Dietary antioxidants and the biochemical response to oxidant inhalation: II. Influence of dietary selenium on the biochemical effects of ozone exposure in mouse lung

Abstract

We examined the influence of dietary selenium (Se) on the pulmonary biochemical response to ozone (O 3) exposure. For 11 weeks, weanling female strain A St mice were fed a test diet containing Se either at 0 ppm (−Se) or 1 ppm (+Se). Each diet contained 55 ppm vitamin E (vit E). Mice from each dietary group were exposed to 0.8 ± 0.05 ppm (1568 ± 98 μg/m 3) O 3 continuously for 5 days. After O 3 exposure, they were killed along with a matched number of unexposed controls, and their lungs were analyzed for various biochemical parameters. The Se contents of lung tissue and whole blood were determined, and the levels were seven- to eightfold higher in +Se mice than in −Se mice, reflecting the Se intake of the animals. In unexposed control mice, Se deficiency caused a decline in glutathione peroxidase (GP) activity relative to +Se group. After O 3 exposure, the GP activity in the −Se group was associated with a lack of stimulation of glutathione reductase (GR) activity and the pentose phosphate cycle (PPC) as assessed by measuring glucose-6-phosphate dehydrogenase (G6PD) and 6-phosphogluconate dehydrogenase (6PGD) activities. In contrast, the +Se group after O 3 exposure exhibited increases in all four enzyme activities. Other parameters, e.g., lung weight, total lung protein, DNA and nonprotein sulfhydryl contents, and O 2 consumption, were not affected by dietary Se in the presence or absence of O 3 exposure. The data indicate that dietary Se alters the GP activity, which in turn influences the GR and PPC activities in the lung evidently through a reduced demand for NADPH. The level of vit E in the lung was found to be twofold higher in the −Se group than in the +Se group, suggesting a compensatory relationship between Se and vit E in the lung. With O 3 exposure, both Se and vit E contents further increased in the lungs of each dietary group. It is plausible that Se and vit E under oxidant stress are “mobilized” to the lung from other body sites.