scholarly journals Molecular Characterization of Reactive Oxygen Species in Myocardial Ischemia-Reperfusion Injury

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Tingyang Zhou ◽  
Chia-Chen Chuang ◽  
Li Zuo
Keyword(s):  
Reactive Oxygen Species ◽  
Myocardial Ischemia ◽  
Energy Demand ◽  
Heart Diseases ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
High Energy ◽  
Protective Mechanism ◽  
Oxygen Species ◽  
Myocardial Ischemia Reperfusion

Myocardial ischemia-reperfusion (I/R) injury is experienced by individuals suffering from cardiovascular diseases such as coronary heart diseases and subsequently undergoing reperfusion treatments in order to manage the conditions. The occlusion of blood flow to the tissue, termed ischemia, can be especially detrimental to the heart due to its high energy demand. Several cellular alterations have been observed upon the onset of ischemia. The danger created by cardiac ischemia is somewhat paradoxical in that a return of blood to the tissue can result in further damage. Reactive oxygen species (ROS) have been studied intensively to reveal their role in myocardial I/R injury. Under normal conditions, ROS function as a mediator in many cell signaling pathways. However, stressful environments significantly induce the generation of ROS which causes the level to exceed body’s antioxidant defense system. Such altered redox homeostasis is implicated in myocardial I/R injury. Despite the detrimental effects from ROS, low levels of ROS have been shown to exert a protective effect in the ischemic preconditioning. In this review, we will summarize the detrimental role of ROS in myocardial I/R injury, the protective mechanism induced by ROS, and potential treatments for ROS-related myocardial injury.

scholarly journals Ambra1 Alleviates Hypoxia/Reoxygenation Injury in H9C2 Cells by Regulating Autophagy and Reactive Oxygen Species

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Lin Zhao ◽  
Liting Cheng ◽  
Yongquan Wu
Keyword(s):  
Reactive Oxygen Species ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Reperfusion Therapy ◽  
Oxygen Species ◽  
H9c2 Cells ◽  
Reoxygenation Injury ◽  
Myocardial Ischemia Reperfusion

Reperfusion therapy is the most important method for treating acute myocardial infarction. However, myocardial ischemia reperfusion injury (MIRI) can offset the benefit of reperfusion therapy and worsen the outcome. In both ischemia and reperfusion, autophagy remains problematic. Activating molecule in Beclin1-regulated autophagy (Ambra1) is an important protein in autophagy regulation, and its function in MIRI remains unclear. Thus, we used H9C2 cells to investigate the function of Ambra1 in MIRI and the underlying mechanisms involved. Hypoxia and reoxygenation of H9C2 cells were used to mimic MIRI in vitro. During hypoxia, autophagy flux was blocked, then recovered in reoxygenation. Ambra1 overexpression increased autophagy in the H9C2 cells, as the LC3B II/I ratio increased, and alleviated cellular necrosis and apoptosis during hypoxia and reoxygenation. This effect was counteracted by an autophagy inhibitor. Knocking down Ambra1 can block autophagy which P62 sediment/supernatant ratio increased while the ratio of LC3B II/I decreased, and worsen outcomes. Ambra1 enhances autophagy in H9C2 cells by improving the stability and activity of the ULK1 complex. Reactive oxygen species (ROS) are an important cause of MIRI. ROS were reduced when Ambra1 was overexpressed and increased when Ambra1 was knocked down, indicating that Ambra1 can protect against hypoxia and reoxygenation injury in H9C2 cells by promoting autophagy and reducing ROS.

Antioxidant pyruvate inhibits cardiac formation of reactive oxygen species through changes in redox state

2000 ◽  
Vol 279 (5) ◽  
pp. H2431-H2438 ◽  
Author(s):  
Eberhard Bassenge ◽  
Olaf Sommer ◽  
Michael Schwemmer ◽  
Rolf Bünger
Keyword(s):  
Reactive Oxygen Species ◽  
Xanthine Oxidase ◽  
Nadh Oxidase ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Oxidase Inhibitor ◽  
Oxygen Species ◽  
Xanthine Oxidase Inhibitor ◽  
Ros Formation ◽  
Myocardial Ischemia Reperfusion

Myocardial ischemia-reperfusion is associated with bursts of reactive oxygen species (ROS) such as superoxide radicals (O2 −·). Membrane-associated NADH oxidase (NADHox) activity is a hypothetical source of O2 −·, implying the NADH concentration-to-NAD+ concentration ratio ([NADH]/[NAD+]) as a determinant of ROS. To test this hypothesis, cardiac NADHox and ROS formation were measured as influenced by pyruvate or l-lactate. Pre- and postischemic Langendorff guinea pig hearts were perfused at different pyruvate/l-lactate concentrations to alter cytosolic [NADH]/[NAD+]. NADHox and ROS were measured with the use of lucigenin chemiluminescence and electron spin resonance, respectively. In myocardial homogenates, pyruvate (0.05, 0.5 mM) and the NADHox blocker hydralazine markedly inhibited NADHox (16 ± 2%, 58 ± 9%). In postischemic hearts, pyruvate (0.1–5.0 mM) dose dependently inhibited ROS up to 80%. However,l-lactate (1.0–15.0 mM) stimulated both basal and postischemic ROS severalfold. Furthermore,l-lactate-induced basal ROS was dose dependently inhibited by pyruvate (0.1–5.0 mM) and not the xanthine oxidase inhibitor oxypurinol. Pyruvate did not inhibit ROS from xanthine oxidase. The data suggest a substantial influence of cytosolic NADH on cardiac O2 −· formation that can be inhibited by submillimolar pyruvate. Thus cytotoxicities due to cardiac ischemia-reperfusion ROS may be alleviated by redox reactants such as pyruvate.

Reactive oxygen species generated during myocardial ischemia enable energetic recovery during reperfusion

2002 ◽  
Vol 283 (4) ◽  
pp. H1656-H1661 ◽  
Author(s):  
Paul F. Klawitter ◽  
Holt N. Murray ◽  
Thomas L. Clanton ◽  
Mark G. Angelos
Keyword(s):  
Reactive Oxygen Species ◽  
Myocardial Ischemia ◽  
Reactive Oxygen ◽  
High Energy ◽  
High Energy Phosphates ◽  
Oxygen Species ◽  
Sprague Dawley ◽  
Additional Group ◽  
Rat Hearts ◽  
Superoxide Scavenger

We studied the differences between the functional and bioenergetic effects of antioxidants (AOX) administered before or after myocardial ischemia. Sprague-Dawley rat hearts were perfused with a modified Krebs-Henseleit solution and bubbled with 95% O2-5% CO2. The protocol consisted of 10 min of baseline perfusion, 20 min of global ischemia, and 30 min of reperfusion. An AOX, either 1,2-dihydroxybenzene-3,5-disulfonate (Tiron), a superoxide scavenger, or N-acetyl-l-cysteine, was infused during either baseline or reperfusion. An additional group received deferoxamine as a bolus before ischemia. Hearts were freeze-clamped at baseline, at end of ischemia, and at end of reperfusion for analysis of high-energy phosphates. All AOX, when given before ischemia, inhibited recovery of ATP compared with controls. Both Tiron and deferoxamine also inhibited recovery of phosphocreatine. AOX given before ischemia decreased the efficiency of contraction during reperfusion compared with controls. All of the changes in energetics and efficiency brought on by preischemic AOX treatment could be blocked by a preconditioning stimulus. This suggests that reactive oxygen species, which are generated during ischemia, enhance bioenergetic recovery by increasing the efficiency of contraction.

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