{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,16]],"date-time":"2026-06-16T21:44:59Z","timestamp":1781646299987,"version":"3.54.5"},"reference-count":48,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2012,2,10]],"date-time":"2012-02-10T00:00:00Z","timestamp":1328832000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The FEBS Journal"],"published-print":{"date-parts":[[2012,3]]},"abstract":"<jats:p>There is increasing evidence that hyperoxia, particularly at the time of birth, may result in neurological injury, in particular to the susceptible vasculature of these tissues. This study was aimed at determining whether overexpression of extracellular superoxide dismutase (EC\u2010SOD) is protective against brain injury induced by hyperoxia. Transgenic (TG) mice (with an extra copy of the human extracellular superoxide dismutase gene) and wild\u2010type (WT) neonate mice were exposed to hyperoxia (95% of <jats:italic>F<\/jats:italic><jats:sub>i<\/jats:sub><jats:sc>o<\/jats:sc><jats:sub>2<\/jats:sub>) for 7\u2003days after birth versus the control group in room air. Brain positron emission tomography (PET) scanning with fludeoxyglucose (FDG) isotope uptake was performed after exposure. To assess apoptosis induced by hyperoxia exposure, caspase\u20033 ELISA and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining were performed. Quantitative western blot for the following inflammatory markers was performed: glial fibrillary acidic protein, ionized calcium\u2010binding adaptor molecule\u20031, macrophage\u2010inhibiting factor, and phospho\u2010AMP\u2010activated protein kinase. PET scanning with FDG isotope uptake showed significantly higher uptake in the WT hyperoxia neonate brain group (0.14\u2003\u00b1\u20030.03) than in both the TG group (0.09\u2003\u00b1\u20030.01) and the control group (0.08\u2003\u00b1\u20030.02) (<jats:italic>P<\/jats:italic>\u2003&lt;\u20030.05). Histopathological investigation showed more apoptosis and dead neurons in hippocampus and cerebellum brain sections of WT neonate mice after exposure to hyperoxia than in TG mice; this finding was also confirmed by TUNEL staining. The caspase\u20033 assay confirmed the finding of more apoptosis in WT hyperoxia neonates (0.814\u2003\u00b1\u20030.112) than in the TG hyperoxic group (0.579\u2003\u00b1\u20030.144) (<jats:italic>P<\/jats:italic>\u2003&lt;\u20030.05); this finding was also confirmed by TUNEL staining. Quantitative western blotting for the inflammatory and metabolic markers showed significantly higher expression in the WT group than in the TG and control groups. Thus, overexpression of EC\u2010SOD in the neonate brain offers significant protection against hyperoxia\u2010induced brain damage.<\/jats:p>","DOI":"10.1111\/j.1742-4658.2012.08478.x","type":"journal-article","created":{"date-parts":[[2012,1,12]],"date-time":"2012-01-12T20:29:45Z","timestamp":1326400185000},"page":"871-881","source":"Crossref","is-referenced-by-count":27,"title":["Overexpression of extracellular superoxide dismutase has a protective role against hyperoxia\u2010induced brain injury in neonatal 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