{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,23]],"date-time":"2026-01-23T18:10:14Z","timestamp":1769191814404,"version":"3.49.0"},"reference-count":66,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2005,8,17]],"date-time":"2005-08-17T00:00:00Z","timestamp":1124236800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurochemistry"],"published-print":{"date-parts":[[2005,11]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Reactive oxygen species (ROS) are known to be involved in the pathogenesis of traumatic brain injury (TBI). Previous studies have shown that the susceptibility of mice to TBI\u2010induced formation of cortical lesion is determined by the expression levels of copper\u2010zinc and manganese superoxide dismutase (CuZnSOD and MnSOD, respectively). However, the underlying biochemical mechanisms are not understood. In this study, we measured the efficiency of mitochondrial respiration in mouse brains with altered expression of these two enzymes. While controlled cortical impact injury (CCII) with a deformation depth of 2\u2003mm caused a drastic decrease in NAD\u2010linked bioenergetic capacity in brain mitochondria of wild\u2010type mice, the functional decrease was not observed in brains of littermate transgenic mice overexpressing CuZnSOD or MnSOD. In addition, a 1\u2003mm CCII greatly compromised brain mitochondrial function in mice deficient in CuZnSOD or MnSOD, but not wild\u2010type mice. Inclusion of the calcium\u2010chelating agent, EGTA, in the assay solution could completely prevent dysfunction of oxidative phosphorylation in all mitochondrial samples, suggesting that the observed impairment of mitochondrial function was a result of calcium overloading. In conclusion, our results imply that mitochondrial dysfunction induced by superoxide anion radical contributes to lesion formation in mouse brain following physical trauma.<\/jats:p>","DOI":"10.1111\/j.1471-4159.2005.03412.x","type":"journal-article","created":{"date-parts":[[2005,10,10]],"date-time":"2005-10-10T16:44:10Z","timestamp":1128962650000},"page":"732-744","source":"Crossref","is-referenced-by-count":47,"title":["Prevention of mitochondrial dysfunction in post\u2010traumatic mouse brain by superoxide dismutase"],"prefix":"10.1111","volume":"95","author":[{"given":"Ye","family":"Xiong","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Feng\u2010Shiun","family":"Shie","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jing","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Chuan\u2010Pu","family":"Lee","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ye\u2010Shih","family":"Ho","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2005,8,17]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0076-6879(84)05016-3"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1007\/BF02815368"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-291X(75)80188-4"},{"key":"e_1_2_7_5_1","doi-asserted-by":"publisher","DOI":"10.1021\/ic00216a003"},{"key":"e_1_2_7_6_1","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-4615-9035-4_5"},{"key":"e_1_2_7_7_1","doi-asserted-by":"publisher","DOI":"10.1042\/bj1340707"},{"key":"e_1_2_7_8_1","doi-asserted-by":"publisher","DOI":"10.1016\/0891-5849(89)90056-7"},{"key":"e_1_2_7_9_1","first-page":"S1","article-title":"Involvement of lipid peroxidation in CNS injury","volume":"9","author":"Braughler J. 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