scholarly journals Mitochondrial ROS generation and function in skeletal muscle from older subjects (863.5)

2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
Giorgos Sakellariou ◽  
Adam Lightfoot ◽  
Timothy Pearson ◽  
Nicola Wells ◽  
Alastair Gilmore ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Ros Generation ◽  
Mitochondrial Ros ◽  
Older Subjects ◽  
And Function

Stanozolol treatment decreases the mitochondrial ROS generation and oxidative stress induced by acute exercise in rat skeletal muscle

2011 ◽  
Vol 110 (3) ◽  
pp. 661-669 ◽  
Author(s):  
Ana Saborido ◽  
Alba Naudí ◽  
Manuel Portero-Otín ◽  
Reinald Pamplona ◽  
Alicia Megías
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Fatty Acid Composition ◽  
Mitochondrial Membrane ◽  
Acute Exercise ◽  
Ros Generation ◽  
Ros Production ◽  
Rat Skeletal Muscle ◽  
Mitochondrial Ros ◽  
Exercise Induced

Anabolic androgenic steroids are used in the sport context to enhance muscle mass and strength and to increase muscle fatigue resistance. Since muscle fatigue has been related to oxidative stress caused by an exercise-linked reactive oxygen species (ROS) production, we investigated the potential effects of a treatment with the anabolic androgenic steroid stanozolol against oxidative damage induced on rat skeletal muscle mitochondria by an acute bout of exhaustive exercise. Mitochondrial ROS generation with complex I- and complex II-linked substrates was increased in exercised control rats, whereas it remained unchanged in the steroid-treated animals. Stanozolol treatment markedly reduced the extent of exercise-induced oxidative damage to mitochondrial proteins, as indicated by the lower levels of the specific markers of protein oxidation, glycoxidation, and lipoxidation, and the preservation of the activity of the superoxide-sensitive enzyme aconitase. This effect was not due to an enhancement of antioxidant enzyme activities. Acute exercise provoked changes in mitochondrial membrane fatty acid composition characterized by an increased content in docosahexaenoic acid. In contrast, the postexercise mitochondrial fatty acid composition was not altered in stanozolol-treated rats. Our results suggest that stanozolol protects against acute exercise-induced oxidative stress by reducing mitochondrial ROS production, in association with a preservation of mitochondrial membrane properties.

Effect of Partial Denervation on Mitochondrial ROS Generation in Skeletal Muscle; a Role in Sarcopenia?

2016 ◽  
Vol 100 ◽  
pp. S86-S87
Author(s):  
Natalie Pollock ◽  
Caroline Amy Staunton ◽  
Aphrodite Vasilaki ◽  
Anne McArdle ◽  
Malcolm J Jackson
Keyword(s):  
Skeletal Muscle ◽  
Ros Generation ◽  
Partial Denervation ◽  
Mitochondrial Ros

scholarly journals Curcumin Ameliorates Heat-Induced Injury through NADPH Oxidase–Dependent Redox Signaling and Mitochondrial Preservation in C2C12 Myoblasts and Mouse Skeletal Muscle

2020 ◽  
Vol 150 (9) ◽  
pp. 2257-2267 ◽  
Author(s):  
Tianzheng Yu ◽  
Jacob Dohl ◽  
Li Wang ◽  
Yifan Chen ◽  
Heath G Gasier ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Nadph Oxidase ◽  
Tissue Injury ◽  
Heat Exposure ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Mitochondrial Morphology ◽  
Ros Production ◽  
C2c12 Myoblasts ◽  
Mitochondrial Ros ◽  
And Function

