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- W2029872768 abstract "VASCULAR endothelial cells (EC) are the prime target in ischemia-reperfusion injury. Indeed, such cytotoxicity is believed to be one of the main underlying etiologies in ischemia-reperfusion injury of the endothelium that may occur after cold preservation of solid organs for transplantation. Early posttransplant graft function is largely influenced by the viability of the EC secondary to a production of reactive oxygen species (ROS) such as O2 , H2O2, or NO z . These ROS participate in the development of cellular damage particularly by attacking cellular proteins, DNA, and lipids, eventually leading to cellular death. Recent study has shown that various types of EC injury by ROS are characterized by morphologic and biologic features that are consistent with apoptosis. We conducted an in vitro study on how porcine aortic EC develops apoptosis from injury by ROS. For this purpose, we used S-nitrosoN-acetyl-DL-penicillamine (SNAP) as a donor for NO z and 3-morpholynosidnomine-N-ethylcarbamide (SIN-1) as for peroxinitrite (ONOO)." @default.
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- W2029872768 date "2000-02-01" @default.
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- W2029872768 title "Free radicals and apoptosis of the endothelial cells" @default.
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- W2029872768 doi "https://doi.org/10.1016/s0041-1345(99)00861-1" @default.
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