Redox-dependent increases in glutathione reductase and exercise preconditioning: role of NADPH oxidase and mitochondria

Frasier, Chad R.; Moukdar, Fatiha; Patel, H.; Sloan, Ruben C.; Stewart, Luke M.; Alleman, Rick J.; Favor, Justin D. La; Brown, David A.

doi:10.1093/cvr/cvt009

Cited by 64 publications

(68 citation statements)

References 77 publications

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“…Notably, exercisebased cardiac rehabilitation has been shown to improve exercise tolerance and reduce mortality in CAD patients [11][12][13]. Meanwhile, it has been documented in animal models produce preconditioning stimuli [14][15][16][17][18][19], thus making the heart more resistant to cardiac injury following myocardial ischemia-reperfusion (I/R) [20][21][22][23]. Also, it has previously been demonstrated that long-term exercise training (e.g.…”

Section: Introductionmentioning

confidence: 99%

Exercise Training Protects Against Acute Myocardial Infarction via Improving Myocardial Energy Metabolism and Mitochondrial Biogenesis

Tao

Bei

Lin

et al. 2015

Cell Physiol Biochem

104

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Background/Aims: Acute myocardial infarction (AMI) represents a major cause of morbidity and mortality worldwide. Exercise has been proved to reduce myocardial ischemia-reperfusion (I/R) injury However it remains unclear whether, and (if so) how, exercise could protect against AMI. Methods: Mice were trained using a 3-week swimming protocol, and then subjected to left coronary artery (LCA) ligation, and finally sacrificed 24 h after AMI. Myocardial infarct size was examined with triphenyltetrazolium chloride staining. Cardiac apoptosis was determined by TUNEL staining. Mitochondria density was checked by Mito-Tracker immunofluorescent staining. Quantitative reverse transcription polymerase chain reactions and Western blotting were used to determine genes related to apoptosis, autophagy and myocardial energy metabolism. Results: Exercise training reduces myocardial infarct size and abolishes AMI-induced autophagy and apoptosis. AMI leads to a shift from fatty acid to glucose metabolism in the myocardium with a downregulation of PPAR-α and PPAR-γ. Also, AMI induces an adaptive increase of mitochondrial DNA replication and transcription in the acute phase of MI, accompanied by an activation of PGC-1α signaling. Exercise abolishes the derangement of myocardial glucose and lipid metabolism and further enhances the adaptive increase of mitochondrial biogenesis. Conclusion: Exercise training protects against AMI-induced acute cardiac injury through improving myocardial energy metabolism and enhancing the early adaptive change of mitochondrial biogenesis.

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Section: Introductionmentioning

confidence: 99%

Exercise Training Protects Against Acute Myocardial Infarction via Improving Myocardial Energy Metabolism and Mitochondrial Biogenesis

Tao

Bei

Lin

et al. 2015

Cell Physiol Biochem

104

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“…In most studies, an increase in the activity of the enzyme glutathione reductase was observed after exercise (22). However, some studies have observed an increase in the catalase activity after exercise (23,24) some observed no change (25,26), and some found even lower (27) activity that could have implications on the role of the increase in glutathione as coenzyme glutathione oxidase.…”

Section: Discussionmentioning

confidence: 99%

The Effects of Copenhagen Football Test on Glutathione Reductase and Catalase Activity in Female Football Players

et al. 2017

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Background: Changes in oxidative stress in response to vigorous exercise is of prime importance. In this area, the changes of catalase activity and glutathione reductase are very important. However, the results of the activity of antioxidants, particularly in erythrocytes, are not unified. Football is a heavy exercise. Therefore, the present study aimed at analyzing the effects of Copenhagen football test on the glutathione reductase and catalase activity.

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“…Exercise is known to protect against arrhythmia (27,30,36,60), as well as other postischemic damage, such as myocardial stunning (11,46,66) and infarction (14,29,58,59). Despite the clear beneficial effect, the underlying cellular mechanisms are not completely understood.…”

Section: New and Noteworthymentioning

confidence: 99%

“…Several factors, including various genetic abnormalities, channelopathies, compromised autonomic function, left ventricular hypertrophy, and acute coronary syndromes, are known to influence the susceptibility to arrhythmia (26, 53, 68). During acute coronary syndromes, the reperfusion of previously ischemic tissue leads to a burst in reactive oxygen species (ROS), a significant contributor to electromechanical dysfunction (3,10,48,75).Exercise is known to protect against arrhythmia (27,30,36,60), as well as other postischemic damage, such as myocardial stunning (11,46,66) and infarction (14,29,58,59). Despite the clear beneficial effect, the underlying cellular mechanisms are not completely understood.…”

mentioning

confidence: 99%

Exercise-induced protection against reperfusion arrhythmia involves stabilization of mitochondrial energetics

Alleman

Tsang

Ryan

et al. 2016

American Journal of Physiology-Heart and Circulatory Physiology

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Mitochondria influence cardiac electrophysiology through energy- and redox-sensitive ion channels in the sarcolemma, with the collapse of energetics believed to be centrally involved in arrhythmogenesis. This study was conducted to determine if preservation of mitochondrial membrane potential (ΔΨm) contributes to the antiarrhythmic effect of exercise. We utilized perfused hearts, isolated myocytes, and isolated mitochondria exposed to metabolic challenge to determine the effects of exercise on cardiac mitochondria. Hearts from sedentary (Sed) and exercised (Ex; 10 days of treadmill running) Sprague-Dawley rats were perfused on a two-photon microscope stage for simultaneous measurement of ΔΨm and ECG. After ischemia-reperfusion, the collapse of ΔΨm was commensurate with the onset of arrhythmia. Exercise preserved ΔΨm and decreased the incidence of fibrillation/tachycardia (P < 0.05). Our findings in intact hearts were corroborated in isolated myocytes exposed to in vitro hypoxia-reoxygenation, with Ex rats demonstrating enhanced redox control and sustained ΔΨm during reoxygenation. Finally, we induced anoxia-reoxygenation in isolated mitochondria using high-resolution respirometry with simultaneous measurement of respiration and H2O2 Mitochondria from Ex rats sustained respiration with lower rates of H2O2 emission than Sed rats. Exercise helps sustain postischemic mitochondrial bioenergetics and redox homeostasis, which is associated with preserved ΔΨm and protection against reperfusion arrhythmia. The reduction of fatal ventricular arrhythmias through exercise-induced mitochondrial adaptations indicates that mitochondrial therapeutics may be an effective target for the treatment of heart disease.

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Redox-dependent increases in glutathione reductase and exercise preconditioning: role of NADPH oxidase and mitochondria

Abstract: Adaptive cardioprotective signalling is triggered by reactive oxygen species from NADPH oxidase, and leads to improved glutathione replenishment through redox-dependent modifications in GR.

Cited by 64 publications

References 77 publications

Exercise Training Protects Against Acute Myocardial Infarction via Improving Myocardial Energy Metabolism and Mitochondrial Biogenesis

Exercise Training Protects Against Acute Myocardial Infarction via Improving Myocardial Energy Metabolism and Mitochondrial Biogenesis

The Effects of Copenhagen Football Test on Glutathione Reductase and Catalase Activity in Female Football Players

Exercise-induced protection against reperfusion arrhythmia involves stabilization of mitochondrial energetics

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