EXPOSURE TO CRYSTALLINE SILICA OR TREATMENT WITH CHLORPHENTERMINE INCREASES VITAMIN-E LEVELS IN RAT ALVEOLAR-LAVAGE MATERIALS

Previous studies have shown that vitamin E may be an integral part of lung surfactant and may function to protect this material from oxidant damage. Therefore, we measured the vitamin E levels in alveolar lavag e materials from rats exposed to crystalline silica or treated with ch lorphentermine (CP), two treatments that are known to increase surfact ant phospholipids (PL) by different mechanisms. Silica exposure leads to increased PL synthesis, and CP treatment causes a reduction in PL d egradation. Two different silica preparations, HCl-washed and unwashed silica, were used because exposure to each of them leads to different degrees of phospholipidosis. Exposure to HCl-washed silica results in a more than 17-fold increase in lavage PL and protein levels and a 12 .2-fold increase in the amount of vitamin E. Exposure to unwashed sili ca leads to an approximately 7-fold increase in PL and proteins and a 5.8-fold increase in lavage vitamin E. Following treatment of rats wit h CP, there is a 15- to 19-fold increase in lavage Pi. and proteins an d a 13.6-fold increase in vitamin E. When the results are expressed as micrograms vitamin E per milligram of lavage PL or protein, there is not much difference between controls and each treatment group. Because surfactant synthesis occurs in the endoplasmic reticulum, we also mea sured vitamin E in lung microsomes. Both silica exposure and CP treatm ent also lead to 1.8- to 2.5-fold increases, respectively, in the lung microsomal levels of vitamin E. These results demonstrate that alveol ar lavage vitamin E levels are elevated along with lavage PL and prote ins, and lung microsomal vitamin E levels are increased following expo sure of rats to silica or treatment of the animals with CP.