Effects of long-term ozone exposure and dietary vitamin E in rats

Rats fed on a vitamin E-deficient diet (E-depleted group) and a vitamin E-supplemented diet (E-supplemented group) were exposed to 0.3 ppm ozone for three hours daily, five days a week for seven months. Then animals from each group were sacrificed, and electron microscopic studies on the lung and biochemical examinations on the lung and liver were performed. 1) Vitamin E concentration in serum decreased following ozone exposure in the E-supplemented group, whereas it remained unaffected the E-depleted group. 2) Both TAB value and % release of lysosomal enzyme (acid phosphatase) of the liver were increased in vitamin E-depleted air-exposed rats, and showed even higher values following ozone exposure. Levels of both components were highest in the vitamin E-depleted ozone-exposed rats, thus demonstrating that there are a marked increase in lipid peroxide and the increased labilization of lysosomes in this instance. 3) Arachidonic acid (20:4) of total lipid, phospholipid and lecithin in the lung tissue showed a tendency to decrease in vitamin E-depleted air-exposed rats. Those in the ozone-exposed animals showed in both groups a tendency to increase in total lipid and lecithin, and to decrease in phospholipid. However, a change in the fatty acid composition following ozone exposure was generally mild. 4) The fatty acid composition of phospholipid in lung washings did not show a remarkable change following ozone exposure in either group, thus suggesting that it has the resistivity to oxidation. 5) Morphological observations on the lung with the scanning and transmission electron microscopes did not reveal any clear differences between the two groups. The defensive effect of vitamin E on ozone toxicity induced by long-term exposure to ozone was not made clear by the morphological or biochemical examination of the lung. However, biochemical findings in liver of rats exposed to ozone suggested the possibility that vitamin E deficiency permits the damaging effects of lipid peroxidation on biological membranes.