Adaptation to Ozone in Rats and Its Association with Ascorbic Acid in the Lung

• Published in: Fundamental and applied toxicology 1996-05, Vol.31 (1), p.56-64
• Main Authors: Wiester, M.J., Tepper, J.S., Winsett, D.W., Crissman, K.M., Richards, J.H., Costa, D.L.
• Format: Article
• Language: English
• Subjects: Adaptation, Physiological - drug effects; Animals; Antioxidants - metabolism; Ascorbic Acid - pharmacology; Biological and medical sciences; Bronchoalveolar Lavage Fluid - cytology; Chemical and industrial products toxicology. Toxic occupational diseases; Gas, fumes; Lung - drug effects; Lung - physiology; Male; Medical sciences; Oxidants, Photochemical - toxicity; Ozone - toxicity; Rats; Rats, Inbred F344; Respiratory Function Tests; Toxicology
• ISSN: 0272-0590; 1095-6832
• DOI: 10.1006/faat.1996.0075

Ozone (O3) adaptation is a well-known, but poorly understood phenomenon that has been demonstrated in humans and laboratory animals. This study examined pulmonary function and bronchoalveolar lavage fluid (BALF) parameters in O3-adapted F-344 rats to explore possible mechanisms of adaptation. Of particular interest was ascorbic acid (AA), an antioxidant reported to be protective against O3injury and found to be increased in O3-adapted rats. Adaptation was induced by exposure to 0.25 ppm O3, 12 hr/day for 6 or 14 weeks and evaluated with a challenge test, one that reexposed rats to 1.0 ppm O3and measured attenuation in the O3effect on frequency of breathing. Pulmonary function was assessed 1 day postexposure and adaptation and BALF were evaluated 1, 3, and 7 days postexposure. Results showed that forced vital capacity increased over time but decreased due to exposure and that the 14-week, O3-exposed rats had an increase in forced expiratory flow rate. All of the O3-exposed rats that were tested demonstrated adaptation on Postexposure Days 1, 3, and 7, but it was diminished on Day 7. Adaptation was also more pronounced in rats exposed for 14 weeks. Except for AA, BALF levels of total protein, potassium, lysozyme, uric acid, and α-tocopherol were unaffected by O3exposure. Lactic acid dehydrogenase, alkaline phosphatase, glucose-6-phosphate dehydrogenase, and total glutathione were also assayed but were always below detectable limits. Ascorbic acid concentrations were elevated on Days 1, 3, and 7, showing postexposure patterns similar to those found for adaptation. Significant correlation was found between AA concentration and the magnitude of adaptation (r= 0.91,p< 0.002). We conclude that AA may play an important role in mechanisms associated with O3adaptation in rats.