scholarly journals Effects of aging and exercise training on eNOS uncoupling and reactive oxygen species signaling in the endothelium of skeletal muscle arterioles

2009 ◽  
Author(s):  
Amy L. Sindler
Keyword(s):  
Reactive Oxygen Species ◽  
Skeletal Muscle ◽  
Exercise Training ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Enos Uncoupling ◽  
Effects Of Aging ◽  
Reactive Oxygen Species Signaling

scholarly journals Lack of Endothelial α1AMPK Reverses the Vascular Protective Effects of Exercise by Causing eNOS Uncoupling

Antioxidants ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 1974
Author(s):  
Thomas Jansen ◽  
Miroslava Kvandová ◽  
Isabella Schmal ◽  
Sanela Kalinovic ◽  
Paul Stamm ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Endothelial Cells ◽  
Exercise Training ◽  
Uncoupling Protein ◽  
Reactive Oxygen ◽  
Voluntary Exercise ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Oxygen Species ◽  
Enos Uncoupling

Voluntary exercise training is an effective way to prevent cardiovascular disease, since it results in increased NO bioavailability and decreased reactive oxygen species (ROS) production. AMP-activated protein kinase (AMPK), especially its α1AMPK subunit, modulates ROS-dependent vascular homeostasis. Since endothelial cells play an important role in exercise-induced changes of vascular signaling, we examined the consequences of endothelial-specific α1AMPK deletion during voluntary exercise training. We generated a mouse strain with specific deletion of α1AMPK in endothelial cells (α1AMPKflox/flox x TekCre+). While voluntary exercise training improved endothelial function in wild-type mice, it had deleterious effects in mice lacking endothelial α1AMPK indicated by elevated reactive oxygen species production (measured by dihydroethidum fluorescence and 3-nitrotyrosine staining), eNOS uncoupling and endothelial dysfunction. Importantly, the expression of the phagocytic NADPH oxidase isoform (NOX-2) was down-regulated by exercise in control mice, whereas it was up-regulated in exercising α1AMPKflox/flox x TekCre+ animals. In addition, nitric oxide bioavailability was decreased and the antioxidant/protective nuclear factor erythroid 2-related factor 2 (Nrf-2) response via heme oxygenase 1 and uncoupling protein-2 (UCP-2) was impaired in exercising α1AMPKflox/flox x TekCre+ mice. Our results demonstrate that endothelial α1AMPK is a critical component of the signaling events that enable vascular protection in response to exercise. Moreover, they identify endothelial α1AMPK as a master switch that determines whether the effects of exercise on the vasculature are protective or detrimental.

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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