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To assess the role of oxidative stress in the pathogenesis of this injury, we measured histopathological damage, lipid peroxidation products, enzymatic activities of catalase and glutathione peroxidase, and hydrogen peroxide (H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>) concentration in these animals before and after hypoxic\u2013ischemic injury. Lipid peroxidation products were significantly increased 2 hours after the insult in both transgenic and nontransgenic brains in hippocampus, the most damaged brain region. Catalase activity did not increase in response to SOD1 overexpression or injury in either group. However, glutathione peroxidase activity, unchanged in response to overexpression, decreased significantly 24 hours after injury in both groups. At 24 hours after injury, greater H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> accumlation was observed in transgenic brains. Because SOD1 dismutates superoxide to H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>, overexpression of SOD1 in the presence of developmentally low activities of the catalytic enzymes glutathione peroxidase and catalase leads to an increased production of H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>, and may explain the increased brain injury observed after hypoxia\u2013ischemia in neonatal SOD1 mice.<\/jats:p>","DOI":"10.1002\/ana.410440311","type":"journal-article","created":{"date-parts":[[2005,1,1]],"date-time":"2005-01-01T15:21:43Z","timestamp":1104592903000},"page":"357-364","source":"Crossref","is-referenced-by-count":161,"title":["Copper\/zinc superoxide dismutase transgenic brain accumulates hydrogen peroxide after perinatal hypoxia ischemia"],"prefix":"10.1002","volume":"44","author":[{"given":"Heather J.","family":"Fullerton","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jeremy 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