Biochemical and morphologic responses of rat nasal epithelia to hyperoxia

While performing its functions in olfaction, modification of inspired air, and protection of the lower respiratory tract from high concentrations of potentially harmful inhalants, the nasal mucosa can be injured by a number of inhalants. In this study, F344/N male rats were exposed to filtered air or hyperoxia (85 or 87% oxygen), 24 hr/day, 7 days/week, for 1 (acute exposure) or 11 (chronic exposure) weeks. There were distinct differences between the different epithelial regions examined in replicative and morphologic responses as well as altered enzyme activities in response to oxygen exposure. Neither acute nor chronic hyperoxic exposure caused degenerative, necrotizing, or inflammatory changes in any of the nasal epithelial examined. Hyperoxia-induced hypertrophy, but not hyperplasia, of the non-ciliated cuboidal (NCC) epithelium occurred after both acute and chronic exposure. Cell replication was increased in portions of the NCC and respiratory epithelia after acute hyperoxia exposure. There were significant increases, compared to controls, in the specific activity of glucose-6-phosphate dehydrogenase in the nasal turbinates, maxilloturbinates, and lateral wall epithelium (NCC epithelium), the nasal septum (respiratory epithelium), and the ethmoturbinates (olfactory epithelium), and in the specific activity of glutathione peroxidase in the NCC epithelium and ethmoturbinates after acute hyperoxia exposure. The specific activity of cytochrome P450-dependent monooxygenase-catalyzed O-deethylation of 3-cyano-7-ethoxycoumarin was significantly decreased, compared to controls, in the NCC epithelium. These results suggest that hyperoxia exposure induces morphologic and biochemical alterations in nasal epithelia which appear to be protective responses of certain cell types to hyperoxia.