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|M.S.Q111.H3_4213 AUG 2007_uh.pdf||Version for UH users||2.7 MB||Adobe PDF||View/Open|
|M.S.Q111.H3_4213 AUG 2007_r.pdf||Version for non-UH users. Copying/Printing is not permitted||2.7 MB||Adobe PDF||View/Open|
|Title:||The effect of SOD-2 knockout and overexpression on brain injury after ischemia and reperfusion in hyperglycemic mice|
|Keywords:||Superoxide dismutase -- Physiological effect|
Cerebral ischemia -- Pathophysiology
|Abstract:||Reactive oxygen radicals (ROS) play important roles in tissue damage caused by cerebral ischemia and reperfusion. Previous studies have shown that mitochondrial specific SOD (SOD-2) plays a protective role as an antioxidant defense in ischemic neuronal injury. One of the important contributors to the adverse effects of hyperglycemia on ischemic brain is the overproduction of superoxide anions. Our studies in mice with hyperglycemia showed that after ischemia and reperfusion, the deficiency of SOD-2 activity in heterozygous SOD-2 KO mice enhanced the production of superoxide anion, increased the infarct volume and exacerbated DNA oxidative damage; whereas the overexpressing of SOD-2 in heterozygous SOD-2 Tg mice, only slightly decreased the superoxide anion production after ischemia and reperfusion, but did not attenuate DNA damage or decrease the infarct volume due to the increased production of hydrogen peroxide from superoxide anion, which was increased in hyperglycemia condition.|
|Description:||Thesis (M.S.)--University of Hawaii at Manoa, 2007.|
Includes bibliographical references (leaves 40-51).
ix, 51 leaves, bound ill. (some col.) 29 cm
|Rights:||All UHM dissertations and theses are protected by copyright. They may be viewed from this source for any purpose, but reproduction or distribution in any format is prohibited without written permission from the copyright owner.|
|Appears in Collections:||M.S. - Molecular Biosciences and Bioengineering|
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