scholarly journals Reactive oxygen species contribute to Ca2+signals produced by osmotic stress in mouse skeletal muscle fibres

2008 ◽  
Vol 586 (1) ◽  
pp. 197-210 ◽  
Author(s):  
Adriano S. Martins ◽  
Vyacheslav M. Shkryl ◽  
Martha C. Nowycky ◽  
Natalia Shirokova
Keyword(s):  
Reactive Oxygen Species ◽  
Skeletal Muscle ◽  
Osmotic Stress ◽  
Reactive Oxygen ◽  
Muscle Fibres ◽  
Oxygen Species ◽  
Mouse Skeletal Muscle ◽  
Skeletal Muscle Fibres

scholarly journals Role of reactive oxygen species in contraction-mediated glucose transport in mouse skeletal muscle

2006 ◽  
Vol 575 (1) ◽  
pp. 251-262 ◽  
Author(s):  
Marie E. Sandström ◽  
Shi-Jin Zhang ◽  
Joseph Bruton ◽  
José P. Silva ◽  
Michael B. Reid ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Skeletal Muscle ◽  
Glucose Transport ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Mouse Skeletal Muscle

Proton leak induced by reactive oxygen species produced during in vitro anoxia/reoxygenation in rat skeletal muscle mitochondria

2006 ◽  
Vol 38 (1) ◽  
pp. 23-32 ◽  
Author(s):  
Rachel Navet ◽  
Ange Mouithys-Mickalad ◽  
Pierre Douette ◽  
Claudine M. Sluse-Goffart ◽  
Wieslawa Jarmuszkiewicz ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Skeletal Muscle ◽  
Reactive Oxygen ◽  
Proton Leak ◽  
Oxygen Species ◽  
Rat Skeletal Muscle ◽  
Muscle Mitochondria ◽  
Skeletal Muscle Mitochondria

scholarly journals Stretch-stimulated glucose uptake in skeletal muscle is mediated by reactive oxygen species and p38 MAP-kinase

2009 ◽  
Vol 587 (13) ◽  
pp. 3363-3373 ◽  
Author(s):  
Melissa A. Chambers ◽  
Jennifer S. Moylan ◽  
Jeffrey D. Smith ◽  
Laurie J. Goodyear ◽  
Michael B. Reid
Keyword(s):  
Reactive Oxygen Species ◽  
Skeletal Muscle ◽  
Map Kinase ◽  
Glucose Uptake ◽  
Reactive Oxygen ◽  
P38 Map Kinase ◽  
Oxygen Species

Reactive oxygen species formation in the transition to hypoxia in skeletal muscle

2005 ◽  
Vol 289 (1) ◽  
pp. C207-C216 ◽  
Author(s):  
Li Zuo ◽  
Thomas L. Clanton
Keyword(s):  
Reactive Oxygen Species ◽  
Skeletal Muscle ◽  
Acute Hypoxia ◽  
Low Frequency ◽  
Metabolic Stress ◽  
Reactive Oxygen ◽  
Fluorescence Signal ◽  
Oxygen Species ◽  
Peroxidase Mimic ◽  
Intracellular Ros

Many tissues produce reactive oxygen species (ROS) during reoxygenation after hypoxia or ischemia; however, whether ROS are formed during hypoxia is controversial. We tested the hypothesis that ROS are generated in skeletal muscle during exposure to acute hypoxia before reoxygenation. Isolated rat diaphragm strips were loaded with dihydrofluorescein-DA (Hfluor-DA), a probe that is oxidized to fluorescein (Fluor) by intracellular ROS. Changes in fluorescence due to Fluor, NADH, and FAD were measured using a tissue fluorometer. The system had a detection limit of 1 μM H2O2 applied to the muscle superfusate. When the superfusion buffer was changed rapidly from 95% O2 to 0%, 5%, 21%, or 40% O2, transient elevations in Fluor were observed that were proportional to the rise in NADH fluorescence and inversely proportional to the level of O2 exposure. This signal could be inhibited completely with 40 μM ebselen, a glutathione peroxidase mimic. After brief hypoxia exposure (10 min) or exposure to brief periods of H2O2, the fluorescence signal returned to baseline. Furthermore, tissues loaded with the oxidized form of the probe (Fluor-DA) showed a similar pattern of response that could be inhibited with ebselen. These results suggest that Fluor exists in a partially reversible redox state within the tissue. When Hfluor-loaded tissues were contracted with low-frequency twitches, Fluor emission and NADH emission were significantly elevated in a way that resembled the hypoxia-induced signal. We conclude that in the transition to low intracellular Po2, a burst of intracellular ROS is formed that may have functional implications regarding skeletal muscle O2-sensing systems and responses to acute metabolic stress.

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