Skeletal muscle reactive oxygen species: A target of good cop/bad cop for exercise and disease

Mason, Shaun; Wadley, Glenn D.

doi:10.1179/1351000213y.0000000077

Cited by 48 publications

(40 citation statements)

References 94 publications

(145 reference statements)

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“…However, chronically elevated ROS levels are detrimental to skeletal muscle and surrounding healthy tissue (Mason and Wadley 2014) and, therefore, may have negative effects on the adaptations to acute inflammation. For example, human supplementation with a powerful antioxidant and anti-inflammatory agent Nacetylcysteine (NAC) (Uraz and others 2013) inhibits fatigue and blunts muscle force reduction 24-48 h after eccentric exercise; however, long-term muscle function is hampered (Michailidis and others 2013).…”

Section: Introductionmentioning

confidence: 99%

Regulation of Granulocyte Colony-Stimulating Factor and Its Receptor in Skeletal Muscle Is Dependent Upon the Type of Inflammatory Stimulus

Wright

Brown

Gatta

et al. 2015

Journal of Interferon & Cytokine Research

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The cytokine granulocyte colony-stimulating factor (G-CSF) binds to its receptor (G-CSFR) to stimulate hematopoietic stem cell mobilization, myelopoiesis, and the production and activation of neutrophils. In response to exercise-induced muscle damage, G-CSF is increased in circulation and G-CSFR has recently been identified in skeletal muscle cells. While G-CSF/G-CSFR activation mediates pro- and anti-inflammatory responses, our understanding of the role and regulation in the muscle is limited. The aim of this study was to investigate, in vitro and in vivo, the role and regulation of G-CSF and G-CSFR in skeletal muscle under conditions of muscle inflammation and damage. First, C2C12 myotubes were treated with lipopolysaccharide (LPS) with and without G-CSF to determine if G-CSF modulates the inflammatory response. Second, the regulation of G-CSF and its receptor was measured following eccentric exercise-induced muscle damage and the expression levels we investigated for redox sensitivity by administering the antioxidant N-acetylcysteine (NAC). LPS stimulation of C2C12 myotubes resulted in increases in G-CSF, interleukin (IL)-6, monocyte chemoattractant protein-1 (MCP-1), and tumor necrosis factor-α (TNFα) messenger RNA (mRNA) and an increase in G-CSF, IL-6, and MCP-1 release from C2C12 myotubes. The addition of G-CSF following LPS stimulation of C2C12 myotubes increased IL-6 mRNA and cytokine release into the media, however it did not affect MCP-1 or TNFα. Following eccentric exercise-induced muscle damage in humans, G-CSF levels were either marginally increased in circulation or remain unaltered in skeletal muscle. Similarly, G-CSFR levels remained unchanged in response to damaging exercise and G-CSF/G-CSFR did not change in response to NAC. Collectively, these findings suggest that G-CSF may cooperate with IL-6 and potentially promote muscle regeneration in vitro, whereas in vivo aseptic inflammation induced by exercise did not change G-CSF and G-CSFR responses. These observations suggest that different models of inflammation produce a different G-CSF response.

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Section: Introductionmentioning

confidence: 99%

Regulation of Granulocyte Colony-Stimulating Factor and Its Receptor in Skeletal Muscle Is Dependent Upon the Type of Inflammatory Stimulus

Wright

Brown

Gatta

et al. 2015

Journal of Interferon & Cytokine Research

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“…It is well-known that exercise induced metabolic stress by the generation of wide range of reactive oxygen species (Mason et al, 2014). Reactive oxygen species, in turn, react with cellular lipids producing lipid peroxides within tissues (Zsolt et al, 2013).…”

Section: Resultsmentioning

confidence: 99%

Effects of L-Ascorbic Acid and Alpha-Tocopherol on Biochemical Parameters of Swimming-Induced Oxidative Stress in Serum of Guinea Pigs

Bursać-Mitrović¹,

Мilоvаnоvić²,

Mitić³

et al. 2016

Afr J Tradit Complement Altern Med

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Background: The purpose of this study is to determine the effect of L-ascorbic acid and alpha-tocopherol as well as combination of these vitamins with or without exposure to physical exercise on intensity of lipid peroxidation, activity of xanthine oxidase, activity of total antioxidative system, concentration of glutathione, and activity of catalase in the serum of guinea pigs. Materials and Methods: The experimental measurements of intensity of lipid peroxidation, activity of xanthine oxidase, activity of total antioxidative system, concentration of glutathione, and activity of catalase were done in the serum of guinea pigs. The animals were exposed to the test load to achieve exhaustion and the test was terminated when the animal for the third time to sink into the water. Results:The results of this study demonstrated that endurance exercise of guinea pigs induced oxidative stress response in terms of increased lipid peroxidation and activity of xanthine oxidase in the serum of experimental animals. Our study investigated the antioxidant activity of L-ascorbic acid and alpha-tocopherol also measuring three protective markers in the serum: total antioxidant activity, content of glutathione and activity of catalase. The results obtained show that the vitamins influence the concentrations of above mentioned biochemical parameters, which points out their protective effect of swimming-induced oxidative stress. Conclusion: Single or combined administration of L-ascorbic acid and alpha-tocopherol caused significant inhibition of these markers indicating the important antioxidant activity of the vitamins. Results lead to conclude that the combined treatments with vitamins with or without exposure to physical exercise showed the clear synergistic effect..

