Ischemic preconditioning in the rat hippocampus increasesantioxidant activities but does not affect the level of hydroxylradicals during subsequent severe ischemia

• Published in: Experimental & molecular medicine pp. 556 - 563
• Main Authors: Yun-Sik Choi, 조경옥, Eun-Jeong Kim, 성기욱, 김성윤
• Format: Journal Article
• Language: Korean
• Published: 생화학분자생물학회 01.08.2007
• Subjects: 생화학
• ISSN: 1226-3613; 2092-6413

Several studies have demonstrated that ischemic pre-conditioning increases superoxide dismutase activ-ity, but it is unclear how ischemic preconditioning duction during subsequent severe ischemia and re-perfusion in the hippocampus. To answer this ques-tion, we investigated whether ischemic precondition-ing in the hippocampal CA1 region increases the activities of antioxidant enzymes glutathione perox-idase and catalase, resulting in a decrease in the level of hydroxyl radicals during subsequent severe ischemia-reperfusion. Transient forebrain ischemia was induced by four-vessel occlusion in rats. ation was performed and a 15-min severe ischemia was induced three days later. Ischemic precondition-ing preserved the CA1 hipocampal neurons follow-ing severe ischemia. The concentration of 2,3-dihy-droxybenzoic acid, an indicator of hydroxyl radical, was measured using in vivo microdialysis technique combined with HPLC. The ischemia-induced increase in the ratio of 2,3-dihydroxybenzoic acid concen-between preconditioned and control groups. On the other hand, activities of the antioxidant enzymes glu-tathione peroxidase-1 and catalase were significantly increased at 3 days after ischemic preconditioning in the hippocampus. Our results suggest that, in pre-conditioned rats, while hydrogen peroxide is gen-erated from severe ischemia, the activity of catalase and glutathione peroxidase-1 is correspondingly in-xide. However, our results show that the enhanced activity of these antioxidant enzymes in precondi-tioned rats is not suficient to decrease hydroxyl radi-cal levels during subsequent severe ischemia-re-perfusion. KCI Citation Count: 17