Alterations in superoxide dismutase, glutathione peroxidase and catalase activities in experimental cerebral ischemia-reperfusion

Abstract

Free radicals are thought to be the most important cause of the reperfusion injury subsequent to ischemia. The antioxidant status of the tissue affected by ischemia-reperfusion is of great importance for the primary endogenous defense against the free radical induced injury. This investigation was performed to evaluate the antioxidant enzyme capacity of the brain tissue in the ischemia-reperfusion period using an experimental global moderate (penumbral) ischemia model on rat brains. Experiments were performed on 45 male Sprague Dawley rats. Ischemia was induced by bilateral vertebral arteries cauterization and temporary bilateral carotid arteries occlusion and sustained for 10 minutes. At the end of ischemia (0 min reperfusion) and various reperfusion periods (20 min, 60 min, 240 min), rats were decapitated and brains were frozen in liquid nitrogen. Changes in the intracellular antioxidant enzyme (superoxide dismutase, glutathione peroxidase and catalase) activities were assessed in the rat brain tissues, by spectrophotometric methods. In all moderate ischemia-reperfusion groups, superoxide dismutase activities were found to have decreased significantly compared to the sham operated controls (P < 0.05). During ischemia superoxide dismutase activity was lowered to 31% of that of the control group. The decreases were more significant in reperfusion groups, particularly in 60 min reperfusion (40%). Relatively smaller but still significant diminution was observed in glutathione peroxidase activities (P < 0.05). The ratio of diminution was striking in 20 min and 60 min reperfusion groups with 26% of the sham operated rats. Conversely, moderate ischemia-reperfusion caused significant increase in catalase activities (P < 0.05). The increment was 63% of the preischemic level with 10 min of moderate ischemia. In conclusion, activities of the major antioxidant enzymes were changed significantly in moderate brain ischemia-reperfusion. These results suggest that the disturbance in oxidant-antioxidant balance might play a part in rendering the tissue more vulnerable to free radical induced injuries.

Protective Effects of Minocycline against Short-Term Ischemia-Reperfusion Injury in Rat Brain

“…In the present study, SOD levels did not differ among groups. This is not consistent with some reports of cerebral I/R studies [42,43,44]. However, there are conflicting reports.…”

The Parkinson's disease gene DJ-1 is also a key regulator of stroke-induced damage

“…Equally important, they likely activate specific signaling pathways that initiate adaptive or death responses (8). This ability to control ROS is critical in stroke, and neuronal damage occurs if the ''oxidant-antioxidant'' balance is disturbed in favor of excess oxidative stress during ischemia/ reperfusion (9,10). Therefore, ROS management plays a central role in the pathogenesis of stroke.…”

Rat Beyinlerinde Global İskemi-Reperfüzyon Hasarı Üzerine Kafeik Asit Fenetil Esterin Nöroprotektif Etkisi

“…Similar to our study, it is demonstrated that ischemic circumstances lead to the accumulation of hypoxanthine and stimulates XO activity [29] . The activity of GSH-Px, which detoxifies H 2 O 2 while oxidizing reduced GSH to oxidized GSSG, was depressed during I/R [4] . In the present study, cerebral cortex GSH-Px activity significantly decreased after 24 h ischemia.…”

“…Transient focal and global cerebral I/R triggers a plethora of cellular and molecular events that promotes neuronal cell death in several regions of the brain due to glutamate excitotoxicity, oxidative stress, inflammation and apoptosis [1][2][3][4] . Studies show that nitric oxide (NO) has beneficial properties to I/R injury including increase of blood flow produced by cerebral vasodilatation and inhibition of inflammation [1,5] .…”