Rationale/ Hypothesis: Reactive oxygen species, including lipid hydroperoxides, play a critical role as second messengers in many physiological processes in the body. Heightened reactive oxygen species production at the time of birth imposes an oxidative stress upon the lung, which may trigger postnatal alveologenesis and physiological lung cell apoptosis in the neonatal rat.
Methods: Neonatal rats were subcutaneously injected daily with vehicle (corn oil) or diphenyl-phenyl diamine for the first 6 days of life to study alveologenesis and physiological lung cell apoptosis. Add-back experiments were conducted with a prototypic lipid hydroperoxide, t-butyl hydroperoxide.
Main Results: Treatment with diphenyl-phenyl diamine resulted in parenchymal thickening, reduced numbers of secondary crests and enlarged air spaces, all consistent with the inhibition of alveologenesis and reduced physiological lung cell apoptosis.
Conclusion: Following an oxidative stress at birth, lipid hydroperoxide formation triggers postnatal alveologenesis and physiological lung cell apoptosis in the neonatal rat.
| Identifer | oai:union.ndltd.org:TORONTO/oai:tspace.library.utoronto.ca:1807/33251 |
| Date | 20 November 2012 |
| Creators | Jamal, Mobin |
| Contributors | Tanswell, Keith |
| Source Sets | University of Toronto |
| Language | en_ca |
| Detected Language | English |
| Type | Thesis |
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