽  
Target Cells ◽  
Past Century ◽  
Oxygen Species ◽  
Toxic Species ◽  
Dynamic Scenario

Generation of reactive oxygen species (ROS) is a ubiquitous phenomenon in eukaryotic cells' life. Up to the 1990s of the past century, ROS have been solely considered as toxic species resulting in oxidative stress, pathogenesis and aging. However, there is now clear evidence that ROS are not merely toxic species but also—within certain concentrations—useful signaling molecules regulating physiological processes. During intense skeletal muscle contractile activity myotubes' mitochondria generate high ROS flows: this renders skeletal muscle a tissue where ROS hold a particular relevance. According to their hormetic nature, in muscles ROS may trigger different signaling pathways leading to diverging responses, from adaptation to cell death. Whether a “positive” or “negative” response will prevail depends on many variables such as, among others, the site of ROS production, the persistence of ROS flow or target cells' antioxidant status. In this light, a specific threshold of physiological ROS concentrations above which ROS exert negative, toxic effects is hard to determine, and the concept of “physiologically compatible” levels of ROS would better fit with such a dynamic scenario. In this review these concepts will be discussed along with the most relevant signaling pathways triggered and/or affected by ROS in skeletal muscle.

Hypoxia-induced reactive oxygen species formation in skeletal muscle

2007 ◽  
Vol 102 (6) ◽  
pp. 2379-2388 ◽  
Author(s):  
Thomas L. Clanton
Keyword(s):  
Reactive Oxygen Species ◽  
Skeletal Muscle ◽  
Molecular Mechanisms ◽  
Cell Injury ◽  
Cell Function ◽  
Contractile Activity ◽  
Reactive Oxygen ◽  
Hypoxic Exposure ◽  
Ros Production ◽  
Oxygen Species

The existence of hypoxia-induced reactive oxygen species (ROS) production remains controversial. However, numerous observations with a variety of methods and in many cells and tissue types are supportive of this idea. Skeletal muscle appears to behave much like heart in that in the early stages of hypoxia there is a transient elevation in ROS, whereas in chronic exposure to very severe hypoxia there is evidence of ongoing oxidative stress. Important remaining questions that are addressed in this review include the following. Are there levels of Po2 in skeletal muscle, typical of physiological or mildly pathophysiological conditions, that are low enough to induce significant ROS production? Does the ROS associated with muscle contractile activity reflect imbalances in oxygen uptake and demand that drive the cell to a more reduced state? What are the possible molecular mechanisms by which ROS may be elevated in hypoxic skeletal muscle? Is the production of ROS in hypoxia of physiological significance, both with respect to cell signaling pathways promoting cell function and with respect to damaging effects of long-term exposure? Discussion of these and other topics leads to general conclusions that hypoxia-induced ROS may be a normal physiological response to imbalance in oxygen supply and demand or environmental stress and may play a yet undefined role in normal response mechanisms to these stimuli. However, in chronic and extreme hypoxic exposure, muscles may fail to maintain a normal redox homeostasis, resulting in cell injury or dysfunction.

scholarly journals Reactive oxygen species formation during tetanic contractions in single isolated Xenopus myofibers

2011 ◽  
Vol 111 (3) ◽  
pp. 898-904 ◽  
Author(s):  
Li Zuo ◽  
Leonardo Nogueira ◽  
Michael C. Hogan
Keyword(s):  
Reactive Oxygen Species ◽  
Skeletal Muscle ◽  
Real Time ◽  
Contractile Activity ◽  
Reactive Oxygen ◽  
Ros Generation ◽  
Oxygen Species ◽  
Fatigue Development ◽  
Species Formation ◽  
Significant Difference

Contracting skeletal muscle produces reactive oxygen species (ROS) that have been shown to affect muscle function and adaptation. However, real-time measurement of ROS in contracting myofibers has proven to be difficult. We used amphibian ( Xenopus laevis) muscle to test the hypothesis that ROS are formed during contractile activity in isolated single skeletal muscle fibers and that this contraction-induced ROS formation affects fatigue development. Single myofibers were loaded with 5 μM dihydrofluorescein-DA (Hfluor-DA), a fluorescent probe that reacts with ROS and results in the formation of fluorescein (Fluor) to precisely monitor ROS generation within single myofibers in real time using confocal miscroscopy. Three identical periods of maximal tetanic contractions (1 contraction/3 s for 2 min, separated by 60 min of rest) were conducted by each myofiber ( n = 6) at 20°C. Ebselen (an antioxidant) was present in the perfusate (10 μM) during the second contractile period. Force was reduced by ∼30% during each of the three contraction periods, with no significant difference in fatigue development among the three periods. The Fluor signal, indicative of ROS generation, increased significantly above baseline in both the first (42 ± 14%) and third periods (39 ± 10%), with no significant difference in the increase in fluorescence between the first and third periods. There was no increase of Fluor in the presence of ebselen during the second contractile period. These results demonstrated that, in isolated intact Xenopus myofibers, 1) ROS can be measured in real time during tetanic contractions, 2) contractile activity induced a significant increase above resting levels of ROS production, and 3) ebselen treatment reduced ROS generation to baseline levels but had no effect on myofiber contractility and fatigue development.

scholarly journals A Study on Myogenesis by Regulation of Reactive Oxygen Species and Cytotoxic Activity by Selenium Nanoparticles

Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1727
Author(s):  
Sang-Cheol Lee ◽  
Na-Hyun Lee ◽  
Kapil D. Patel ◽  
Soo-Kyung Jun ◽  
Jeong-Hui Park ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Skeletal Muscle ◽  
Contractile Activity ◽  
Reactive Oxygen ◽  
Selenium Nanoparticles ◽  
C2c12 Cells ◽  
Myoblast Differentiation ◽  
Oxygen Species ◽  
Protective Effects ◽  
Intracellular Ros