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“…Reactive oxygen species (ROS) and reactive nitrogen species are free radicals produced in myocytes, endothelium, and extracellular space from peroxisomes, SR, PLA 2 , nicotinamide adenine dinucleotide phosphate (NADPH) oxidases, xanthine oxidases (XO), and nitric oxide (NO) synthases (111,139). However, mitochondria of skeletal muscle cells are the predominant source of ROS (139).…”

Section: Mitochondria An Important Source Of Reactive Oxygen Speciesmentioning

confidence: 99%

Chronology of mitochondrial and cellular events during skeletal muscle ischemia-reperfusion

Paradis

Charles

Meyer

et al. 2016

American Journal of Physiology-Cell Physiology

104

127

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Peripheral artery disease (PAD) is a common circulatory disorder of the lower limb arteries that reduces functional capacity and quality of life of patients. Despite relatively effective available treatments, PAD is a serious public health issue associated with significant morbidity and mortality. Ischemia-reperfusion (I/R) cycles during PAD are responsible for insufficient oxygen supply, mitochondriopathy, free radical production, and inflammation and lead to events that contribute to myocyte death and remote organ failure. However, the chronology of mitochondrial and cellular events during the ischemic period and at the moment of reperfusion in skeletal muscle fibers has been poorly reviewed. Thus, after a review of the basal myocyte state and normal mitochondrial biology, we discuss the physiopathology of ischemia and reperfusion at the mitochondrial and cellular levels. First we describe the chronology of the deleterious biochemical and mitochondrial mechanisms activated by I/R. Then we discuss skeletal muscle I/R injury in the muscle environment, mitochondrial dynamics, and inflammation. A better understanding of the chronology of the events underlying I/R will allow us to identify key factors in the development of this pathology and point to suitable new therapies. Emerging data on mitochondrial dynamics should help identify new molecular and therapeutic targets and develop protective strategies against PAD.peripheral artery disease; ischemia-reperfusion; skeletal muscle; mitochondria; oxidative stress PERIPHERAL ARTERY DISEASE (PAD) refers to a common circulatory disorder of the lower limb caused by chronic narrowing of the arteries (e.g., stenosis and occlusion) or atherosclerosis. PAD represents a broad spectrum of disease severity, ranging from asymptomatic disease to frequent pain when walking (i.e., intermittent claudication or limping) or critical limb ischemia associated with decubitus pain and/or ulcers (114,126).PAD is known to be associated with reduced functional capacity and quality of life. It is a major cause of limb amputation, as well as an increased risk factor for myocardial infarction, stroke, and death. The incidence of PAD varies with age, from 3-10% in young people to 15-20% in people Ͼ70 yr of age, and is asymptomatic in 40% of the cases (1), with greater prevalence among men. The major PAD risk factors, including smoking, diabetes mellitus, dyslipidemia, hypertension, and obesity, are the same as those for cardiovascular and cerebrovascular diseases (35).Three main complementary treatment options improve the functional status and other clinical outcomes in PAD patients (54). 1) Optimization of medical therapy (i.e., pharmacotherapy) reduces the risk of cardiac ischemia, increases the distance a patient can walk, and improves the functional capacity of patients. 2) When possible, exercise training, a noninvasive and nonpharmacological therapy, improves walking ability and has protective effects in patients with PAD characterized by intermittent claudication and infrainguinal lesions...

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Skeletal muscle reactive oxygen species: A target of good cop/bad cop for exercise and disease

Cited by 48 publications

References 94 publications

Regulation of Granulocyte Colony-Stimulating Factor and Its Receptor in Skeletal Muscle Is Dependent Upon the Type of Inflammatory Stimulus

Regulation of Granulocyte Colony-Stimulating Factor and Its Receptor in Skeletal Muscle Is Dependent Upon the Type of Inflammatory Stimulus

Effects of L-Ascorbic Acid and Alpha-Tocopherol on Biochemical Parameters of Swimming-Induced Oxidative Stress in Serum of Guinea Pigs

Chronology of mitochondrial and cellular events during skeletal muscle ischemia-reperfusion

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