{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,31]],"date-time":"2026-07-31T12:07:14Z","timestamp":1785499634692,"version":"3.56.0"},"reference-count":40,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2007,9,4]],"date-time":"2007-09-04T00:00:00Z","timestamp":1188864000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Institutes of Health","award":["NS33997"],"award-info":[{"award-number":["NS33997"]}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Intl J of Devlp Neuroscience"],"published-print":{"date-parts":[[2008,2]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:label\/><jats:p>Oxidative stress is a critical component of the injury response to hypoxia\u2010ischemia (HI) in the neonatal brain, and this response is unique and at times paradoxical to that seen in the mature brain. Previously, we showed that copper\u2010zinc superoxide\u2010dismutase (SOD1) over\u2010expression is not beneficial to the neonatal mouse brain with HI injury, unlike the adult brain with ischemic injury. However, glutathione peroxidase 1 (GPx1) over\u2010expression is protective to the neonatal mouse brain with HI injury. To further test the hypothesis that an adequate supply of GPx is critical to protection from HI injury, we crossed SOD1 over\u2010expressing mice (hSOD\u2010tg) with GPx1 over\u2010expressing mice (hGPx\u2010tg). Resulting litters contained wild\u2010type (wt), hGPx\u2010tg, hSOD\u2010tg and hybrid hGPx\u2010tg\/hSOD\u2010tg pups, which were subjected to HI at P7. Confirming previous results, the hGPx\u2010tg mice had reduced injury compared to both Wt and hSOD\u2010tg littermates. Neonatal mice over\u2010expressing <jats:italic>both<\/jats:italic> GPx1 and SOD1 also had less injury compared to wt or hSOD\u2010tg alone. A result of oxidative stress after neonatal HI is a decrease in the concentration of reduced (i.e. antioxidant\u2010active) glutathione (GSH). In this study, we tested the effect of systemic administration of \u03b1\u2010lipoic acid on levels of GSH in the cortex after HI. Although GSH levels were restored by 24 h after HI, injury was not reduced compared to vehicle\u2010treated mice. We also tested two other pharmacological approaches to reducing oxidative stress in hSOD\u2010tg and wild\u2010type littermates. Both the specific inhibitor of neuronal nitric oxide synthase, 7\u2010nitroindazole (7NI), and the spin\u2010trapping agent alpha\u2010phenyl\u2010tert\u2010butyl\u2010nitrone (PBN) did not reduce HI injury, however. Taken together, these results imply that H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> is a critical component of neonatal HI injury, and GPx1 plays an important role in the defense against this H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> and is thereby neuroprotective.<\/jats:p><\/jats:sec>","DOI":"10.1016\/j.ijdevneu.2007.08.010","type":"journal-article","created":{"date-parts":[[2007,9,5]],"date-time":"2007-09-05T11:26:49Z","timestamp":1188991609000},"page":"87-92","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":25,"title":["Genetic and pharmacologic manipulation of oxidative stress after neonatal hypoxia\u2010ischemia"],"prefix":"10.1002","volume":"26","author":[{"given":"R. Ann","family":"Sheldon","sequence":"first","affiliation":[{"name":"Neonatal Brain Disorders Center Department of Neurology University of California San Francisco San Francisco CA 94143\u20100663 USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephan","family":"Christen","sequence":"additional","affiliation":[{"name":"Institute for Infectious Diseases University of Berne CH\u20103010 Berne Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Donna M.","family":"Ferriero","sequence":"additional","affiliation":[{"name":"Neonatal Brain Disorders Center Department of Neurology University of California San Francisco San Francisco CA 94143\u20100663 USA"},{"name":"Department of Pediatrics University of California San Francisco San Francisco CA 94143\u20100663 USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2007,9,4]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0165-3806(01)00302-9"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1203\/00006450-199511000-00004"},{"key":"e_1_2_6_4_1","doi-asserted-by":"publisher","DOI":"10.1097\/00008506-199310000-00004"},{"issue":"4","key":"e_1_2_6_5_1","doi-asserted-by":"crossref","first-page":"287","DOI":"10.1016\/j.siny.2007.01.020","article-title":"Anti\u2010oxidant strategies","volume":"12","author":"Buonocore G.","year":"2007","journal-title":"Semin. 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