Effect of vitamin E deficiency and supercritical fluid aerosolized vitamin E supplementation on interleukin-1-induced oxidative lung injury in rats.

We hypothesized that alterations in lung vitamin E levels would impact the development of acute oxidative lung injury. We found that dietary induced deficiency of vitamin E diminished lung tissue levels of vitamin E and increased lung leak following intratracheal administration of interleukin-1 (IL-1) to rats. Conversely, rats administered vitamin E directly to the lungs as an inhaled aerosol (0.3-3 microns particles) formed by supercritical fluid aerosolization (SFA) had increased lung tissue vitamin E levels and decreased IL-1 induced lung leak compared to control rats. Lung myeloperoxidase (MPO) activities, reflecting neutrophil concentrations, were increased in rats given IL-1 intratracheally compared to rats given saline intratracheally but were not different for control or vitamin E depleted rats. Lung MPO activities in rats given IL-1 intratracheally were slightly higher in SFA vitamin E treated rats than in control rats. Our results suggest that vitamin E levels affect susceptibility to IL-1 induced, neutrophil-dependent lung injury. We speculate that supercritical fluid aerosol (SFA) delivery of vitamin E can rapidly increase lung vitamin E levels and decrease acute oxidative lung injury.