scholarly journals Decreased hydrogen peroxide production and mitochondrial respiration in skeletal muscle but not cardiac muscle of the green-striped burrowing frog, a natural model of muscle disuse

2013 ◽  
Vol 217 (7) ◽  
pp. 1087-1093 ◽  
Author(s):  
B. D. Reilly ◽  
A. J. R. Hickey ◽  
R. L. Cramp ◽  
C. E. Franklin
Keyword(s):  
Skeletal Muscle ◽  
Hydrogen Peroxide ◽  
Cardiac Muscle ◽  
Mitochondrial Respiration ◽  
Hydrogen Peroxide Production ◽  
Muscle Disuse

Changes in oxygen tension affect cardiac mitochondrial respiration rate via changes in the rate of mitochondrial hydrogen peroxide production

2009 ◽  
Vol 47 (1) ◽  
pp. 49-56 ◽  
Author(s):  
Carla A. Di Maria ◽  
Marie A. Bogoyevitch ◽  
Douglas J. McKitrick ◽  
Leonard F. Arnolda ◽  
Livia C. Hool ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Oxygen Tension ◽  
Respiration Rate ◽  
Mitochondrial Respiration ◽  
Hydrogen Peroxide Production

scholarly journals Desmin Cytoskeleton Linked to Muscle Mitochondrial Distribution and Respiratory Function

2000 ◽  
Vol 150 (6) ◽  
pp. 1283-1298 ◽  
Author(s):  
Derek J. Milner ◽  
Manolis Mavroidis ◽  
Noah Weisleder ◽  
Yassemi Capetanaki
Keyword(s):  
Skeletal Muscle ◽  
Cardiac Muscle ◽  
Soleus Muscle ◽  
Mitochondrial Respiration ◽  
Respiratory Function ◽  
Structural Defects ◽  
Ultrastructural Observation ◽  
Ultrastructural Studies ◽  
Mitochondrial Distribution

Ultrastructural studies have previously suggested potential association of intermediate filaments (IFs) with mitochondria. Thus, we have investigated mitochondrial distribution and function in muscle lacking the IF protein desmin. Immunostaining of skeletal muscle tissue sections, as well as histochemical staining for the mitochondrial marker enzymes cytochrome C oxidase and succinate dehydrogenase, demonstrate abnormal accumulation of subsarcolemmal clumps of mitochondria in predominantly slow twitch skeletal muscle of desmin-null mice. Ultrastructural observation of desmin-null cardiac muscle demonstrates in addition to clumping, extensive mitochondrial proliferation in a significant fraction of the myocytes, particularly after work overload. These alterations are frequently associated with swelling and degeneration of the mitochondrial matrix. Mitochondrial abnormalities can be detected very early, before other structural defects become obvious. To investigate related changes in mitochondrial function, we have analyzed ADP-stimulated respiration of isolated muscle mitochondria, and ADP-stimulated mitochondrial respiration in situ using saponin skinned muscle fibers. The in vitro maximal rates of respiration in isolated cardiac mitochondria from desmin-null and wild-type mice were similar. However, mitochondrial respiration in situ is significantly altered in desmin-null muscle. Both the maximal rate of ADP-stimulated oxygen consumption and the dissociation constant (Km) for ADP are significantly reduced in desmin-null cardiac and soleus muscle compared with controls. Respiratory parameters for desmin-null fast twitch gastrocnemius muscle were unaffected. Additionally, respiratory measurements in the presence of creatine indicate that coupling of creatine kinase and the adenine translocator is lost in desmin-null soleus muscle. This coupling is unaffected in cardiac muscle from desmin-null animals. All of these studies indicate that desmin IFs play a significant role in mitochondrial positioning and respiratory function in cardiac and skeletal muscle.

scholarly journals Methoxychlor Inhibits Brain Mitochondrial Respiration and Increases Hydrogen Peroxide Production and CREB Phosphorylation

2005 ◽  
Vol 88 (2) ◽  
pp. 495-504 ◽  
Author(s):  
Rosemary A. Schuh ◽  
Tibor Kristián ◽  
Rupesh K. Gupta ◽  
Jodi A. Flaws ◽  
Gary Fiskum
Keyword(s):  
Hydrogen Peroxide ◽  
Mitochondrial Respiration ◽  
Hydrogen Peroxide Production ◽  
Creb Phosphorylation

scholarly journals Intramyocellular ceramides and skeletal muscle mitochondrial respiration are partially regulated by Toll-like receptor 4 during hindlimb unloading

2016 ◽  
Vol 311 (5) ◽  
pp. R879-R887 ◽  
Author(s):  
Oh Sung Kwon ◽  
Daniel S. Nelson ◽  
Katherine M. Barrows ◽  
Ryan M. O'Connell ◽  
Micah J. Drummond
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Respiration ◽  
Hindlimb Unloading ◽  
Model Assessment ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Muscle Disuse ◽  
Ceramide Accumulation

Physical inactivity and disuse result in skeletal muscle metabolic disruption, including insulin resistance and mitochondrial dysfunction. The role of the Toll-like receptor 4 (TLR4) signaling pathway in contributing to metabolic decline with muscle disuse is unknown. Therefore, our goal was to determine whether TLR4 is an underlying mechanism of insulin resistance, mitochondrial dysfunction, and skeletal muscle ceramide accumulation following muscle disuse in mice. To address this hypothesis, we subjected ( n = 6–8/group) male WT and TLR4−/− mice to 2 wk of hindlimb unloading (HU), while a second group of mice served as ambulatory wild-type controls (WT CON, TLR4−/− CON). Mice were assessed for insulin resistance [homeostatic model assessment-insulin resistance (HOMA-IR), glucose tolerance], and hindlimb muscles (soleus and gastrocnemius) were used to assess muscle sphingolipid abundance, mitochondrial respiration [respiratory control ratio (RCR)], and NF-κB signaling. The primary finding was that HU resulted in insulin resistance, increased total ceramides, specifically Cer18:0 and Cer20:0, and decreased skeletal muscle mitochondrial respiration. Importantly, TLR4−/− HU mice were protected from insulin resistance and altered NF-κB signaling and were partly resistant to muscle atrophy, ceramide accumulation, and decreased RCR. Skeletal muscle ceramides and RCR were correlated with insulin resistance. We conclude that TLR4 is an upstream regulator of insulin sensitivity, while partly upregulating muscle ceramides and worsening mitochondrial respiration during 2 wk of HU.

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