ABSTRACT Background Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and the mitochondrial electron transport chain are the primary sources of reactive oxygen species (ROS). Previous studies have shown that severe heat exposure damages mitochondria and causes excessive mitochondrial ROS production that contributes to the pathogenesis of heat-related illnesses. Objectives We tested whether the antioxidant curcumin could protect against heat-induced mitochondrial dysfunction and skeletal muscle injury, and characterized the possible mechanism. Methods Mouse C2C12 myoblasts and rat flexor digitorum brevis (FDB) myofibers were treated with 5 μM curcumin; adult male C57BL/6J mice received daily curcumin (15, 50, or 100 mg/kg body weight) by gavage for 10 consecutive days. We compared ROS levels and mitochondrial morphology and function between treatment and nontreatment groups under unheated or heat conditions, and investigated the upstream mechanism and the downstream effect of curcumin-regulated ROS production. Results In C2C12 myoblasts, curcumin prevented heat-induced mitochondrial fragmentation, ROS overproduction, and apoptosis (all P < 0.05). Curcumin treatment for 2 and 4 h at 37°C induced increases in ROS levels by 42% and 59% (dihydroethidium-derived fluorescence), accompanied by increases in NADPH oxidase protein expression by 24% and 32%, respectively (all P < 0.01). In curcumin-treated cells, chemical inhibition and genetic knockdown of NADPH oxidase restored ROS to levels similar to those of controls, indicating NADPH oxidase mediates curcumin-stimulated ROS production. Moreover, curcumin induced ROS-dependent shifting of the mitochondrial fission–fusion balance toward fusion, and increases in mitochondrial mass by 143% and membrane potential by 30% (both P < 0.01). In rat FDB myofibers and mouse gastrocnemius muscles, curcumin preserved mitochondrial morphology and function during heat stress, and prevented heat-induced mitochondrial ROS overproduction and tissue injury (all P < 0.05). Conclusions Curcumin regulates ROS hormesis favoring mitochondrial fusion/elongation, biogenesis, and improved function in rodent skeletal muscle. Curcumin may be an effective therapeutic target for heat-related illness and other mitochondrial diseases.

scholarly journals Essential Role of Septin 7 in Skeletal Muscle Structure and Function

2020 ◽  
Vol 118 (3) ◽  
pp. 258a
Author(s):  
Laszlo Csernoch ◽  
Mónika Gönczi ◽  
Zsolt Ráduly ◽  
László Szabó ◽  
Nóra Dobrosi ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Essential Role ◽  
Structure And Function ◽  
Muscle Structure ◽  
And Function

scholarly journals β2-adrenergic receptor agonist counteracts skeletal muscle atrophy and oxidative stress in uremic mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Takaaki Higashihara ◽  
Hiroshi Nishi ◽  
Koji Takemura ◽  
Hiroshi Watanabe ◽  
Toru Maruyama ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Adrenergic Receptor ◽  
Culture Media ◽  
Therapeutic Interventions ◽  
Skeletal Muscle Atrophy ◽  
C2c12 Myotubes ◽  
Ros Generation ◽  
Skeletal Muscle Function ◽  
Ros Accumulation ◽  
Β2 Adrenergic Receptor

AbstractIn patients with chronic kidney disease, skeletal muscle dysfunction is associated with mortality. Uremic sarcopenia is caused by ageing, malnutrition, and chronic inflammation, but the molecular mechanism and potential therapeutics have not been fully elucidated yet. We hypothesize that accumulated uremic toxins might exert a direct deteriorative effect on skeletal muscle and explore the pharmacological treatment in experimental animal and culture cell models. The mice intraperitoneally injected with indoxyl sulfate (IS) after unilateral nephrectomy displayed an elevation of IS concentration in skeletal muscle and a reduction of instantaneous muscle strength, along with the predominant loss of fast-twitch myofibers and intramuscular reactive oxygen species (ROS) generation. The addition of IS in the culture media decreased the size of fully differentiated mouse C2C12 myotubes as well. ROS accumulation and mitochondrial dysfunction were also noted. Next, the effect of the β2-adrenergic receptor (β2-AR) agonist, clenbuterol, was evaluated as a potential treatment for uremic sarcopenia. In mice injected with IS, clenbuterol treatment increased the muscle mass and restored the tissue ROS level but failed to improve muscle weakness. In C2C12 myotubes stimulated with IS, although β2-AR activation also attenuated myotube size reduction and ROS accumulation as did other anti-oxidant reagents, it failed to augment the mitochondrial membrane potential. In conclusion, IS provokes muscular strength loss (uremic dynapenia), ROS generation, and mitochondrial impairment. Although the β2-AR agonist can increase the muscular mass with ROS reduction, development of therapeutic interventions for restoring skeletal muscle function is still awaited.

scholarly journals Mapping of the contraction-induced phosphoproteome identifies TRIM28 as a significant regulator of skeletal muscle size and function

Cell Reports ◽  
2021 ◽  
Vol 34 (9) ◽  
pp. 108796
Author(s):  
Nathaniel D. Steinert ◽  
Gregory K. Potts ◽  
Gary M. Wilson ◽  
Amelia M. Klamen ◽  
Kuan-Hung Lin ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Size ◽  
And Function
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