Author： Bermúdez Eliezer
Publisher： Informa Healthcare
ISSN： 1091-7691
Source： Inhalation Toxicology, Vol.13, Iss.1, 2001-01, pp. : 69-84
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Abstract
The toxic effects of nitrogen dioxide (NO2) and ozone (O3) are mediated through the formation of free radicals, which can cause DNA strand breaks. The present study demonstrates that exposure to NO2 and O3 causes a stimulation of poly (ADP-ribose) (poly ADPR) synthetase in alveolar macrophages of rats. Three-month-old male Sprague-Dawley rats, specific pathogen free, were exposed to either 1.2 ppm NO2 or 0.3 ppm O3 alone or a combination of these 2 oxidants continuously for 3 days. The control group was exposed to filtered room air. To evaluate whether exposure to these two oxidants (NO2 and O3) caused DNA damage to lung cells, the activity of poly ADPR synthetase was measured. Cellular DNA repair is dependent upon the formation of poly (ADP-ribose) polymerase, which is catalyzed by poly ADPR synthetase. Poly ADPR synthetase is known to be activated in response of DNA damage. The results showed that the enzyme activity was stimulated after exposure to O3 or exposure to NO2 + O3. Ozone exposure caused a 25% increase in the enzyme activity as compared to the control. Combined exposure to NO2 + O3 showed a 53% increase in the enzyme activity. These results were statistically significant as compared to the control and NO2 exposure groups. Other parameters such as total cell count, cell viability, and differential cell count were also determined. The stimulation of poly ADPR synthetase activity after O3 exposure or NO2 + O3 exposure reflects a response to lung cellular DNA repair, which may be used as an indicator for assessing DNA damage caused by oxidant injury.
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