Does lack of glutathione peroxidase 1 gene expression exacerbate lung injury induced by neonatal hyperoxia in mice?

Supplemental oxygen (O₂) increases the risk of lung injury in preterm infants, owing to an immature antioxidant system. 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^+/+ and GPx1^–/– C57Bl/6J mice were exposed to 21% O₂ (Air) or 40% O₂ (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^+/+Hyp mice and decreased in both GPx1^–/– 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^+/+Air group and a greater proportion of lymphocytes in GPx1^–/–Hyp mice. GPx1 expression was significantly decreased in GPx1^–/– mice; GPx2-4 and catalase expression was increased in GPx1^–/–Hyp mice compared with other groups. Tissue fraction was decreased in GPx1^–/–Air mice; bronchiolar smooth muscle was decreased in GPx1^–/– 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^–/–Hyp mice suggests gene redundancy within the model.

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