Abstract
Rats fed on a vitamin E-deficient diet (E-depleted group) and a vitamin E-supplemented diet (E-supplemented group) were exposed to 0.3ppm of ozone three hours a day, 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 in the E-depleted group. 2) TBA and % release of lysosomal enzyme (acid phosphatase) of the liver were already increased in vitamin E-depleted air-exposed rats, and showed higher values following ozone exposure. Both showed the highest value in vitamin E-depleted ozone-exposed rats, thus demonstrating that there is a marked increase in lipid peroxide and a fall in the 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 both groups, thus suggesting that it has the resistivity to oxidation. 5) Morphological observations on the lung with the scanning and transmission electron microscope did not reveal any clear differences between both groups.
The defensive effect of vitamin E on ozone toxicity induced by long-term exposure to ozone was not made clear by the morphological examination, however, biochemical findings suggested the possibility that this vitamin will play the role of antioxidant effect in vivo.
