Rat Lung Alveolar Type I Epithelial Cell Injury and Response to Hyperoxia

Publisher Website
Google Scholar
Abstract
Hyperoxia has been shown to cause extensive lung injury, which involves all components of the alveolar septum, although the type I epithelium has generally been reported to be resistant to significant injury. Electron microscopic morphometry was performed to define changes in volumes of subcellular components of alveolar epithelial cells in rats exposed to 85% O2 for 0, 7, and 14 d. Because of their large size, type I cells in control animals actually contain a greater volume of most of the organelles involved in cell metabolism than do type II cells. Hyperoxic exposure causes a dramatic change in the subcellular composition of the average type I cell, suggesting significant injury and/or response. Injury was suggested by the finding that lysosomes plus peroxisomes increased 1,250% after 7 d in hyperoxia and remained elevated by 200% after 14 d of exposure. Volumes of mitochondria, rough endoplasmic reticulum, smooth endoplasmic reticulum, and Golgi apparatus increased by 100%, 51%, 91%, and 500%, respectively, after hyperoxia. Qualitative analysis showed an altered, ruffled air border with focal areas of cytoplasmic translucency (suggesting injury) and focal areas of subcellular hypertrophy. Exposure to hyperoxia was associated with more organelles being found in peripheral or attenuated portions of type I alveolar cells. Since the increase in type I organelles exceeds the volume of these organelles in its progenitor, the type II cell, it is likely that hyperoxia causes hypertrophy of the type I alveolar epithelium itself, independent of simple type II cell differentiation. Because of the large size and wide distribution of the type I cell, dramatic shifts in cell substructure caused by hyperoxia are more difficult to detect and require quantitative analysis to fully ascertain the extent of cell alterations.