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Item Description Lin, Yanling en_US 2011-07-22T00:06:25Z 2011-07-22T00:06:25Z 2007 en_US
dc.description Thesis (M.S.)--University of Hawaii at Manoa, 2007. en_US
dc.description Includes bibliographical references (leaves 40-51). en_US
dc.description ix, 51 leaves, bound ill. (some col.) 29 cm en_US
dc.description.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. en_US
dc.language.iso en-US en_US
dc.relation Theses for the degree of Master of Science (University of Hawaii at Manoa). Molecular Biosciences and Bioengineering; no. 4213 en_US
dc.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. en_US
dc.subject Superoxide dismutase -- Physiological effect en_US
dc.subject Cerebral ischemia -- Pathophysiology en_US
dc.title The effect of SOD-2 knockout and overexpression on brain injury after ischemia and reperfusion in hyperglycemic mice en_US
dc.type Thesis en_US
dc.type.dcmi Text en_US

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