scholarly journals Possible role of avian uncoupling protein in down-regulating mitochondrial superoxide production in skeletal muscle of fasted chickens

FEBS Letters ◽  
2006 ◽  
Vol 580 (20) ◽  
pp. 4815-4822 ◽  
Author(s):  
Tomoki Abe ◽  
Ahmad Mujahid ◽  
Kan Sato ◽  
Yukio Akiba ◽  
Masaaki Toyomizu
Keyword(s):  
Skeletal Muscle ◽  
Uncoupling Protein ◽  
Superoxide Production ◽  
Mitochondrial Superoxide ◽  
Avian Uncoupling Protein

scholarly journals Skeletal muscle mitoflashes, pH, and the role of uncoupling protein-3

2019 ◽  
Vol 663 ◽  
pp. 239-248 ◽  
Author(s):  
S. McBride ◽  
L. Wei-LaPierre ◽  
F. McMurray ◽  
M. MacFarlane ◽  
X. Qiu ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Uncoupling Protein ◽  
Uncoupling Protein 3

scholarly journals Hypoxanthine Induces Muscular ATP Depletion and Fatigue via UCP2

2021 ◽  
Vol 12 ◽  
Author(s):  
Cong Yin ◽  
Zewei Ma ◽  
Fan Li ◽  
Chen Duan ◽  
Yexian Yuan ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Fatigue ◽  
Muscle Development ◽  
Uncoupling Protein ◽  
Atp Depletion ◽  
Mitochondrial Uncoupling ◽  
Ucp2 Expression ◽  
Pathological Mechanism ◽  
Abnormal Metabolism

Hypoxanthine (Hx), an intermediate metabolite of the purine metabolism pathway which is dramatically increased in blood and skeletal muscle during muscle contraction and metabolism, is characterized as a marker of exercise exhaustion. However, the physiological effects of Hx on skeletal muscle remain unknown. Herein, we demonstrate that chronic treatment with Hx through dietary supplementation resulted in skeletal muscle fatigue and impaired the exercise performance of mice without affecting their growth and skeletal muscle development. Hx increased the uncoupling protein 2 (UCP2) expression in the skeletal muscle, which led to decreased energy substrate storage and enhanced glycolysis. These effects could also be verified in acute treatment with Hx through intraperitoneal injection. In addition, muscular specifically knockout of UCP2 through intra-muscle tissue injection of adenovirus-associated virus reversed the effects of Hx. In conclusion, we identified a novel role of Hx in the skeletal muscular fatigue mediated by UCP2-dependent mitochondrial uncoupling. This finding may shed light on the pathological mechanism of clinical muscle dysfunctions due to abnormal metabolism, such as muscle fatigue and weakness.

scholarly journals Asymmetric superoxide release inside and outside the mitochondria in skeletal muscle under conditions of aging and disuse

2010 ◽  
Vol 109 (4) ◽  
pp. 1133-1139 ◽  
Author(s):  
Xin Xu ◽  
Chiao-nan (Joyce) Chen ◽  
Edgar A. Arriaga ◽  
LaDora V. Thompson
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Oxidative Damage ◽  
Superoxide Production ◽  
Type I ◽  
Electrophoretic Method ◽  
Specific Product ◽  
Mitochondrial Superoxide ◽  
The Matrix ◽  
Superoxide Release

Superoxide released from mitochondria forms reactive oxygen species that can cause severe oxidative damage and have been associated with aging- and disuse-induced muscle dysfunction. Superoxide is released to both the exterior and the matrix of mitochondria, where oxidative damage is not necessarily the same. This complicates determining the role of mitochondrial superoxide in eliciting oxidative stress in skeletal muscle. A newly developed capillary electrophoretic method analyzes hydroxytriphenylphosphonium ethidium, a superoxide-specific product of triphenylphosphonium hydroethidine, released to outside the mitochondria (supernatant) and retained in the matrix (pellet). In this study, we investigated the mitochondrial superoxide production of soleus (type I) and semimembranosus (type II) muscles of Fischer 344 rats affected by aging (13 vs. 26 mo) and disuse (hindlimb unloading). In agreement with previous studies, overall superoxide production increased with aging and disuse. On the other hand, the new experimental method revealed that superoxide production outside the mitochondria of the soleus does not show a significant age-related increase. Another observation was that the superoxide production increase in the matrix occurs earlier (7 days of disuse) compared with the outside mitochondria (14 days of disuse) in both muscle types. These findings indicate that superoxide release is complex as it occurs asymmetrically at both sides of the mitochondrial inner membrane, and that such release has muscle type and temporal specificity. These findings are important to refine current concepts on oxidative stress associated with muscle aging and disuse.

scholarly journals Altered Mitochondrial Superoxide Production in Skeletal Muscle of an ALS Mouse Model during the Disease Progression

