The effect of dietary vitamin E on pulmonary susceptibility to near ambient levels of ozone was studied in rats. Exposure to 0.7 or 0.8 ppm ozone continuously for 7 days resulted in significant biochemical augmentations in the lungs of both vitamin E-deficient and -supplemented rats. The relative order of the change was glutathione (GSH) peroxidase > lactate dehydrogenase > glucose-6-phosphate (G-6-P) dehydrogenase and pyruvate kinase > reduced glutathione > malic enzyme > glutathione reductase > protein and malic dehydrogenase. Except for malic dehydrogenase, the degrees of biochemical changes were greater in the lungs of vitamin E-deficient rats than those of the supplemented group following ozone exposure, and the differences in the levels of GSH peroxidase, G-6-P dehydrogenase, pyruvate kinase, and GSH were statistically significant. Histological examination of animal lungs revealed that all animals exposed to 0.7 ppm ozone for 7 days had detectable lesions compared to none from the control groups. However, almost all the lungs categorized as having severe lesions by two investigators in a blind study were from rats fed the vitamin E-deficient diet, while nearly all the lungs from the supplemented group had mild lesions. The results suggest that dietary vitamin E alters cellular sensitivity of lung tissue to ozone exposure, and that depletion of dietary vitamin E lowers the threshold concentration of ozone at which effects can be detected.
ASJC Scopus subject areas
- Environmental Science(all)