Ozone causes lipid peroxidation but little antioxidant depletion in exercising and nonexercising hamsters

Ozone (O-3), a major component of urban air pollution, is a strong oxidizin g agent that can cause lung injury and inflammation. In the present study, we investigated the effect of inhalation of O-3 on levels of F-2-isoprostan es in bronchoalveolar lavage fluid (BALF) and on levels of antioxidants in the BALF and plasma of hamsters. Because antioxidants, including urate, asc orbate, GSH, and vitamin E, defend the lungs by reacting with oxidizing age nts, we expected to find a decrease in antioxidant levels after O-3 exposur e. Similarly, we expected an increase in the levels of F-2-isoprostanes, wh ich are lipid peroxidation products. Exposure to 1.0 or 3.0 parts/million ( PPM) O-3 for 6 h resulted in an increase in BALF neutrophil numbers, an ind icator of acute inflammation, as well as elevation of BALF F-2-isoprostanes . The higher dose Of O-3 caused an increase in the BALF level of urate and a decrease in the plasma level of ascorbate, but 1.0 ppm O-3 had no effect on BALF or plasma antioxidant levels. Exposure to 0.12 ppm O-3 had no effec t on BALF neutrophils or F-2-isoprostanes nor on BALF and plasma antioxidan ts. We also investigated the effect Of O-3 exposure of hamsters during exer cise on F-2-isoprostane and antioxidant levels. We found that exposure to 1 .0 PPM O-3 during 1 h of exercise on a laddermill increased BALF levels of F-2-isoprostanes but had no effect on BALF neutrophils or on BALF and plasm a antioxidants. These results indicate that O-3 induces inflammation and bi omolecule oxidation in the lungs, whereas extracellular antioxidant levels are relatively unchanged.