Language
English
Publication Date
8-1-2023
Journal
Redox Biology
DOI
10.1016/j.redox.2023.102790
PMID
37348155
PMCID
PMC10271936
PubMedCentral® Posted Date
6-16-2023
PubMedCentral® Full Text Version
Post-print
Abstract
Oxygen supplementation is life saving for premature infants and for COVID-19 patients but can induce long-term pulmonary injury by triggering inflammation, with xenobiotic-metabolizing CYP enzymes playing a critical role. Murine studies showed that CYP1B1 enhances, while CYP1A1 and CYP1A2 protect from, hyperoxic lung injury. In this study we tested the hypothesis that Cyp1b1-null mice would revert hyperoxia-induced transcriptomic changes observed in WT mice at the transcript and pathway level. Wild type (WT) C57BL/6J and Cyp1b1-null mice aged 8-10 weeks were maintained in room air (21% O
Keywords
Humans, Infant, Newborn, Animals, Mice, Hyperoxia, Cytochrome P-450 CYP1A2, Lung Injury, Cytochrome P-450 CYP1A1, Mice, Inbred C57BL, COVID-19, Oxygen, Bronchopulmonary Dysplasia, Mice, Knockout, Lung, Animals, Newborn, Hyperoxia, Cytochrome P450, CYP1B1, Bronchopulmonary dysplasia, Lung, Oxidative stress
Published Open-Access
yes
Recommended Citation
Grimm, Sandra L; Stading, Rachel E; Robertson, Matthew J; et al., "Loss of Cytochrome P450 (CYP)1B1 Mitigates Hyperoxia Response in Adult Mouse Lung by Reprogramming Metabolism and Translation" (2023). Faculty and Staff Publications. 1930.
https://digitalcommons.library.tmc.edu/baylor_docs/1930
Graphical Abstract
Included in
Biological Phenomena, Cell Phenomena, and Immunity Commons, Life Sciences Commons, Medical Cell Biology Commons, Medical Microbiology Commons, Medical Molecular Biology Commons, Medical Specialties Commons