scholarly journals Ceramides increase mitochondrial ROS generation via altered mitochondrial dynamics in skeletal muscle

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Braden J Tucker ◽  
Melissa E Smith ◽  
Benjamin T Bikman
Keyword(s):  
Skeletal Muscle ◽  
Mitochondrial Dynamics ◽  
Ros Generation ◽  
Mitochondrial Ros

scholarly journals Homocysteine and Mitochondria in Cardiovascular and Cerebrovascular Systems

2020 ◽  
Vol 21 (20) ◽  
pp. 7698 ◽  
Author(s):  
Peter Kaplan ◽  
Zuzana Tatarkova ◽  
Monika Kmetova Sivonova ◽  
Peter Racay ◽  
Jan Lehotsky
Keyword(s):  
Antioxidant Defense ◽  
Current Knowledge ◽  
Mitochondrial Dynamics ◽  
Ros Generation ◽  
Elevated Concentration ◽  
Apoptotic Pathway ◽  
Beneficial Effects ◽  
Mitochondrial Ros ◽  
Mitochondrial Functions ◽  
Altered Gene

Elevated concentration of homocysteine (Hcy) in the blood plasma, hyperhomocysteinemia (HHcy), has been implicated in various disorders, including cardiovascular and neurodegenerative diseases. Accumulating evidence indicates that pathophysiology of these diseases is linked with mitochondrial dysfunction. In this review, we discuss the current knowledge concerning the effects of HHcy on mitochondrial homeostasis, including energy metabolism, mitochondrial apoptotic pathway, and mitochondrial dynamics. The recent studies suggest that the interaction between Hcy and mitochondria is complex, and reactive oxygen species (ROS) are possible mediators of Hcy effects. We focus on mechanisms contributing to HHcy-associated oxidative stress, such as sources of ROS generation and alterations in antioxidant defense resulting from altered gene expression and post-translational modifications of proteins. Moreover, we discuss some recent findings suggesting that HHcy may have beneficial effects on mitochondrial ROS homeostasis and antioxidant defense. A better understanding of complex mechanisms through which Hcy affects mitochondrial functions could contribute to the development of more specific therapeutic strategies targeted at HHcy-associated disorders.

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 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 Mitochondrial Dynamics, ROS, and Cell Signaling: A Blended Overview

Life ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 332
Author(s):  
Valentina Brillo ◽  
Leonardo Chieregato ◽  
Luigi Leanza ◽  
Silvia Muccioli ◽  
Roberto Costa
Keyword(s):  
Molecular Mechanisms ◽  
Mitochondrial Dynamics ◽  
Eukaryotic Cells ◽  
Therapeutic Approaches ◽  
Cellular Functions ◽  
Lipid Trafficking ◽  
Mitochondrial Ros ◽  
Intracellular Organelles ◽  
Proliferation Regulation ◽  
Dynamic Plasticity

Mitochondria are key intracellular organelles involved not only in the metabolic state of the cell, but also in several cellular functions, such as proliferation, Calcium signaling, and lipid trafficking. Indeed, these organelles are characterized by continuous events of fission and fusion which contribute to the dynamic plasticity of their network, also strongly influenced by mitochondrial contacts with other subcellular organelles. Nevertheless, mitochondria release a major amount of reactive oxygen species (ROS) inside eukaryotic cells, which are reported to mediate a plethora of both physiological and pathological cellular functions, such as growth and proliferation, regulation of autophagy, apoptosis, and metastasis. Therefore, targeting mitochondrial ROS could be a promising strategy to overcome and hinder the development of diseases such as cancer, where malignant cells, possessing a higher amount of ROS with respect to healthy ones, could be specifically targeted by therapeutic treatments. In this review, we collected the ultimate findings on the blended interplay among mitochondrial shaping, mitochondrial ROS, and several signaling pathways, in order to contribute to the dissection of intracellular molecular mechanisms involved in the pathophysiology of eukaryotic cells, possibly improving future therapeutic approaches.

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