2014 ◽  
Vol 106 (2) ◽  
pp. 184a
Author(s):  
Chehade Karam ◽  
Jianxun Yi ◽  
Jiajie Xu ◽  
Carlo Manno ◽  
Kaitao Li ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Mouse Model ◽  
Disease Progression ◽  
Superoxide Production ◽  
Mitochondrial Superoxide

Type II skeletal myofibers possess unique properties that potentiate mitochondrial H2O2 generation

2006 ◽  
Vol 290 (3) ◽  
pp. C844-C851 ◽  
Author(s):  
Ethan J. Anderson ◽  
P. Darrell Neufer
Keyword(s):  
Skeletal Muscle ◽  
Mitochondrial Dysfunction ◽  
Complex I ◽  
Basal Respiration ◽  
Superoxide Production ◽  
Complex Iii ◽  
Type I ◽  
Type Ii ◽  
Mitochondrial Content ◽  
Mitochondrial Superoxide

Mitochondrial dysfunction is implicated in a number of skeletal muscle pathologies, most notably aging-induced atrophy and loss of type II myofibers. Although oxygen-derived free radicals are thought to be a primary cause of mitochondrial dysfunction, the underlying factors governing mitochondrial superoxide production in different skeletal myofiber types is unknown. Using a novel in situ approach to measure H2O2 production (indicator of superoxide formation) in permeabilized rat skeletal muscle fiber bundles, we found that mitochondrial free radical leak (H2O2 produced/O2 consumed) is two- to threefold higher ( P < 0.05) in white (WG, primarily type IIB fibers) than in red (RG, type IIA) gastrocnemius or soleus (type I) myofibers during basal respiration supported by complex I (pyruvate + malate) or complex II (succinate) substrates. In the presence of respiratory inhibitors, maximal rates of superoxide produced at both complex I and complex III are markedly higher in RG and WG than in soleus muscle despite ∼50% less mitochondrial content in WG myofibers. Duplicate experiments conducted with ±exogenous superoxide dismutase revealed striking differences in the topology and/or dismutation of superoxide in WG vs. soleus and RG muscle. When normalized for mitochondrial content, overall H2O2 scavenging capacity is lower in RG and WG fibers, whereas glutathione peroxidase activity, which is largely responsible for H2O2 removal in mitochondria, is similar in all three muscle types. These findings suggest that type II myofibers, particularly type IIB, possess unique properties that potentiate mitochondrial superoxide production and/or release, providing a potential mechanism for the heterogeneous development of mitochondrial dysfunction in skeletal muscle.

scholarly journals Mitochondrial superoxide and coenzyme Q in insulin-deficient rats: increased electron leak

2011 ◽  
Vol 301 (6) ◽  
pp. R1616-R1624 ◽  
Author(s):  
Judith A. Herlein ◽  
Brian D. Fink ◽  
Dorlyne M. Henry ◽  
Mark A. Yorek ◽  
Lynn M. Teesch ◽  
...  
Keyword(s):  
Weight Loss ◽  
Electron Transport ◽  
Coenzyme Q ◽  
Tca Cycle ◽  
Diabetic Rats ◽  
Superoxide Production ◽  
Ros Production ◽  
Mitochondrial Superoxide ◽  
Respiratory Parameters

Mitochondrial superoxide is important in the pathogeneses of diabetes and its complications. However, there is uncertainty regarding the intrinsic propensity of mitochondria to generate this radical. Studies to date suggest that superoxide production by mitochondria of insulin-sensitive target tissues of insulin-deficient rodents is reduced or unchanged. Moreover, little is known of the role of the Coenzyme Q (CoQ), whose semiquinone form reacts with molecular oxygen to generate superoxide. We measured reactive oxygen species (ROS) production, respiratory parameters, and CoQ content in mitochondria from gastrocnemius muscle of control and streptozotocin (STZ)-diabetic rats. CoQ content did not differ between mitochondria isolated from vehicle- or STZ-treated animals. CoQ also was unaffected by weight loss in the absence of diabetes (induced by caloric restriction). Under state 4 or state 3 conditions, both respiration and ROS release were reduced in diabetic mitochondria fueled with succinate, glutamate plus malate, or with all three substrates (continuous TCA cycle). However, H2O2 and directly measured superoxide production were substantially increased in gastrocnemius mitochondria of diabetic rats when expressed per unit oxygen consumed. On the basis of substrate and inhibitor effects, the mechanism involved multiple electron transport sites. More limited results using heart mitochondria were similar. ROS per unit respiration was greater in muscle mitochondria from diabetic compared with control rats during state 3, as well as state 4, while the reduction in ROS per unit respiration on transition to state 3 was less for diabetic mitochondria. In summary, ROS production is, in fact, increased in mitochondria from insulin-deficient muscle when considered relative to electron transport. This is evident on multiple energy substrates and in different respiratory states. CoQ is not reduced in diabetic mitochondria or with weight loss due to food restriction. The implications of these findings are discussed.

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