EUK-8 a synthetic catalytic scavenger of reactive oxygen species protects isolated iron-overloaded rat heart from functional and structural damage induced by ischemia/reperfusion

1996 ◽  
Vol 10 (3) ◽  
pp. 331-339 ◽  
Author(s):  
S. Pucheu ◽  
F. Boucher ◽  
T. Sulpice ◽  
N. Tresallet ◽  
Y. Bonhomme ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Rat Heart ◽  
Structural Damage ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Oxygen Species

scholarly journals Treatment of Rats With Hypolipidemic Compound Pirinixic Acid Protects Their Hearts Against Ischemic Injury: Are Mitochondrial KATP Channels and Reactive Oxygen Species Involved?

2013 ◽  
pp. 577-584 ◽  
Author(s):  
M. NEMČEKOVÁ ◽  
S. ČARNICKÁ ◽  
M. FERKO ◽  
M. MURÁRIKOVÁ ◽  
V. LEDVÉNYIOVÁ ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Rat Heart ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Katp Channels ◽  
Ros Generation ◽  
Peroxisome Proliferator ◽  
Oxygen Species ◽  
Protective Effects ◽  
Mitochondrial Katp Channels

Hypolipidemic compound pirinixic acid (WY-14643, WY) is known to exert pleiotropic (other than primary) effects, such as activation of peroxisome proliferator-activated receptors (PPAR-α), transcription factors regulating different cardiac functions. Their role in ischemia-reperfusion (I/R) injury and cardioprotection is less clear, although protective effects of PPAR agonists have been documented. This study was designed to explore the effects of WY on the I/R injury in the rat heart and potential mechanisms involved, including mitochondrial KATP channels (mitoKATP) opening and production of reactive oxygen species (ROS). Langendorff-perfused hearts of rats intragastrally treated with WY (3 mg/kg/day) for 5 days and of control animals were subjected to 30-min global ischemia and 2-h reperfusion with or without 15-min perfusion with mitoKATP blocker 5-hydroxydecanoate (5-HD) prior to I/R. Evaluation of the infarct size (IS, TTC staining) served as the main end-point of protection. Lipid peroxidation (a marker of ROS production) was determined by measurement of myocardial concentration of conjugated dienes (CD), whereas protein expression of endothelial NO synthase was analysed by Western blotting. A 2-fold increase in the cardiac protein levels of eNOS after treatment with WY was accompanied by lower post-I/R levels of CD compared with those in the hearts of untreated controls, although WY itself enhanced ROS generation prior to ischemia. IS was reduced by 47 % in the hearts of WY-treated rats (P<0.05), and this effect was reversed by 5-HD. Results suggest that PPAR-α activation may confer protection against lethal I/R injury in the rat heart that involves up-regulation of eNOS, mitoKATP opening and reduced oxidative stress during I/R.

The Role of Reactive Oxygen Species, Kinases, Hydrogen Sulfide, and Nitric Oxide in the Regulation of Autophagy and Their Impact on Ischemia and Reperfusion Injury in the Heart

2020 ◽  
Vol 16 ◽  
Author(s):  
Andrey Krylatov ◽  
Leonid Maslov ◽  
Sergey Y. Tsibulnikov ◽  
Nikita Voronkov ◽  
Alla Boshchenko ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Hydrogen Sulfide ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Ischemia And Reperfusion ◽  
Oxygen Species ◽  
Ischemia And Reperfusion Injury ◽  
Adaptive Process

: There is considerable evidence in the heart that autophagy in cardiomyocytes is activated by hypoxia/reoxygenation (H/R) or in hearts by ischemia/reperfusion (I/R). Depending upon the experimental model and duration of ischemia, increases in autophagy in this setting maybe beneficial (cardioprotective) or deleterious (exacerbate I/R injury). Aside from the conundrum as to whether or not autophagy is an adaptive process, it is clearly regulated by a number of diverse molecules including reactive oxygen species (ROS), various kinases, hydrogen sulfide (H2S) and nitric oxide (NO). The purpose this review is to address briefly the controversy regarding the role of autophagy in this setting and to examine a variety of disparate molecules that are involved in its regulation.

scholarly journals TRPM2 Non-Selective Cation Channels in Liver Injury Mediated by Reactive Oxygen Species

Antioxidants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1243
Author(s):  
Eunus S. Ali ◽  
Grigori Y. Rychkov ◽  
Greg J. Barritt
Keyword(s):  
Reactive Oxygen Species ◽  
Liver Injury ◽  
Cell Injury ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Cell Types ◽  
Chronic Liver ◽  
Oxygen Species ◽  
Alcoholic Fatty Liver ◽  
Trpm2 Channels

