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Our objective was to determine whether impairing antioxidant defense by decreasing glutathione peroxidase 1 ( GPx1) gene expression increases the injurious effects of hyperoxia (Hyp). GPx1<jats:sup>+\/+<\/jats:sup>and GPx1<jats:sup>\u2212\/\u2212<\/jats:sup>C57Bl\/6J mice were exposed to 21% O<jats:sub>2<\/jats:sub>(Air) or 40% O<jats:sub>2<\/jats:sub>(Hyp) from birth to postnatal day 7 (P7d); they were euthanized on P7d or maintained in air until adulthood [postnatal day 56 (P56d)] to assess short-term and long-term effects, respectively. We assessed lung architecture, three markers of pulmonary oxidative stress (P7d, P56d), macrophages in lung tissue (P7d), immune cells in bronchoalveolar lavage fluid (BALF; P56d), and GPx1-4 and catalase gene expression in lung tissue (P7d, P56d). On P7d, macrophages were decreased by lack of GPx1 expression and further decreased by hyperoxia. GPx1 expression was increased in GPx1<jats:sup>+\/+<\/jats:sup>Hyp mice and decreased in both GPx1<jats:sup>\u2212\/\u2212<\/jats:sup>groups. On P56d, heme oxygenase-1 was increased by hyperoxia when GPx1 was absent. There were significantly more immune cells from Hyp groups than from the GPx1<jats:sup>+\/+<\/jats:sup>Air group and a greater proportion of lymphocytes in GPx1<jats:sup>\u2212\/\u2212<\/jats:sup>Hyp mice. GPx1 expression was significantly decreased in GPx1<jats:sup>\u2212\/\u2212<\/jats:sup>mice; GPx2-4 and catalase expression was increased in GPx1<jats:sup>\u2212\/\u2212<\/jats:sup>Hyp mice compared with other groups. Tissue fraction was decreased in GPx1<jats:sup>\u2212\/\u2212<\/jats:sup>Air mice; bronchiolar smooth muscle was decreased in GPx1<jats:sup>\u2212\/\u2212<\/jats:sup>mice. GPx1 does not clearly exacerbate hyperoxia-induced increases in oxidative stress or lung injury but may alter pulmonary immune function. Increased expression of GPx2-4 and catalase in GPx1<jats:sup>\u2212\/\u2212<\/jats:sup>Hyp mice suggests gene redundancy within the model.<\/jats:p>","DOI":"10.1152\/ajplung.00039.2016","type":"journal-article","created":{"date-parts":[[2017,4,7]],"date-time":"2017-04-07T02:27:36Z","timestamp":1491532056000},"page":"L115-L125","source":"Crossref","is-referenced-by-count":8,"title":["Does lack of<i>glutathione peroxidase 1<\/i>gene expression exacerbate lung injury induced by neonatal hyperoxia in mice?"],"prefix":"10.1152","volume":"313","author":[{"given":"Sheena","family":"Bouch","sequence":"first","affiliation":[{"name":"Development and Stem Cells Program, Monash Biomedicine Discovery Institute, and Department of Anatomy and Developmental Biology, Monash University, Melbourne, Victoria, Australia; and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Megan","family":"O\u2019Reilly","sequence":"additional","affiliation":[{"name":"Development and Stem Cells Program, 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