Oxidative stress ischemia

Stress Heat-fever Heavy metals Oxidant injury Oxidative uncouplers Ischemia... 

Hypoxia-ischemia may initiate apoptosis in parallel with excitotoxicity 565 Triggers of ischemic apoptosis may include decreased supply or sensitivity to neurotrophins, oxidative stress, exposure to inflammatory cytokines or damage to mitochondria 566... 

Oxygen free radicals are required intermediates in many biological reactions but may damage macromolecules during oxidative stress 566 Reactive oxygen species generated during ischemia—reperfusion contribute to the injury 567... 

Reactive oxygen species may modify both the excito-toxic and the apoptotic components of ischemic brain damage. In addition to direct effects of oxidative injury during ischemia-reperfusion, ROS may modify ischemic excitotoxicity by downregulating current through NMDA receptors. However, exposure to oxidative stress can be... 

Gasche, Y., Copin, J. C., Sugawara, T., Fujimura, M. and Chan, P. H. Matrix metalloproteinase inhibition prevents oxidative stress-associated blood-brain barrier disruption after transient focal cerebral ischemia. /. Cereb. Blood Plow Metab. 21 1393-1400,2001. 

D1 (10,17S-docosatriene) from DHA using tandem liquid chromatography-photodiode array-electrospray ionization-tandem mass spectrometry (LC-PDA-ESI-MS-MS)-based lipidomic analysis have been documented in ischemic brain [4] and retinal pigment epithelium [5], This new lipid is called neuroprotectin D1 (1) because of its neuro-protectiveproperties in brain ischemia-reperfusion [4] and in oxidative stress-challenged retinal pigment epithelial cells [5] (2) because of its potent ability to inactivate proapoptotic signaling (see apoptosis, Ch. 35) [5] and (3) because it is the first identified neuroprotective mediator derived from DHA. 

Chen Y-W, Hwang KC, Yen C-C, Lai Y-L (2004) Fullerene derivatives protect against oxidative stress in RAW 264.7 cells and ischemia-reperfused lungs. Am. J. Physiol. 287 R21-R26. 

In addition, there is experimental evidence showing that mitochondrial cardiolipin content markedly decreases following ischemia and reperfusion injury due to cardiolipin peroxidation (Soussi et al., 1990) and that a decrease in the mitochondrial phospholipid cardiolipin occurred in aged rat hearts (Pepe, 2000). These decreases may he attrihutahle to the hydroperoxide-formation of cardiolipin after exposure to intense or repeated oxidative stress during disease state or normal aging, respectively. 

P5 Studies have shown that ebselen is an antiinflammatory and antioxidative agent. Its protective effect has been investigated in oxidative stress related diseases such as cerebral ischemia in recent years. However, experimental evidence also shows that ebselen causes cell death in several different cell types. Whether ebselen will have a beneficial or detrimental effect on cells under ischemic condition is not known. Herein, we studied the effect of ebselen... 

Love S. (1999). Oxidative stress in brain ischemia. Brain Pathol. 9 119-131. 

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