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- W2495259560 abstract "Clinically controlled hepatic ischemia/reperfusion (I/R) injury is either a frequently employed strategy or an unavoidable necessity in liver surgery, which involves temporary cessation of oxygen supply to the liver due to contrived vascular inflow occlusion and acute reoxygenation following restoration of blood flow. Hepatic I/R leads to parenchymal liver damage, which clinically manifests itself through elevation of circulating liver enzymes, liver failure, or early graft failure. The main cause of this hepatic injury is oxidative/nitrosative stress (ONS), which results from the excess production of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in hypoxia-exposed cells upon reoxygenation, exceeding the antioxidative capacity. This subsequently leads to the interaction of these reactive transients with macromolecules, such as lipids, proteins, and nucleic acids, which become dysfunctional. Oxidative stress occurs not only in hepatocytes, but also in endothelial cells and Kupffer cells lining the vascular wall. In the hyperacute phase of hepatic reperfusion, ROS/RNS are produced by hepatocytes, endothelial cells, and Kupffer cells (KCs). In the acute and chronic phase, KCs and neutrophils are mainly responsible for the ROS/RNS production, respectively." @default.
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- W2495259560 date "1975-01-01" @default.
- W2495259560 modified "2023-10-17" @default.
- W2495259560 title "Behavior Modification with Delinquents" @default.
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