Ischemia/Reperfusion Injury

Anaya-Prado, Roberto; Toledo‐Pereyra, Luis H.; Lentsch, Alex B.; Ward, Peter A.

doi:10.1006/jsre.2002.6385

Cited by 203 publications

(174 citation statements)

References 128 publications

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“…Normally, living organisms are protected from the dangerous effects of O 2 À by SOD, which converts O 2 À into H 2 O 2 [68][69][70] . Whereas, during reperfusion of ischemic tissues, these natural defences may not be overcome and H 2 O 2 is converted into OH , this transformation has the capacity to damage a wide range of biomolecules species containing amino acids, membrane proteins and nucleic acids [71][72][73] . CAT is an oxidoreductase that catalyzes the conversion of H 2 O 2 to H 2 O and O 2 .…”

Section: Resultsmentioning

confidence: 99%

A comparative study on the antioxidant effects of hesperidin and ellagic acid against skeletal muscle ischemia/reperfusion injury

Akdemir

Gülçın

Karagöz

et al. 2016

Journal of Enzyme Inhibition and Medicinal Chemistry

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The antioxidant effects of ellagic acid (EA) and hesperidin (HES) against skeletal muscle ischemia/reperfusion injury (I/R) were performed. Hindlimb ischemia has been induced by tourniquet occlusion for 2 h on left hindlimb. At the end of ischemia, the tourniquate has been removed and initiated reperfusion for 2 h. EA (100 mg/kg) has been applied orally before ischemia/reperfusion in the EA + I/R group. HES (100 mg/kg) has been given orally in the HES + I/R group. The left gastrocnemius muscle has been harvested and stored immediately at À80 C until assessed for the levels of MDA and antioxidant enzymes activities. MDA level has statistically increased in I/R group (p50.05) compared to other groups. The muscle tissue antioxidant enzymes activities were lower than the other groups in the I/R group (p50.05). EA and HES treatments significantly reversed the damage level in I/R, also activity of tissue SOD increased in the EA + I/R and HES + I/R groups.

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Section: Resultsmentioning

confidence: 99%

A comparative study on the antioxidant effects of hesperidin and ellagic acid against skeletal muscle ischemia/reperfusion injury

Akdemir

Gülçın

Karagöz

et al. 2016

Journal of Enzyme Inhibition and Medicinal Chemistry

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“…However, during oxidative stress conditions, the balance between ROS and antioxidants shifts toward the former, resulting in liver damage [51].…”

Section: Ischemia/reperfusion Liver Injury and Free Radicalsmentioning

confidence: 99%

Role of free radicals in liver diseases

2009

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Reactive oxygen and nitrogen species (ROS and RNS) are produced by metabolism of normal cells. However, in liver diseases, redox is increased thereby damaging the hepatic tissue; the capability of ethanol to increase both ROS/RNS and peroxidation of lipids, DNA, and proteins was demonstrated in a variety of systems, cells, and species, including humans. ROS/RNS can activate hepatic stellate cells, which are characterized by the enhanced production of extracellular matrix and accelerated proliferation. Cross-talk between parenchymal and nonparenchymal cells is one of the most important events in liver injury and fibrogenesis; ROS play an important role in fibrogenesis throughout increasing platelet-derived growth factor. Most hepatocellular carcinomas occur in cirrhotic livers, and the common mechanism for hepatocarcinogenesis is chronic inflammation associated with severe oxidative stress; other risk factors are dietary aflatoxin B 1 consumption, cigarette smoking, and heavy drinking. Ischemia-reperfusion injury affects directly on hepatocyte viability, particularly during transplantation and hepatic surgery; ischemia activates Kupffer cells which are the main source of ROS during the reperfusion period. The toxic action mechanism of paracetamol is focused on metabolic activation of the drug, depletion of glutathione, and covalent binding of the reactive metabolite N-acetyl-pbenzoquinone imine to cellular proteins as the main cause of hepatic cell death; intracellular steps critical for cell death include mitochondrial dysfunction and, importantly, the formation of ROS and peroxynitrite. Infection with hepatitis C is associated with increased levels of ROS/RNS and decreased antioxidant levels. As a consequence, antioxidants have been proposed as an adjunct therapy for various liver diseases.

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“…4 The pathophysiology of ischemiareperfusion injury is complex, with activation of neutrophils and release of reactive oxygen species and other inflammatory mediators. 5 Since it was demonstrated that specific complement inhibition with soluble complement receptor 1 (sCR1) markedly attenuated the tissue damage in experimental myocardial infarction, 6 a large body of evidence has accumulated demonstrating an essential role for complement in ischemia-reperfusion injury. This is supported by studies showing a therapeutic benefit of complement blockade in various ischemia-reperfusion injury models, as reviewed elsewhere.…”

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confidence: 99%

Mechanism of Complement Activation and Its Role in the Inflammatory Response After Thoracoabdominal Aortic Aneurysm Repair

et al. 2003

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Background-Complement activation contributes to ischemia-reperfusion injury. Patients undergoing thoracoabdominal aortic aneurysm (TAAA) repair suffer extensive ischemia-reperfusion and considerable systemic inflammation. Methods and Results-The degree and mechanism of complement activation and its role in inflammation were investigated in 19 patients undergoing TAAA repair. Patients undergoing open infrarenal aortic surgery (nϭ5) or endovascular descending aortic aneurysm repair (nϭ6) served as control subjects. Substantial complement activation was seen in TAAA patients but not in controls. C1rs-C1-inhibitor complexes increased moderately, whereas C4bc, C3bBbP, C3bc, and the terminal SC5b-9 complex (TCC) increased markedly after reperfusion, reaching a maximum 8 hours after reperfusion. Interleukin (IL)-1␤, tumor necrosis factor ␣ (TNF-␣), and IL-8 increased significantly in TAAA patients but not in controls, peaking at 24 hours postoperatively and correlating closely with the degree of complement activation. IL-6 and IL-10 increased to a maximum 8 hours after reperfusion in the TAAA patients, were not correlated with complement activation, and increased moderately in the control subjects. Myeloperoxidase and lactoferrin increased markedly before reperfusion in all groups, whereas sICAM-1, sP-selectin, and sE-selectin were unchanged.No increase was observed in complement activation products, IL-1␤, TNF-␣, or IL-8 in a mannose-binding lectin (MBL)-deficient TAAA patient, whereas IL-6, IL-10, myeloperoxidase, and lactoferrin increased as in the controls. Two other MBL-deficient TAAA patients receiving plasma attained significant MBL levels and showed complement and cytokine patterns identical to the MBL-sufficient TAAA patients. Conclusions-The data suggest that complement activation during TAAA repair is MBL mediated, amplified through the alternative pathway, and responsible in part for the inflammatory response.

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Ischemia/Reperfusion Injury

Cited by 203 publications

References 128 publications

A comparative study on the antioxidant effects of hesperidin and ellagic acid against skeletal muscle ischemia/reperfusion injury

A comparative study on the antioxidant effects of hesperidin and ellagic acid against skeletal muscle ischemia/reperfusion injury

Role of free radicals in liver diseases

Mechanism of Complement Activation and Its Role in the Inflammatory Response After Thoracoabdominal Aortic Aneurysm Repair

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