Ischemic reperfusion

Tso and Lam suggested that astaxanthin could be useful for prevention and treatment of neuronal damage associated with age-related macular degeneration and may also be effective in treating ischemic reperfusion injury, Alzheimer s disease, Parkinson s disease, spinal cord injuries, and other types of central nervous system injuries. Astaxanthin was found to easily cross the blood-brain barrier and did not form crystals in the eye. 

A.Vanella, C. di Giacomo, V. Sorrenti, A. Russo, C. Castorina, A. Campisi, M. Renis, and J.R. Perez-Polo, Free radical scavenger depletion in post-ischemic reperfusion brain damage. Neurochem. Res. 18,... 

A3 adenosine receptor knockout mice were protected from renal failure caused by ischemic-reperfusion injury or by myoglobinuria (Lee et al. 2003). A similar protection was achieved with A3 antagonists whereas agonists worsened the condition confirming A3 receptors as a potential target in the treatment of renal failure. 

Harrison GJ, Cerniway RJ, Peart J, Berr SS, Ashton K, Regan S, Matherne GP, Headrick JP (2002) Effects of A3 adenosine receptor activation and gene knock-out in ischemic-reperfusion mouse heart. Cardiovasc Res 53(1) 147-155... 

Peart J, Flood A, Linden J, Matherne GP, Headrick JP (2002) Adenosine-mediated cardioprotection in ischemic-reperfused mouse heart. J Cardiovasc Pharmacol 39(1) 117-129 Peart J, Willems L, Headrick JP (2003) Receptor and non-receptor-dependent mechanisms of cardioprotection with adenosine. Am J Physiol Heart Circ Physiol 284(2) H519-H527 Peart JN, Headrick JP (2008) Sustained cardioprotection exploring unconventional modalities. Vascular Pharmacol 49(2-3) 63-70... 

Bushell AJ, Klenerman L, Taylor S, Davies H, Grierson I, Helliwell TR, Jackson MJ (2002b) Ischemic preconditioning of skeletal muscle. 1. Protection against the structural changes induced by ischemic/reperfusion injury. J Bone Joint Surg 84-B l 184-1188... 

Szabo ME, Galiyas E, Bak I, Rakotovao A, Boucher F, de Leiris J, Nagy N, Varga E, Tosaki A. 2004 Heme oxygenase-1-related carbon monoxide and flavonoids in ischemic/reperfused rat retina. Invest Ophthalmol Vis Sci 45 3727-3232. 

With this cautionary remark in mind, we would like to mention some studies where attempts have been made to monitor OH production and a variety of conditions, including stressed systems dextran sulfate-induced colitis (Blackburn et al. 1998), diabetes patients (Ghiselli et al. 1992), obstructive jaundice of rats (Tsay et al. 1998), ischemic reperfused mycocardium (Das et al. 1989), activated human neutrophils (Kaur et al. 1988), healthy humans (Grootveld and Halliwell 1988), fecal flora (Owen et al. 1996), in chondrocytes and cartilage (Tiku et al. 1998). 

Das DK, George A, Liu X, Rao PS (1989) Detection of hydroxyl radical in the mitochondria of ischemic reperfused myocardium by trapping with salicylate. Biochem Biophys Res Commun 165 1004-1009... 

Chen, W., Bennett, C. F., Wang, M. E., Dragun, D., Tian, L., Stecker, K., Clark, J. H., Kahan, B. D. and Stepkowski, S. M. (1999). Perfusion of kidneys with unformulated naked intercellular adhesion molecule-1 antisense oligodeoxynucleotides prevents ischemic/reperfusion injury. Transplantation 68, 880-887. 

Persad, S., Takeda, S., Panagia, V., and Dhalla, N.S. 1997. p-adrcnoccptor-linkcd signal transduction in ischemic-reperfused heart and scavenging of oxyradicals. J. Mol. Cell. Cardiol. 29 545-558. 

Cordis, G.A., Maulik, G., Bagchi, D., Riedel, W., and Das, D.K. 1998b. Detection of oxidative DNA damage to ischemic reperfused rat hearts by 8-hydroxydeoxyguanosine formation. J. Mol. Cell. Cardiol. 30 1939-1944. 

Cargnoni, A., Ceconi, C., Gaia, G., Agnoletti, L., and Ferrari, R. 2002. Cellular thiols redox status a switch for NF-kB activation during myocardial post-ischemic reperfusion. J. Mol. Cell. Cardiol. 34 997-1005. 

Gauthamna, K., Maulik, M., Kumari, R., Manchanda, S.C., Dinda, A.K., and Maulik, S.K. 2001. Effect on chronic treatment with bark of Terminalia arjuna a study of the isolated ischemic-reperfused rat heart. J. Ethnopharmacol. 75, 197—201. 

Studies in various animal models and in human hearts suggest that apoptosis does occur in ischemia/reperfusion injury of the heart, though the relative contribution of apoptosis in comparison with necrosis to cell loss in ischemia/ reperfusion injury is still controversial. Cardiomyocyte apoptosis was first reported by Gottlieb et al. [107], who studied the ischemia/reperfusion in rabbit hearts and found the hallmark of apoptosis in ischemic/reperfused hearts but not in the normal or ischemic-only rabbit hearts. Identification of apoptosis was based on the presence of fragmented DNA in electrophoretic gels, on in situ nick end-labeling assays, and on electron microscopy. They concluded that apoptosis may be a specific feature of reperfusion injury in cardiac myocytes. Subsequent studies have shown that apoptosis probably occurs both in ischemia and reperfusion [108], It appears that apoptosis is more prominent after ischemia followed by reperfusion than after ischemia alone [109, 110],... 

In the absence of strong chelating agents, lactoferrin, transferrin and ceruloplasmin do not promote hydroxyl-radical production at pH 7.4 [158,159], which is consistent with their protecting role at sites of inflammation. At present, the possible involvement of ferritin and that of the iron-transit pool in Fenton-type reactions cannot be excluded, and this may be of great importance in some pathophysiological situations such as post-ischemic reperfusion of tissues. 

The use of chopped samples indicates marked differences in ESR spectra of the control, ischemic, and post-ischemic reperfused myocardium. Processing... 

The ESR spectral parameters of post-ischemic reperfused samples are similar to those of the control (Table 1). However, the spectral amplitude is consistently increased by a factor of two or more. Therefore, reperfusion of the ischemic myocardium results in an increase in the production of radicals. However, direct ESR evidence for the production of oxy radicals in ischemic and reperfused heart tissues is still lacking. 

---