Time Course of Peripheral Oxidative Stress as Consequence of Global Ischaemic Brain Injury in Rats

Abstract

Free radicals play an important role in the pathogenesis of brain injury. This study evaluates the potential relationship between ischaemia/reperfusion (I/R)-induced brain injury, peripheral oxidative stress (lymphocyte DNA damage), plasma antioxidant potential and uric acid levels. We observed that 15 min of ischaemia were sufficient to significantly increase lymphocyte DNA damage that remained elevated at the end of early (3 h) reperfusion and at later (72 h) reperfusion time; this parameter was not significantly increased, when compared to preoperated levels. In parallel, antioxidant potential was elevated after 15 min of ischaemia, remained high at early (3 h) reperfusion and decreased again with longer (72 h) reperfusion. A close association between the plasma antioxidant status and the uric acid content has been confirmed by findings that changes in TRAP values positively correlate with uric acid concentration in rat plasma after ischaemic injury. Moreover, results of in vitro experiments with extra uric acid addition to control plasma have shown that uric acid contributes to a greater part of TRAP values. These results indicate a similar time course of brain I/R-associated oxidative stress and peripheral antioxidant defence status and/or oxidative stress in animal experiments.

Transient Forebrain Ischemia Impact on Lymphocyte DNA Damage, Glutamic Acid Level, and SOD Activity in Blood

“…Similar experiment studied relationship between ischemic/reperfusion injury and peripheral oxidative stress represented by DNA damage of peripheral lymphocytes was performed in the same model of brain ischemia, but with longer period of blood supply restriction (Sivonova et al 2008). Authors investigated that cerebral ischemia and subsequent reperfusion affects not only brain antioxidant capacity but also peripheral system.…”

Molecular Mechanisms Leading to Neuroprotection/Ischemic Tolerance: Effect of Preconditioning on the Stress Reaction of Endoplasmic Reticulum

“…Global forebrain ischemia was induced by the standard four-vessel occlusion model as was recently described (Lehotský et al 2004;Sivonová et al 2008;Uríková et al 2006;Urban et al 2008). Briefly, on day 1, both vertebral arteries were irreversibly occluded for 10 min.…”

Molecular Analysis of Endoplasmic Reticulum Stress Response After Global Forebrain Ischemia/Reperfusion in Rats: Effect of Neuroprotectant Simvastatin

“…Global forebrain ischemia was induced by the standard four-vessel occlusion model (Lehotský et al 2004;Sivonová et al 2008;Uríková et al 2006). Briefly, on day 1, both vertebral arteries were irreversibly occluded for 10 min by thermo coagulation through the alar foramina after anesthesia with 2,5% halothane in a mixture of oxygen/nitrous oxide (30%/ 70%), without any visible influence on the animals.…”