scholarly journals Does Oxidative Stress Change During Orthotopic Liver Transplantation?

2017 ◽  
Vol 3 (2) ◽  
pp. 1-5
Author(s):  
Dimitrios Tsikas
Keyword(s):  
Oxidative Stress ◽  
Liver Transplantation ◽  
Orthotopic Liver Transplantation ◽  
Nitrosative Stress ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Enzymatic Reactions ◽  
Time Duration ◽  
Oxidative And Nitrosative Stress ◽  
Concentration Changes

In clinical ischemia/reperfusion injury, damage resulting from oxidative and nitrosative stress is generally considered crucial for graft functioning. Yet, there is increasing evidence that modern clinical transplantation including orthotopic liver transplantation (OLT) is not associated with elevation of oxidative and nitrosative stress upon organ reoxygenation. We measured two currently used biomarkers of oxidative stress, i.e., 15(S)-8-iso-prostaglandin F2a  (15(S)-8-iso-PGF2a) and cis-epoxyoctadecanoic acid (cis-EpOA), in human plasma during the entire time duration of OLT in eight patients suffering from end-stage liver disease. No considerable concentration changes of 15(S)-8-iso-PGF2a and cis-EpOA were observed, indicating lack of oxidative stress. Previously, we found in the same patients that nitrosative stress, measured as 3-nitrotyrosine and 3-nitrotyrosinoalbumin. Yet, as 15(S)-8-iso-PGF2a, cis-EpOA and 3-nitrotyrosine are produced both by chemical and enzymatic reactions, the current concepts of oxidative and nitrosative stress require reconsideration.

scholarly journals Early cytokine signatures of ischemia/reperfusion injury in human orthotopic liver transplantation

JCI Insight ◽  
2016 ◽  
Vol 1 (20) ◽  
Author(s):  
Rebecca A. Sosa ◽  
Ali Zarrinpar ◽  
Maura Rossetti ◽  
Charles R. Lassman ◽  
Bita V. Naini ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Reperfusion Injury ◽  
Orthotopic Liver Transplantation ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion

Proteomic analysis of liver tissues subjected to early ischemia/reperfusion injury during human orthotopic liver transplantation

PROTEOMICS ◽  
2006 ◽  
Vol 6 (11) ◽  
pp. 3455-3465 ◽  
Author(s):  
Carlo Vascotto ◽  
Laura Cesaratto ◽  
Chiara D'Ambrosio ◽  
Andrea Scaloni ◽  
Claudio Avellini ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Reperfusion Injury ◽  
Orthotopic Liver Transplantation ◽  
Proteomic Analysis ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Liver Tissues

scholarly journals MicroRNA-141-3p Attenuates Oxidative Stress-induced Hepatic Ischemia Reperfusion Injury via Keap1/Nrf2 Pathway

2021 ◽  
Author(s):  
Tingting Li ◽  
Qingsong Chen ◽  
Jiangwen Dai ◽  
Zuotian Huang ◽  
Yunhai Luo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Transplantation ◽  
Reperfusion Injury ◽  
Inflammatory Responses ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Hepatic Ischemia ◽  
Hepatic Ischemia Reperfusion

Abstract Hepatic ischemia reperfusion injury (IRI) is a major factor affecting the prognosis of liver transplantation through a series of severe cell death and inflammatory responses. MicroRNA-141-3p (miR-141-3p) has been reported to be associated with hepatic steatosis and other liver diseases. However, the potential role of miR-141-3p in hepatic IRI is currently unknown. In the present study, we found that miR-141-3p levels were negatively correlated with alanine aminotransferase (ALT)/aspartate aminotransferase (AST) in liver transplantation patients. The results demonstrated that miR-141-3p was decreased in mouse liver tissue after hepatic IRI in mice and in hepatocytes after hypoxia/reoxygenation (H/R). Overexpression of miR-141-3p directly decreased Kelch-like ECH-associated protein 1 (Keap1) levels and attenuated cell apoptosis in vivo and in vitro, while inhibition of miR-141-3p facilitated apoptosis. Further experiments revealed that overexpression of miR-141-3p also attenuated oxidative stress-induced damage in hepatocytes under H/R conditions. Taken together, our results indicate that miR-141-3p plays a major role in hepatic IRI through the Keap1 signaling pathway, and the present study suggests that miR-141-3p might have a protective effect on hepatic IRI to some extent.

scholarly journals Oxidative Stress as a Mediator of Cardiovascular Disease

2009 ◽  
Vol 2 (5) ◽  
pp. 259-269 ◽  
Author(s):  
Maqsood M. Elahi ◽  
Yu Xiang Kong ◽  
Bashir M. Matata
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Nitrosative Stress ◽  
Ischemia Reperfusion Injury ◽  
Cell Damage ◽  
Ischemia Reperfusion ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Redox Balance ◽  
Reactive Oxidant Species ◽  
Reactive Oxidant

During physiological processes molecules undergo chemical changes involving reducing and oxidizing reactions. A molecule with an unpaired electron can combine with a molecule capable of donating an electron. The donation of an electron is termed as oxidation whereas the gaining of an electron is called reduction. Reduction and oxidation can render the reduced molecule unstable and make it free to react with other molecules to cause damage to cellular and sub-cellular components such as membranes, proteins and DNA. In this paper, we have discussed the formation of reactive oxidant species originating from a variety of sources such as nitric oxide (NO) synthase (NOS), xanthine oxidases (XO), the cyclooxygenases, nicotinamide adenine dinucleotide phosphate (NAD(P)H) oxidase isoforms and metal-catalyzed reactions. In addition, we present a treatise on the physiological defences such as specialized enzymes and antioxidants that maintain reduction-oxidation (redox) balance. We have also given an account of how enzymes and antioxidants can be exhausted by the excessive production of reactive oxidant species (ROS) resulting in oxidative stress/nitrosative stress, a process that is an important mediator of cell damage. Important aspects of redox imbalance that triggers the activity of a number of signaling pathways including transcription factors activity, a process that is ubiquitous in cardiovascular disease related to ischemia/reperfusion injury have also been presented.

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