TRPM2 channels admit Ca2+ and Na+ across the plasma membrane and release Ca2+ and Zn2+ from lysosomes. Channel activation is initiated by reactive oxygen species (ROS), leading to a subsequent increase in ADP-ribose and the binding of ADP-ribose to an allosteric site in the cytosolic NUDT9 homology domain. In many animal cell types, Ca2+ entry via TRPM2 channels mediates ROS-initiated cell injury and death. The aim of this review is to summarise the current knowledge of the roles of TRPM2 and Ca2+ in the initiation and progression of chronic liver diseases and acute liver injury. Studies to date provide evidence that TRPM2-mediated Ca2+ entry contributes to drug-induced liver toxicity, ischemia–reperfusion injury, and the progression of non-alcoholic fatty liver disease to cirrhosis, fibrosis, and hepatocellular carcinoma. Of particular current interest are the steps involved in the activation of TRPM2 in hepatocytes following an increase in ROS, the downstream pathways activated by the resultant increase in intracellular Ca2+, and the chronology of these events. An apparent contradiction exists between these roles of TRPM2 and the role identified for ROS-activated TRPM2 in heart muscle and in some other cell types in promoting Ca2+-activated mitochondrial ATP synthesis and cell survival. Inhibition of TRPM2 by curcumin and other “natural” compounds offers an attractive strategy for inhibiting ROS-induced liver cell injury. In conclusion, while it has been established that ROS-initiated activation of TRPM2 contributes to both acute and chronic liver injury, considerable further research is needed to elucidate the mechanisms involved, and the conditions under which pharmacological inhibition of TRPM2 can be an effective clinical strategy to reduce ROS-initiated liver injury.

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 Metformin Protects H9C2 Cardiomyocytes from High-Glucose and Hypoxia/Reoxygenation Injury via Inhibition of Reactive Oxygen Species Generation and Inflammatory Responses: Role of AMPK and JNK

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Mingyan Hu ◽  
Ping Ye ◽  
Hua Liao ◽  
Manhua Chen ◽  
Feiyan Yang
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Viability ◽  
High Glucose ◽  
Molecular Mechanisms ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Compound C ◽  
Hypoxia Reoxygenation

Metformin is a first-line drug for the management of type 2 diabetes. Recent studies suggested cardioprotective effects of metformin against ischemia/reperfusion injury. However, it remains elusive whether metformin provides direct protection against hypoxia/reoxygenation (H/R) injury in cardiomyocytes under normal or hyperglycemic conditions. This study in H9C2 rat cardiomyoblasts was designed to determine cell viability under H/R and high-glucose (HG, 33 mM) conditions and the effects of cotreatment with various concentrations of metformin (0, 1, 5, and 10 mM). We further elucidated molecular mechanisms underlying metformin-induced cytoprotection, especially the possible involvement of AMP-activated protein kinase (AMPK) and Jun NH(2)-terminal kinase (JNK). Results indicated that 5 mM metformin improved cell viability, mitochondrial integrity, and respiratory chain activity under HG and/or H/R (P<0.05). The beneficial effects were associated with reduced levels of reactive oxygen species generation and proinflammatory cytokines (TNF-α, IL-1α, and IL-6) (P<0.05). Metformin enhanced phosphorylation level of AMPK and suppressed HG + H/R induced JNK activation. Inhibitor of AMPK (compound C) or activator of JNK (anisomycin) abolished the cytoprotective effects of metformin. In conclusion, our study demonstrated for the first time that metformin possessed direct cytoprotective effects against HG and H/R injury in cardiac cells via signaling mechanisms involving activation of AMPK and concomitant inhibition of JNK.

scholarly journals The role of reactive oxygen species in the infarct-limiting effect of hypoxic preconditioning

2021 ◽  
Vol 20 (2) ◽  
pp. 87-91
Author(s):  
A. S. Sementsov ◽  
N. V. Naryzhnaya ◽  
M. A. Sirotina ◽  
L. N. Maslov
Keyword(s):  
Reactive Oxygen Species ◽  
Coronary Artery ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Hypoxic Preconditioning ◽  
Male Rats ◽  
Oxygen Species ◽  
Infarct Size Reduction

Introduction. Increased resistance of the heart to ischemia/reperfusion (I/R) is an urgent aim of physiology, pharmacology, and cardiac surgery, since I/R injury of the heart is often the cause of cardiogenic shock and subsequent death of patients in the postoperative period. Materials and methods. The study was carried out in male rats which were subjected to coronary artery occlusion (45 min) and reperfusion (2 h). Before coronary occlusion, early hypoxic preconditioning (HP) was modeled. The rats were subjected to six sessions of hypoxia (8 % O2, 10 min) and reoxygenation (21 % O2, 10 min) 30 min before coronary artery occlusion. The rats were injected with the following drugs: 1,3-dimethylthiourea (DMTM), 2-mercaptopropionyl glycine (2-MPG), deferoxamine. Results. It was found that HP contributes to infarct size reduction by 30 %. Preliminary administration of DMTM, 2-MPG, deferoxamine eliminated the infarct-reducing effect of HP. Conclisuon. The obtained data indicate that reactive oxygen species are involved in the cardioprotective effect of HP.

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