Effect of glutathione reductase (Gsr) deficiency on lung transcriptomics in embryonic mice and neonatal and adult mice exposed to hyperoxia.

Gsr is an antioxidant enzyme responsible for maintaining the supply of reduced glutathiones which reduce reactive oxigen species and maintain cellular redox balance. However, the the role for Gsr in the developemnt of oxidative lung injury is not well characterized. We used microarray analysis to identify Gsr-dependent genes and pathways in embyronic, neonate, and adult lungs. We also determined Gsr-dependent lung transcriptomics in mouse neonates and adults which were neonatally exposed to hyperoxia (O2) or air. Lungs from Gsr-wildtype (Gsr-WT, C3H/HeN) and Gsr-knockout (Gsr-KO) embryos were isolated at embryonic day 19 (E19). Lungs from Gsr-wildtype and Gsr-knockout mice exposed to room air or hyperoxia during postnatal days 0-5 (P0-P5) were collected at P5 and P56. Lung total RNA was isolated and hybridization on Affymetrix Mouse 430_2 arrays.