Mechanisms of cell death in oxidant stress and ischemia‐reperfusion injury
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چکیده
منابع مشابه
Oxidant stress, mitochondria, and cell death mechanisms in drug-induced liver injury: lessons learned from acetaminophen hepatotoxicity.
Hepatotoxicity is a serious problem during drug development and for the use of many established drugs. For example, acetaminophen overdose is currently the most frequent cause of acute liver failure in the United States and Great Britain. Evaluation of the mechanisms of drug-induced liver injury indicates that mitochondria are critical targets for drug toxicity, either directly or indirectly th...
متن کاملMechanisms of cell injury and death.
Control of the rate of cell death relative to the rate of cell division maintains organ integrity and physiological homeostasis. Cell death is valuable for the organism because it removes terminally injured or unwanted cells that utilize valuable substrates and nutrients. Likewise, cell death also has value for the species, as it provides a mechanism for eliminating terminally injured individua...
متن کاملNeutrophil and Kupffer cell-induced oxidant stress and ischemia-reperfusion injury in rat liver.
The hypothesis that Kupffer cells and infiltrating neutrophils generate reactive oxygen in the hepatic sinusoids and may contribute to ischemia-reperfusion injury in the liver was investigated in a model of partial no-flow ischemia and reperfusion in male Fischer rats in vivo. During the reperfusion period of 60 min, plasma concentrations of glutathione disulfide (GSSG; index of oxidant stress)...
متن کاملOxidant stress and endothelial cell dysfunction.
Reactive oxygen species (ROS) are generated at sites of inflammation and injury, and at low levels, ROS can function as signaling molecules participating as signaling intermediates in regulation of fundamental cell activities such as cell growth and cell adaptation responses, whereas at higher concentrations, ROS can cause cellular injury and death. The vascular endothelium, which regulates the...
متن کاملAcetaminophen-induced oxidant stress and cell injury in cultured mouse hepatocytes: protection by N-acetyl cysteine.
The increase in cellular and mitochondrial glutathione disulfide (GSSG) levels and the GSSG:GSH ratio after acetaminophen (AAP) overdose suggest the involvement of an oxidant stress in the pathophysiology. However, the initial severe depletion of hepatocellular glutathione makes quantitative assessment of the oxidant stress difficult. Therefore, we tested the hypothesis that oxidant stress prec...
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ژورنال
عنوان ژورنال: The FASEB Journal
سال: 2007
ISSN: 0892-6638,1530-6860
DOI: 10.1096/fasebj.21.5.a448-c