For in vivo experiments rats were exposed to O3 either acutely (2 p.p.m., 4 to 8 hours) or chronically (0.8 p.p.m., 10 days). For in vitro experiments rat lung homogenate was exposed to 2 to 3 p.p.m. O3 for 30 minutes. It was observed that following in vivo acute exposures lung sulfhydryl (SH) levels decreased 18 per cent (p < 0.005) for protein fraction (PSH) and 41 per cent (p < 0.005) for nonprotein fraction (NPSH). In vitro exposure led to a 20 per cent (p < 0.01) loss for PSH and 95 per cent (p < 0.001) for NPSH. The results suggest that loss of lung SH is an important consequence of acute O3 stress. In addition, following in vivo acute exposures there was a 15 to 30 per cent (p < 0.05) depression in activities of several enzymes containing SH at the functional sites, viz., glucose-6-phosphate dehydrogenase (G6PD), glutathione reductase (GR), and cytochrome c reductases related to succinate and NADH. In contrast to preceding results, lung SH was maintained at normal levels under chronic O3 exposure, and there was a 32 per cent (p < 0.005) rise in G6PD activity and a 20 per cent (p < 0.05) increase in cytochrome c reductase activities. These results suggest that lungs of the chronically exposed animals acquired a metabolic adaptation. The maintenance of normal SH levels might be related to enhanced G6PD activity observed. Increased formation of NADPH by G6PD can lead to an establishment of normal sulfhydryl-disulfide equilibrium in lung by a series of enzymatic (e.g., disulfide reductase) and nonenzymatic (e.g., disulfide exchange) reactions.
|Original language||English (US)|
|Number of pages||8|
|Journal||The Journal of Laboratory and Clinical Medicine|
|State||Published - 1972|
ASJC Scopus subject areas
- Pathology and Forensic Medicine