Reactive oxygen species (ROS) are continuously produced by skeletal muscle during contractile activity and even at rest. However, the ROS generated from excessive exercise or traumatic damage may produce more ROS than can be neutralized by an antioxidant capacity, which can be harmful to muscle function. In particular, selenium is a known antioxidant that regulates physiological functions such as cell differentiation and anti-inflammatory function. In this study, we developed nano-sized antioxidative biomaterials using selenium to investigate the protective and differentiation effects against C2C12 myoblasts in an H2O2-induced oxidative stress environment. The selenium nanoparticles (SeNPs) were produced with a size of 35.6 ± 4.3 nm and showed antioxidant effects according to the 3,3′,5,5′-tetramethylbenzidine assay. Then, SeNPs were treated to C2C12 cells with or without H2O2. Our results showed that SeNPs reduced C2C12 apoptosis and intracellular ROS levels. Additionally, SeNPs effectively up-regulated in the presence of H2O2, MyoD, MyoG, α-actinin, and myosin heavy chain, which are well known to increase during myoblast differentiation as assayed by qRT-PCR, immunocytochemistry-staining, western blotting. These results demonstrate that SeNPs can accelerate differentiation with its protective effects from the ROS environment and can be applied to the treatment of skeletal muscle in a cellular redox environment.

Effect of prior chronic contractile activity on mitochondrial function and apoptotic protein expression in denervated muscle

2008 ◽  
Vol 105 (1) ◽  
pp. 114-120 ◽  
Author(s):  
Michael F. N. O'Leary ◽  
David A. Hood
Keyword(s):  
Reactive Oxygen Species ◽  
Skeletal Muscle ◽  
Protein Expression ◽  
Reactive Oxygen Species Production ◽  
Contractile Activity ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Chronic Stimulation ◽  
Apoptotic Protein ◽  
Species Production

Skeletal muscle is highly adaptable in response to increases and decreases in contractile activity. The purpose of this study was to determine whether the preconditioning of skeletal muscle has a protective effect against subsequent denervation-induced apoptotic protein expression. To investigate this, we chronically stimulated the tibialis anterior and extensor digitorum longus muscles for 7 days (10 Hz, 3 h/day) before 7 days of denervation. Denervation reduced total cytochrome- c oxidase activity by 39%, which was likely a consequence of a decrease in subsarcolemmal (SS) mitochondria. This decrease in the SS subfraction was prevented by prior chronic stimulation and, as a result, maintained total mitochondrial content at control levels. The expression of Bax was elevated 2.2-fold by denervation, and prior chronic stimulation did not attenuate this increase. This produced a increase in the Bax-to-Bcl-2 ratio, indicating greater muscle apoptotic susceptibility. Denervation also decreased state 3 respiration in SS and intermyofibrillar mitochondria and elevated state 4 reactive oxygen species production within both mitochondrial subfractions. These changes were not prevented by prior chronic stimulation. Furthermore, the antioxidant protein MnSOD was also reduced by denervation, whereas Beclin-1 was markedly elevated. This suggests that autophagic cell death could also play a significant part in denervation-induced muscle atrophy. Thus, despite prior chronic stimulation, denervation increases the apoptotic susceptibility of skeletal muscle by altering the Bax-to-Bcl-2 ratio, by increasing reactive oxygen species production, and by reducing the expression of MnSOD. Whether a more extensive stimulation paradigm would be more effective in attenuating apoptosis before muscle disuse remains to be determined.

Oxidative stress and disuse muscle atrophy

2007 ◽  
Vol 102 (6) ◽  
pp. 2389-2397 ◽  
Author(s):  
Scott K. Powers ◽  
Andreas N. Kavazis ◽  
Joseph M. McClung
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Skeletal Muscle ◽  
Cell Signaling ◽  
Signaling Pathways ◽  
Muscle Atrophy ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Disuse Muscle Atrophy ◽  
Cell Signaling Pathways

Skeletal muscle inactivity is associated with a loss of muscle protein and reduced force-generating capacity. This disuse-induced muscle atrophy results from both increased proteolysis and decreased protein synthesis. Investigations of the cell signaling pathways that regulate disuse muscle atrophy have increased our understanding of this complex process. Emerging evidence implicates oxidative stress as a key regulator of cell signaling pathways, leading to increased proteolysis and muscle atrophy during periods of prolonged disuse. This review will discuss the role of reactive oxygen species in the regulation of inactivity-induced skeletal muscle atrophy. The specific objectives of this article are to provide an overview of muscle proteases, outline intracellular sources of reactive oxygen species, and summarize the evidence that connects oxidative stress to signaling pathways contributing to disuse muscle atrophy. Moreover, this review will also discuss the specific role that oxidative stress plays in signaling pathways responsible for muscle proteolysis and myonuclear apoptosis and highlight gaps in our knowledge of disuse muscle atrophy. By presenting unresolved issues and suggesting topics for future research, it is hoped that this review will serve as a stimulus for the expansion of knowledge in this exciting field.

Proton leak induced by reactive oxygen species produced during in vitro anoxia/reoxygenation in rat skeletal muscle mitochondria

2006 ◽  
Vol 38 (1) ◽  
pp. 23-32 ◽  
Author(s):  
Rachel Navet ◽  
Ange Mouithys-Mickalad ◽  
Pierre Douette ◽  
Claudine M. Sluse-Goffart ◽  
Wieslawa Jarmuszkiewicz ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Skeletal Muscle ◽  
Reactive Oxygen ◽  
Proton Leak ◽  
Oxygen Species ◽  
Rat Skeletal Muscle ◽  
Muscle Mitochondria ◽  
Skeletal Muscle Mitochondria
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