Oxidant stress reperfusion

Eventually, after 40-50 min of oxidant stress, intracellular calcium increased. These changes were irreversible when cells were reperfused with control buffer at the end of the protocol. Redrawn with permission from Burton et al. (1990). 

Although it is widely accepted that ischaemia/ reperfusion-induced oxidant stress is associated with a reduction of Na/K ATPase activity, it is difficult to determine which features of this process are responsible for this effect. A classical approach to this type of problem has been to determine the effect of the application of selected metabolites or agents on the activity of the enzyme of interest, an approach that has been exploited for the sarcolemmal Na/K ATPase and glutathione (Haddock et al., 1990). The application of GSH (O.l-l.OmM) induces a concentration-dependent increase in the activity of a bovine isolated ventricular Na/K ATPase preparation (determined by the ouabain-sensitive hydrolysis of ATP to release inorganic phosphate). In the presence of 1 mM GSH there was a 38% stimulation of activity compared to untreated control... 

Ferrari, R., Ceconi, C., Curello, S., Caignoni, A., De Giuli, F. and Visioli, O. (1992). Occurrence of oxidative stress during myocardial reperfusion. Mol. Cell. Biochem. Ill, 61-69. 

Metzger, J., Dore, S.P. and Layterberg, B.H. (1988). Oxidant stress during reperfusion of ischaemic liver no evidence for a role of xanthine oxidase. Hepatology 8, 580-584. 

Hepatic reperfusion injury is not a phenomenon connected solely to liver transplantation but also to situations of prolonged hypoperfusion of the host s own liver. Examples of this occurrence are hypovolemic shock and acute cardiovascular injur) (heart attack). As a result of such cessation and then reintroduction of blood flow, the liver is damaged such that centrilobular necrosis occurs and elevated levels of liver enzymes in the serum can be detected. Particularly because of the involvement of other organs, the interpretation of the role of free radicals in ischaemic hepatitis from this clinical data is very difficult. The involvement of free radicals in the overall phenomenon of hypovolemic shock has been discussed recently by Redl et al. (1993). More specifically. Poll (1993) has reported preliminary data on markers of free-radical production during ischaemic hepatitis. These markers mostly concerned indices of lipid peroxidation in the serum and also in the erythrocytes of affected subjects, and a correlation was seen with the extent of liver injury. The mechanisms of free-radical damage in this model will be difficult to determine in the clinical setting, but the similarity to the situation with transplanted liver surest that the above discussion of the role of XO activation, Kupffer cell activation and induction of an acute inflammatory response would be also relevant here. It will be important to establish whether oxidative stress is important in the pathogenesis of ischaemic hepatitis and in the problems of liver transplantation discussed above, since it would surest that antioxidant therapy could be of real benefit. 

Omar, B., McCord, J. and Downey, J. (1991). Ischaemia reperfusion. In Oxidative Stress Oxidants and Antioxidants (ed. H. Sies) pp. 493-528. Academic Press, London. 

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... 

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. 

Grezzana, T.J. et al. (2004) Oxidative stress, hepatocellular integrity, and hepatic function after initial reperfusion in human hepatic transplantation. Transplantation Proceedings, 36 (4), 843-845. 

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