CHRONIC INHALATION EXPOSURE TO OZONE AND NITRIC-ACID ELEVATES STRESS-INDUCIBLE HEAT-SHOCK PROTEIN-70 IN THE RAT LUNG

The ability of urban oxidant and acid air pollutants to induce heat sh ock proteins (HSPs) in the mammalian lung is not known. Such proteins are known to be correlated with environmental stress and pathophysiolo gical conditions. In this study, stress-inducible HSP 70 was assessed by slot-blotting in rat lungs (N = 10 per group) following inhalation exposures for 4 h per day, 3 days per week for 40 weeks to the followi ng pollutants: (a) purified air; (b) 0.15 ppm ozone (O-3); (c) 50 mu g /m(3) nitric acid (HNO3); or (d) a combination of both 0.15 ppm O-3 an d 50 mu g/m(3) HNO3. At 24 h following the last exposure, samples from the right apical lobe of the lung were obtained for either slot-blott ing or gel electrophoretic separation, subsequent protein immunoblotti ng, and chemiluminescence detection of HSP 70 levels. Experiments demo nstrate that stress-inducible HSP 70 was present constitutively in the control lungs and was separable from the constitutive form of HSP 70. Slot-blotting analysis demonstrate that the O-3 and HNO3 exposures al one produced significant elevations of HSP 70. Specifically, either O- 3 or HNO3 alone significantly elevated lung stress-inducible HSP 70 le vels by 277% and 221%, respectively, above control levels. The group e xposed to combined O-3 and HNO3 showed a 177% elevation in lung stress -inducible HSP 70 that was significantly greater than the group inhali ng purified air, but this effect was less than the effects of either p ollutant component alone. Moreover, all exposure groups were significa ntly different from one another. These results indicate that stress-in ducible HSP 70 in the rat lung is highly elevated after chronic inhala tion exposures to both O-3 and HNO3 when administered either alone or in combination within the range of urban ambient concentrations.